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by Dr. Geoffrey Sher on December 1, 2015

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

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

Dear Patients,

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

– Geoffrey Sher, MD

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  • Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 25, 2017 reply

    Hi Jessica,

    I really do not know how far out I am booked. Call Julie at 800-780-7437 and ask her directly. Also, the consultation can be effected just as well, via Skype.

    Geoff Sher

  • Aziza Solomon - July 24, 2017 reply

    Also an extremely thing that I forgot to mention is: I have hyperhidrosis- which is an unclassified excessive sweating problem. I currently take glycopyrolate 2x a day/2mg dose. Will this drug cause interactions with any IUI medications? I already know stimulating myself with hormones will cause side effects of hot flashes that will only exacerbate my condition. Should I even try the IUI approach. I did inform my current doctor of this, but he has no insight as to how this would for me….

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 25, 2017 reply

    Hi Aziza,

    I have no knowledge of possible effects of this drug. I would need to (and would) research this since it would be the first time in a career of 35y that I will have been confronted by this issue.

    Geoff Sher

    Aziza Solomon - August 17, 2017 reply

    Thank you for your responses Dr. Sher! I appreciate it.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - August 18, 2017 reply

    You are very welcome!

    Geoff Sher

  • Aziza Solomon - July 24, 2017 reply

    Hi Dr. Sher,

    I am 35. In January I had 25 fibroids along with an ovarian cyst removed. As of June 2017, my HSG revealed a healthy uterine cavity with 4 more budding fibroids, a blocked tube, but a healthy ovary and an open tube on one side. The fertility clinic suggested that I start IUI rounds. I have never even tried to become pregnant naturally before, so I dont know of my chances in that aspect. Should I start with IUI or should I try the insemination at home?
    Any guidance you can provide will be helpful.

    Thanks,
    Aziza Solomon

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 25, 2017 reply

    Before even contemplating treatment of any type, a thorough evaluation of your uterus and pelvic anatomy is essential. This will likely at the very least require a laparoscopy and hysteroscopy. Then we should talk.

    Fibroids or leiomyomas are non-malignant muscle tumors that grow in the uterine wall. They can be found in about one out of every five (1:5) women >30Y of age. Fibroids are far more prevalent in African Americans and women and less frequent in other ethnic groups (i.e. Caucasians and Asians).
    Fibroids, enlarge and/or distort uterine configuration. They can produce symptoms such as heavy, painful and prolonged menstrual periods. Other symptoms include pain with intercourse, backache, severe abdominal pain when large fibroids run out of blood supply or when superficial fibroids on a stem (pedunculated) undergo twisting (torsion). Sometimes fibroids will protrude into the uterine cavity, cause severe cramping and bleeding and so irritate the uterine lining as to compromise embryo attachment (anatomical implantation dysfunction). Women with fibroids are also at greater risk of miscarriage, premature delivery, malposition of the baby (mandating cesarean delivery) and an increased risk of bleeding after birth (post-partum hemorrhage)
    Diagnosis can be made by one or more of the following symptoms/presentations: Symptomatology, pelvic examination pelvic ultrasound, hysterosalpingogram (HSG), sonohysterogram (HSN), CT-scan or MRI..
    Fibroids are classified as:
    • Submucosal: Here the fibroid grows just under the lining of the uterine cavity (mucosa) or protrudes into the uterine cavity. They might mold into the underlying uterine muscle (sessile) or be on a stalk (pedunculated). Submucosal fibroids can change the shape of the uterine cavity, irritate the lining and prevent implantation, cause miscarriage. These lesions must be removed in their entirety prior to undertaking embryo transfer, usually hysteroscopically. (see below)
    • Subserosal: – Here the tumors grow under the outer layer (serosa) of the uterus. These fibroids will not compromise implantation, but if they are large, causing severe pain, and especially if they are multiple, pedunculated and thus at risk of undergoing torsion (twisting) the3y should be removed, usually laparoscopically. (See below).
    • Intramural: – when the fibroids develop within the muscular wall of the uterus. This is the commonest presentation. Unless they are large and multiple and do not encroach on the uterine cavity, they can be left alone Surgical removal is usually by laparoscopy or laparotomy/abdominal open incision (See below)
    The uterus is composed of a thick layer of smooth muscle (myometrium) surrounding the endometrial lining into which the embryo implants and which serves to protect and nourish a growing pregnancy. These tumors are rarely malignant (see below). Fibroid tumors, even large ones, can occur without producing any symptoms at all.
    For the most part, only those fibroids that impinge upon the uterine (endometrial) cavity (submucosal) affect fertility. Exceptions include large fibroids in the muscle wall of the uterus (intramural) that can block the openings of the fallopian tubes as they enter the uterus, and where multiple fibroids cause abnormal uterine contraction patterns.
    In some cases multiple uterine fibroids may so deprive the uterine lining (endometrium) of blood flow, that the delivery of estrogen to the endometrium is curtailed to the point that the lining cannot thicken sufficient to support a pregnancy. This can result in early 1st trimester (prior to the 13th week of pregnancy) miscarriages. Large or multiple fibroids, by curtailing the ability of the uterus to stretch in order to accommodate the spatial needs of a rapidly growing pregnancy, may precipitate 2nd trimester (beyond the 13th week) miscarriages and/or trigger the onset of premature labor.
    Sizable fibroid tumors are usually easily identified by simple vaginal examination. However, even the smallest fibroid can be identified by transvaginal ultrasound. Sometimes it is difficult to tell if the fibroid is impinging on the uterine cavity. In such cases, a hysteroscopy (where a telescope like instrument, inserted via the vagina into the uterine cavity) or a sonohysterogram where injected fluid, distends the uterine cavity allowing for examination of its inner configuration can help distinguish between intramural and submucosal fibroids. CT scan and MRI can also be used to distinguish between fibroid tumors and another condition that also involves affects the uterine muscular wall, known as adenomyosis. This condition is characterized by endometrial tissue growing deeply into the uterine wall.. Given the often-diffuse nature of adenomyosis, it can be very difficult to remove surgically. This contrasts with fibroid tumors, which are well defined and are usually easily removed.
    Surgical Treatment: The mainstay for the treatment of fibroid tumors is surgical removal (myomectomy). Small, asymptomatic fibroids that do not impinge upon the endometrial cavity will usually not require treatment other than observation and vigilance. Large fibroids and submucosal fibroids should be removed prior to starting fertility treatments such as In Vitro Fertilization (IVF) in order to decrease the chance of implantation failure, miscarriage, pregnancy complications and premature labor. Intramural and subserosal fibroids are readily removable by laparoscopic resection or via an abdominal incision. The former allows for a more rapid convalescence and is ideal for the removal of small and accessible superficial fibroid tumors, while the latter approach is preferred for treating larger and less accessible fibroids.
    Myomectomy can affect fertility in several ways. If the endometrial cavity is entered during the surgery, there is a possibility of post adhesions forming within the uterine cavity. This should always be checked by the performance of a hysteroscopy or through a \sonohysterogram, prior to beginning fertility treatment. Because myomectomy can be bloody, there is a high likelihood of post-operative abdominal adhesion formation, which could bind down or encase the ovaries, preventing the release of the eggs, or block the ends of the fallopian tubes. For this reason, it is important that myomectomies be formed only by accomplished surgeons, who are familiar with techniques to limit blood loss and prevent adhesion formation.
    Regardless of whether the laparoscopic or abdominal approach is employed, adequate closure of the uterine wall is essential in order to reduce the subsequent risk of uterine rupture during pregnancy or labor. This is one of the main arguments used against the use of laparoscopic removal of large, multiple or remotely situated fibroids. While laparoscopic myomectomy requires but a few days (at most) for post-operative convalescence, abdominal myomectomy usually requires 6-8 weeks of recovery time. When myomectomy necessitates or results in the uterine cavity being entered (purposefully or inadvertently), it should always be followed up with a “2nd look” hysteroscopy to rule out scar tissue formation, which occurs frequently in the presence of submucosal fibroids.
    Uterine polyps (and in some cases, also submucosal fibroids), can usually be removed hysteroscopically (through the vagina). This eliminates the need for abdominal surgery and greatly reduces the recovery time. Hysteroscopic surgery is only useful if the majority of the fibroid protrudes into the endometrial cavity, ensuring that the tumor defect will not be too large. This surgery is often done under laparoscopic guidance, to reduce the risk of uterine perforation. After hysteroscopic surgery it is often advisable to prescribe cyclical hormonal therapy for a few months to encourage regeneration of the endometrial lining over the area of tumor defect and healing of the uterine muscle. A 2nd look hysteroscopy should be performed a few months later in all cases, to rule out scar tissue formation even if it means delaying or deferring the initiation of definitive fertility treatment.
    Medical Treatment: The growth of fibroid tumors is estrogen-dependent. Thus when a woman enters menopause and stops making female hormones, fibroids tend to shrink in size on their own. Conditions that mimic menopause can also reduce the size of fibroid tumors. The most common of theses treatment is with a medication such as leuprolide acetate (Lupron), which shuts off the communication of the brain with the ovaries, preventing hormone production. However, this type of medication can only be taken for a limited period (usually 6 months) and once the medication is stopped the fibroids will usually regain their original size within a few months. The medication is therefore only a “temporary fix,” used mostly to decrease the size of large fibroids in order to make their ultimate surgical removal easier, or to help a woman bridge the gap until spontaneous menopause sets in. For the majority of women there is no major benefit from Lupron therapy prior to surgery.
    Embolization of Fibroid Tumors: Myomectomy always carries the small (although infrequent) risk that severe, uncontrollable intra-operative bleeding could require the performance of a hysterectomy (complete removal of the uterus) as a life saving measure. Moreover, some women are poor candidates for surgery. This is where a new procedure known as embolization comes in. Embolization is a procedure in which small particles are injected into the arteries of the uterus under radiological guidance to shut off the blood supply to the fibroids, in the hope that they will “shrink” and perhaps, even disappear.
    Embolization is relatively new to the field of gynecology and little is known about its potential effects on future fertility. We are concerned that in the process of shutting off the blood supply to the uterus, it will permanently so reduce endometrial blood flow, as to compromise embryo implantation. For this reason, I do not currently recommend this therapy for women who still wish to conceive and carry a baby in their uterus. At present, it seems best suited for symptomatic women who are finished with their childbearing or who are planning to use a gestational surrogate.
    Malignant Change in Fibroid Tumors: Fibroids rarely undergo malignant change. The reported incidence is less than 1 in 2000 cases. Fibroids usually grow very slowly (over a number of years). However, when growth occurs rapidly over a month or two, especially in older women who have large fibroids, it should raise the suspicion of this very rare but extremely serious complication.

    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • IVF Failure and Implantation Dysfunction:
    • The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
    • Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
    • Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
    • Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
    • Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
    • Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
    • Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
    • Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
    • Endometrial Thickness, Uterine Pathology and Immunologic Factors
    • 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
    • Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
    • A personalized, stepwise approach to IVF
    • The Basic Infertility Work-Up
    • Uterine Fibroids and Fertility
    • Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & Con’s!
    • IUI-Reflecting upon its Use and Misuse: Time for a Serious “Reality Check”.
    • Micro-IVF: Often Preferable to Ovarian Stimulation with or Without IUI
    • Induction of Ovulation With Clomiphene Citrate: Mode of Action, Indications, Benefits, Limitations and Contraindications for its ue
    • Clomiphene Induction of Ovulation: Its Use and Misuse!
    If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher

  • Ananya - July 24, 2017 reply

    I am 35 and my husband will be 36 this year. We have sperm motility issues. We have had one IVF (ICSI) cycle where one early morula (fragmented), and two early blastocysts (highly fragmented – graded poor) were transferred and the cycle failed. We moved on to do a second cycle for which we transferred one early morula (>40% fragmented, graded poor) and the cycle failed again. However from this second cycle, we have two frozen hatching blastocysts (graded excellent quality) that we plan to transfer later this month. I just had a hysteroscopy done last week and the doctor said that the uterus looks great. Could the reason for the early failures be only embryo quality? How do you see our chances for this FET cycle? We plan to transfer just one frozen blast.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 24, 2017 reply

    It likely is an embryo quality issue, which although it can be due to sperm quality, is more likely a stimulation issue.

    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
    • Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
    • The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
    • Blastocyst Embryo Transfers Should be the Standard of Care in IVF
    • Why did my IVF Fail
    • 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 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
    • 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.
    • Male Infertility
    • Hormonal Treatment of Male Infertility
    • Antisperm Antibodies, Infertility and the Role of IVF with Intracytoplasmic Sperm Injection (ICSI)
    • Testicular Sperm Extraction (TESE) and Testicular Sperm Aspiration (TESA): Surgical Approaches for Accessing Sperm from men who have no sperm in their ejaculates (Azoospermia)
    • Varicocele and Male Infertility: When and how should it be treated?
    • The Sperm Chromatin Structure Assay (SCSA): A Measure of the Potential of Sperm to Help Propagate a Viable Pregnancy
    If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com.

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

    Ananya - July 24, 2017 reply

    Thank you Dr. Sher. Just another question, what do you feel are our chances with this FET given that this is the first time we have frozen blasts with good quality? Also missed mentioning earlier, we used donor sperm for the second cycle. What would your suggestions be for the FET medication ?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 25, 2017 reply

    Anannya,

    I cannot inset myself into your treatment. I also cannot offer statistics when I do not have any details on your case and have no knowledge of the clinic you are attending.

    I wish you good luck but if you do not succeeed and are not in the midst of treatment, I would be happy to interact with you at your request.

    Good luck!

    Geoff Sher

  • Jessica milz - July 24, 2017 reply

    hello dr. Sher i also forgot to mention what’s the success rate with someone with pocos and hypothyroidisum I just turned 34 and I feel like I need to get it done now or at least try to do what I can to get Ivf done never done it before but I hope it will work thank u for taking the time to read and respond to message very much appreatiate

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 24, 2017 reply

    Thanks for communicating.

    Herewith a few articles relating to 1) an under-active thyroid and its link to infertility and of]ten also repeated failed IVF and 2) to PCOS.

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

    2)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.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.

    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
    • The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
    • Blastocyst Embryo Transfers Should be the Standard of Care in IVF
    • IVF: How Many Attempts should be considered before Stopping?
    • “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
    • IVF Failure and Implantation Dysfunction:
    • The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
    • Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
    • Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
    • Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
    • Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
    • Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
    • Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
    • Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
    • Endometrial Thickness, Uterine Pathology and Immunologic Factors
    • Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
    • A personalized, stepwise approach to IVF
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    • The Role of Nutritional Supplements in Preparing for IVF

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

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

    Geoffrey Sher MD

  • Cynthia - July 23, 2017 reply

    Hello Dr. Sher,
    My husband and I have been trying for over a year before we looked for answered. I had stage 4 endometriosis discovered June 2016. I had a laparoscopy done June 2016 by my new OBGYN. I had a cyst removed and some fibrosis. My doctor cleared as much scar tissue as possible left from the endometriosis. We tried Clomid for 3 months afterward and still nothing. Jan 2017 I did my IVF retrieval. 18 eggs retrieve, 8 matured and tested with PGS 7 are genetically perfect. I was hyper stimulated and so my first implantation was March 1, 2017. My beta was strong but unfortunately miscarriage 2 weeks later. Did a hysteroscopy April 2017 by my RE to remove a small septum, clear up the miscarriage and drain a chocolate cyst I have in my left ovary. Start acupuncture to help the blood flow in May per my own research. Second implantation June 13, 2017, with a perfect lining and perfect levels per our doctor. Eight days later beta came back at 8. I am 33 and my husband is 38. Our embryos are healthy and strong. We are lost we don’t know what to do and our doctor just says these things happen. Do you have any insight?

    Thank you,
    Cynthia

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 24, 2017 reply

    Hi Cynthia,

    From what you are telling me, you clearly have an implantation dysfunction which given your endometriosis is very likely to be immunologic in nature.

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

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

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

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

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

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

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

    1. Controlled Ovulation stimulation (COS) with/without intrauterine insemination (IUI): Toxins in the peritoneal secretions of women with endometriosis exert a negative effect on fertilization potential regardless of how sperm reaches the fallopian tubes. This helps explain why COS with or without IUI will usually not improve the chances of pregnancy (over no treatment at all) in women with endometriosis. IVF is the only way by which to bypass this problem.
    2. Laparoscopy or Laparotomy Surgery aimed at restoring the anatomical integrity of the fallopian tubes does not counter the negative influence of toxic peritoneal factors that inherently reduce the chances of conception in women with endometriosis four to six fold. Nor does it address the immunologic implantation dysfunction (IID) commonly associated with this condition. Pelvic surgery is relatively contraindicated for the treatment of infertility associated with endometriosis, when the woman is more than 35 years of age. With the pre-menopause approaching, such women do not have the time to waste on such less efficacious alternatives. In contrast, younger women who have time on their side might consider surgery as a viable option. Approximately 30 -40 percent of women under 35 years of age with endometriosis will conceive with in two to three years following corrective pelvic surgery.
    3. Sclerotherapy for ovarian endometriomas (“chocolate” cysts). About 15 years ago I introduced “sclerotherapy”, a relatively non-invasive, safe and effective outpatient method to permanently eliminate endometriomas without surgery being required. Sclerotherapy for ovarian endometriomas involves needle aspiration of the liquid content of the endometriotic cyst, followed by the injection of 5% tetracycline into the cyst cavity. Treatment results in disappearance of the lesion within 6-8 weeks, in more than 75% of cases so treated. Ovarian sclerotherapy can be performed under local anesthesia or under general anesthesia. It has the advantage of being an ambulatory office- based procedure, at low cost, with a low incidence of significant post-procedural pain or complications and the avoidance of the need for laparoscopy or laparotomy
    4. The role of selective immunotherapy More than half of women who have endometriosis harbor antiphospholipid antibodies (APA) that can compromise development of the embryo’s root system (trophoblast). In addition and far more serious, is the fact that in about one third of cases endometriosis, regardless of its severity is associated with NKa and cytotoxic uterine lymphocytes (CTL) which can seriously jeopardize implantation. This immunologic implantation dysfunction (IID) is diagnosed by testing the woman’s blood for APA, for NKa (using the K-562 target cell test or by endometrial biopsy for cytokine activity) and, for CTL (by a blood immunophenotype). Activated NK cells attack the invading trophoblast cells (developing “root system” of the embryo/early conceptus) as soon as it tries to gain attachment to the uterine wall. In most cases, this results in rejection of the embryo even before the pregnancy is diagnosed and sometimes, in a chemical pregnancy or an early miscarriage. . As such, many women with endometriosis, rather than being infertile, in the strict sense of the word, often actually experience repeated undetected “mini-miscarriages”.

    Women who harbor APA’s often experience improved IVF birth rates when heparinoids (Clexane/Lovenox) are administered from the onset of ovarian stimulation with gonadotropins until the 10th week of pregnancy. NKa is treated with a combination of Intralipid (IL) and steroid therapy: Intralipid (IL) is a solution of small lipid droplets suspended in water. When administered intravenously, IL provides essential fatty acids, linoleic acid (LA), an omega-6 fatty acid, alpha-linolenic acid (ALA), an omega-3 fatty acid.IL is made up of 20% soybean oil/fatty acids (comprising linoleic acid, oleic acid, palmitic acid, linolenic acid and stearic acid) , 1.2% egg yolk phospholipids (1.2%), glycerin (2.25%) and water (76.5%).IL exerts a modulating effect on certain immune cellular mechanisms largely by down-regulating NKa.

    The therapeutic effect of IL/steroid therapy is likely due to an ability to suppress pro-inflammatory cellular (Type-1) cytokines such as interferon gamma and TNF-alpha. IL/steroids down-regulates NKa within 2-3 weeks of treatment the vast majority of women experiencing immunologic implantation dysfunction. In this regard IL is just as effective as Intravenous Gamma globulin (IVIg) but at a fraction of the cost and with a far lower incidence of side-effects. Its effect lasts for 4-9 weeks when administered in early pregnancy.
    5. The role of IVF: The toxic pelvic environment caused by endometriosis, profoundly reduces natural fertilization potential. As a result normally ovulating infertile women with endometriosis and patent Fallopian tubes are much less likely to conceive naturally, or by using fertility agents alone (with or without intrauterine (IUI) insemination. The only effective way to bypass this adverse pelvic environment is through IVF. I am not suggesting here that all women who have endometriosis require IVF! Rather, I am saying that in cases where the condition is further compromised by an IID associated with NKa and/or for older women(over 35y) who have diminished ovarian reserve (DOR) where time is of the essence, it is my opinion that IVF is the treatment of choice.

    Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
    a. A“ thin uterine lining”
    b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
    c. Immunologic implantation dysfunction (IID)
    d. Endocrine/molecular endometrial receptivity issues
    Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.

    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
    • The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
    • Blastocyst Embryo Transfers Should be the Standard of Care in IVF
    • IVF: How Many Attempts should be considered before Stopping?
    • “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
    • IVF Failure and Implantation Dysfunction:
    • The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
    • Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
    • Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
    • Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
    • Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
    • Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
    • Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
    • Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
    • Endometrial Thickness, Uterine Pathology and Immunologic Factors
    • Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
    • A personalized, stepwise approach to IVF
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    • The Role of Nutritional Supplements in Preparing for IVF.•
    . Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF
    • Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
    • Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
    • Treating Ovarian Endometriomas with Sclerotherapy.
    • Induction of Ovulation With Clomiphene Citrate: Mode of Action, Indications, Benefits, Limitations and Contraindications for its ue
    • Clomiphene Induction of Ovulation: Its Use and Misuse!

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

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

    Geoffrey Sher MD

  • Crystal Helton - July 23, 2017 reply

    Dr sher,
    I realized that I had inadvertently taken 2ml instead of .2ml of delestrogen for my upcoming fresh embryo transfer scheduled for julu 30th. How likely do you think it is that my transfer will be cancelled due to this huge mistake? Thank you

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 23, 2017 reply

    It is not ideal but I doubt the transfer would be canceled.

    Good luck!

    Geoff Sher

  • Kat - July 22, 2017 reply

    Dr. Sher,
    I am 41 y/o and my 2nd ER (per your agonist/antagonist protocol by my RE in So. Cal, who uses your protocols) resulted in 16 eggs, 15 mature, 13 fertilized and 2 Day 6 blasts and 2 Day 7 blasts. One Day 6 6BA blast tested as PGS normal. For my age, I felt these results were average, statistically-speaking. I had an HSG test done within 12 months prior to the FET, and had a fibroid removed 8 months prior to the FET. I underwent immune and thrombo panel testing as a precaution (per my request, even though I had no history of previous pregnancies and/or miscarriages), which revealed immune and blood clotting issues, although no thyroid or NK killer cell issues), so addressed those issues with BA, Lovenox and Metanx. Prior to the FET, my lining measured at 12 mm with triple stripe. My first beta was negative (less than 2), so the embryo did not implant. Can you opine on whether this was just “bad luck” or whether there is anything I or my RE could do differently this next time around? I have no more embryos, so would need to do another ER and FET.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 23, 2017 reply

    Hi Kat!

    Day 7 blastocysts are in my opinion VERY unlikely to be “competent” so you will need to go again. However, before doing so, we really should talk.

    I suggest you call Julie (my concierge) at 800-780-7437 or email her at http://www.julied@sherivf.com) she will set up a Skype consultation with me so we can talk.

    Geoff Sher

    Kat - July 23, 2017 reply

    The blast we transferred was a Day 6 PGS tested normal embryo, not a Day 7. Does this change your response?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 23, 2017 reply

    A day-6 PGS-normal blastocyst has a good chance!

    Geoff Sher

    Kat - July 23, 2017

    But our Day 6 z PGS normal blast didn’t implant. Was it just “bad luck”, considering the other factors I mentioned? I’m worried that if I or my RE don’t do anything differently (but not sure if anything could even be done differently?) the next one won’t implant either. Or perhaps that is just the odds I need to accept?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 24, 2017

    It sounds like an implantation dysfunction, possibly immunologic in origin. We should talk.

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

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

    Geoffrey S

  • Sofy - July 22, 2017 reply

    Hi Dr Sher, is AFC directly related to AMH?
    My AFC was 10 in 2014 and is still 10 now. I had my AMH done this year and it is 5.7 pmol. Is it then likely it would have also been this number in 2014 since my AFC has not changed?

    Thank you.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 22, 2017 reply

    The low AMH,if accurately measured (and I would repeat it to be sure), suggests diminished ovarian reserve and that in spite of your AFC being 10 (which commonly is an inaccurate measurement), suggests that there will likely be a problem with response to ovarian stimulation. In my opinion, this demands a robust, FSHr-dominant , strategically chosen protocol for ovarian stimulation.

    In my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”.
    Women who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.

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

    Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.

    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
    • A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
    • Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
    • Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
    • Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
    • The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
    • Blastocyst Embryo Transfers should be the Standard of Care in IVF
    • Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
    • Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
    • Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
    • Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
    • Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
    • Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
    • PGS in IVF: Are Some Chromosomally Abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
    • PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
    • Traveling for IVF from Out of State/Country–
    • A personalized, stepwise approach to IVF
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    • The Role of Nutritional Supplements in Preparing for IVF
    • Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
    • IVF Egg Donation: A Comprehensive Overview

    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • Vanessa - July 21, 2017 reply

    Hi Dr.Sher,

    I just got my fertility report for my 11 embryos and only 3 blastocysts made it to freeze for day 5 but I was told that the other 7 were between 7-8 cells and could still catch up over the weekend. I’m only 32 and I’m doing PGS testing. With the embryos only being 7-8 cells on day 5 do you think they’ll develop into blastocysts by this weekend for freeze and PGS? They’re going to call me Monday with the final result but I’m going crazy over here!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 22, 2017 reply

    Unfortunately, it is unlikely that these embryos will make blastocyst by day day 6. It could be a matter of reviewing and revising your protocol for ovarian stimulation.

    Here is the protocol I advise for women, <40Y who have adequate ovarian reserve.
    My advice is to use a long pituitary down regulation protocol starting on a BCP, and overlapping it with Lupron 10U daily for three (3) days and then stopping the BCP but continuing on Lupron 10u daily (in my opinion 20U daily is too much) and await a period (which should ensue within 5-7 days of stopping the BCP). At that point an US examination is done along with a baseline measurement of blood estradiol to exclude a functional ovarian cyst and simultaneously, the Lupron dosage is reduced to 5U daily to be continued until the hCG (10,000u) trigger. An FSH-dominant gonadotropin such as Follistim, Puregon or Gonal-f daily is started with the period for 2 days and then the gonadotropin dosage is reduced and a small amount of menotropin (Menopur---no more than 75U daily) is added. This is continued until US and blood estradiol levels indicate that the hCG trigger be given, whereupon an ER is done 36h later. I personally would advise against using Lupron in “flare protocol” arrangement (where the Lupron commences with the onset of gonadotropin administration.
    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation (COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas
    • Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
    • A personalized, stepwise approach to IVF
    • “Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • Joanna Troccoli - July 21, 2017 reply

    What is the lowest you have seen an initial beta be at 7 days past a 5 day transfer that resulted in a healthy baby?
    I’ve read anything below 5 is negative and above 25 is positive but what about that in between stage? Does that always mean miscarriage?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 21, 2017 reply

    I have seen cases where even with an initial hCG level of zero, a late implantation has resulted in a viable pregnancy. However, I like the 1st beta to be >10MIU/ml.

    Geoff Sher

    Joanna Troccoli - July 21, 2017 reply

    Thank you … my first beta at 7 days past a 5 day transfer was a 6.7…. guess all I can do is wait for 2 test

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 22, 2017 reply

    Good luck!

    Geoff Sher

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 22, 2017 reply

    Good luck

    Geoff Sher

  • Paulina - July 21, 2017 reply

    Dr. Sher,
    How often do you recommend completion of a saline ultrasound/hysteroscopy to check for fibroids, polyps and scar tissue? We have had one doctor that recommends hysteroscopy every 6 months and another that recommends only saline ultrasound every 12 months. What do you/your clinic recommend?
    Thank you,
    Paulina

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 21, 2017 reply

    I believe this should be done a year before ET.

    Geoff Sher

  • Sarah - July 21, 2017 reply

    Hi Dr Sher,
    Is there a minimum and maximum
    amount of days you should be on the BCP ahead of an IVF cycle? I have no DOR and results appear normal for my age of 35/36 yo.
    Thanks – have a good weekend

    Sarah - July 21, 2017 reply

    Ps A natural cycle is not possible due to travel arrangements

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 21, 2017 reply

    I do not believe in the efficacy or advantage of NC-IVF.

    Geoff Sher

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 21, 2017 reply

    In my opinion …at least 10 days, but no maximum, provided an overlap down-regulation protocol is used.

    Geoff Sher

    Sarah - July 21, 2017 reply

    No down regulation protocol seems to be used at my clinic. I plan to be on the BCP for 17 days, then a break, then 18 days then a break to start stims – do you think this is okay? My alternative is to be on it 42 days straight before starting stims – do you have any views? … thanks

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 22, 2017 reply

    Very respectfully,

    I believe that fertility doctors have different approaches. I personally not used this approach.

    Geoff Sher

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 22, 2017 reply

    Very respectfully, opinions differ. I personally would not use this approach.

    Here is the protocol I advise for women, <40Y who have adequate ovarian reserve.
    My advice is to use a long pituitary down regulation protocol starting on a BCP, and overlapping it with Lupron 10U daily for three (3) days and then stopping the BCP but continuing on Lupron 10u daily (in my opinion 20U daily is too much) and await a period (which should ensue within 5-7 days of stopping the BCP). At that point an US examination is done along with a baseline measurement of blood estradiol to exclude a functional ovarian cyst and simultaneously, the Lupron dosage is reduced to 5U daily to be continued until the hCG (10,000u) trigger. An FSH-dominant gonadotropin such as Follistim, Puregon or Gonal-f daily is started with the period for 2 days and then the gonadotropin dosage is reduced and a small amount of menotropin (Menopur---no more than 75U daily) is added. This is continued until US and blood estradiol levels indicate that the hCG trigger be given, whereupon an ER is done 36h later. I personally would advise against using Lupron in “flare protocol” arrangement (where the Lupron commences with the onset of gonadotropin administration.
    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation (COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas
    • Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
    • A personalized, stepwise approach to IVF
    • “Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • Paulina - July 20, 2017 reply

    Dr Sher,
    Over the past 12 months, I have undergone 4 IVF cycles, one transfer and two ERA’s. In both ERA cycles and the transfer cycle I started taking estrace early in the cycle to help build my uterine lining. It has been almost a year since I had a saline ultrasound and hysteroscopy completed. Now I am preparing for another transfer with only 3 PGS normal embryos remaining (from a donor) after failing the first transfer. My concern is that the significant estrogen intake since the last testing will result in polyps or fibroids that will decrease chances of pregnancy. Knowing that I have a limited number of embryos, what do you recommend I do? Should I hold off on the transfer until I have another saline ultrasound, or proceed with transfer (I already started transfer protocol and lining looks good)? Is it true that taking estrogen from IVF can promote fibroids/polyps that may decrease chances of pregnancy?
    Thanks so much for your help!
    Paulina

    Paulina - July 21, 2017 reply

    As a follow up to my prior question, if your answer is YES to having another saline ultrasound, do you think it is ok to have the saline ultrasound completed 13 days before the transfer (during the transfer cycle)?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 21, 2017 reply

    If a HSN is done, it should be done in a preceding cycle go the one where an FET is done.

    Geoff Sher

    Paulina - July 21, 2017 reply

    Thank you! Would you recommend a hysteroscopy or a saline ultrasound?
    I previously had a hysteroscopy almost a year ago and also a saline ultrasound 1.5 years ago (different doctors). Both came back clear.
    Thanks again,
    Paulina

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 21, 2017

    Respectfully,

    If the hysteroscopy was normal a year ago, in my opinion, unless something new has come up to indicate a repeat, I wold not!

    Geoff Sher

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 21, 2017 reply

    In do not believe that appropriately prescribed hormone therapy will promote polyp growth.

    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?. In your case, the fact that embryo quality was confirmed renders this more likely to be an implantation issue.
    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:

    Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
    a. A“ thin uterine lining”
    b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
    c. Immunologic implantation dysfunction (IID)
    d. Endocrine/molecular endometrial receptivity issues
    Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.

    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
    • The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
    • Blastocyst Embryo Transfers Should be the Standard of Care in IVF
    • IVF: How Many Attempts should be considered before Stopping?
    • “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
    • IVF Failure and Implantation Dysfunction:
    • The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
    • Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
    • Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
    • Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
    • Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
    • Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
    • Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
    • Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
    • Endometrial Thickness, Uterine Pathology and Immunologic Factors
    • Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
    • A personalized, stepwise approach to IVF
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    • The Role of Nutritional Supplements in Preparing for IVF
    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • Anna - July 20, 2017 reply

    Hello,
    I am 34 years old and had 5 failed IUI attempts. Based on my fertility work up my RE said I had no fertility issues. Nevertheless, I did not continue with IUI I decided to do IVF. I recently completed my first cycle and I’m not too familiar with protocols used. I only started to look into protocol types when I learned that the result of my cycle was not what I expected. The doctor was able to retrieve 6 eggs, 2 of which fertilized by ICSI. One embryo was frozen at 3 days and the second one I wanted to push to day 5. Both are great quality apparently although I don’t know very much about grading. My RE decided I should do a FET as my progesterone was too high. I am currently taking medication in preparation for the transfer which will be in 5 days. My lining is 12 mm and no concerns are seen there. My questions are is there anything I can do to prepare for this transfer? Anything I can do after to increase the success of the cycle? Or will
    It ultimately depend on my embryo quality if everything else seems normal. Any advice is appreciated. I guess I’m
    Concerned that if I only have 2 embryos from the Ivf cycle chances are they are poor quality? Or is that not the case necessarily. Thank you

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 21, 2017 reply

    Respectfully, this is not an optimal response. I suggest that the protocol used for ovarian stimulation should be carefully reviewed and revised.

    Here is the protocol I advise for women, <40Y who have adequate ovarian reserve.
    My advice is to use a long pituitary down regulation protocol starting on a BCP, and overlapping it with Lupron 10U daily for three (3) days and then stopping the BCP but continuing on Lupron 10u daily (in my opinion 20U daily is too much) and await a period (which should ensue within 5-7 days of stopping the BCP). At that point an US examination is done along with a baseline measurement of blood estradiol to exclude a functional ovarian cyst and simultaneously, the Lupron dosage is reduced to 5U daily to be continued until the hCG (10,000u) trigger. An FSH-dominant gonadotropin such as Follistim, Puregon or Gonal-f daily is started with the period for 2 days and then the gonadotropin dosage is reduced and a small amount of menotropin (Menopur---no more than 75U daily) is added. This is continued until US and blood estradiol levels indicate that the hCG trigger be given, whereupon an ER is done 36h later. I personally would advise against using Lupron in “flare protocol” arrangement (where the Lupron commences with the onset of gonadotropin administration.
    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation (COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas
    • Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
    • A personalized, stepwise approach to IVF
    • “Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

    Anna - July 21, 2017 reply

    So do you think I’m wasting my time going ahead with the frozen embryo transfer? I do have 2 embryos.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 21, 2017 reply

    Frankly that decision is one to be made between you and your treating RE.

    Geoff Sher

  • Julia - July 20, 2017 reply

    I have just had a donor egg cycle. The donor was 31, AMH 10. She did not respond will to stimulation and produced 4 eggs of which only 3 fertilised normally. All 3 turned into hatching blastocysts and one was transferred. I got a positive urine test 10dpo. I used a clearblue digital test and it indicated 1-2 weeks pregnant up until the afternoon of 14dpo where it changed to 2-3 weeks pregnant. 17dpo the test showed 1-2 weeks pregnant again so I took a blood test which has come in at only 65.
    I had a hysteroscopy 3 months prior to transfer.
    It looks like this pregnancy is failing and I’m trying to understand why. The donor did not produce many eggs – should this have been known from her screening? What is the most likely reason for the embryo to fail? If it was egg quality then why did it implant?
    I have 2 frozen blastocycsts and I am emotional that these will also fail.
    Any insights would be appreciated..
    J

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 20, 2017 reply

    Perhaps the protocol used for ovarian stimulation needs to be adjusted next time round

    Here is the protocol I advise for women, <40Y who have adequate ovarian reserve.
    My advice is to use a long pituitary down regulation protocol starting on a BCP, and overlapping it with Lupron 10U daily for three (3) days and then stopping the BCP but continuing on Lupron 10u daily (in my opinion 20U daily is too much) and await a period (which should ensue within 5-7 days of stopping the BCP). At that point an US examination is done along with a baseline measurement of blood estradiol to exclude a functional ovarian cyst and simultaneously, the Lupron dosage is reduced to 5U daily to be continued until the hCG (10,000u) trigger. An FSH-dominant gonadotropin such as Follistim, Puregon or Gonal-f daily is started with the period for 2 days and then the gonadotropin dosage is reduced and a small amount of menotropin (Menopur---no more than 75U daily) is added. This is continued until US and blood estradiol levels indicate that the hCG trigger be given, whereupon an ER is done 36h later. I personally would advise against using Lupron in “flare protocol” arrangement (where the Lupron commences with the onset of gonadotropin administration.
    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation (COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas
    • Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
    • A personalized, stepwise approach to IVF
    • “Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • Jessica - July 20, 2017 reply

    Good morning Dr.Sher! I saw a documentary about your practice on Netflix. It was very touching and connceted to me in some way. I’m currently going through infertility treatments with Kaiser Permanente Reproductive Endocrinology. I’ve done 3 prior cycles with clomid all chemical pregnancies with a prior doctor. With Kaiser I’ve donde 2 cycles with clomid+trigger+endometrin inserts and one with injectibles (menopu+trigger+PIO) and also all ended in chemical pregnancies. I currently take prenantals, fertileaid,ovaboost,and dhea. I’m interested in the Immunologic Implantation Dysfunction treatment. We live in the Orange County area. Thank You Very Much!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 20, 2017 reply

    Implantation dysfunction is a very common (often overlooked) cause of “unexplained” infertility and of treatment 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 failure in such women. Common sense dictates that implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
    a. A“ thin uterine lining”
    b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
    c. Immunologic implantation dysfunction (IID)
    d. Endocrine/molecular endometrial receptivity issues
    Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.

    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
    • The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
    • Blastocyst Embryo Transfers Should be the Standard of Care in IVF
    • IVF: How Many Attempts should be considered before Stopping?
    • “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
    • IVF Failure and Implantation Dysfunction:
    • The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
    • Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
    • Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
    • Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
    • Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
    • Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
    • Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
    • Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
    • Endometrial Thickness, Uterine Pathology and Immunologic Factors
    • Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
    • A personalized, stepwise approach to IVF
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    • The Role of Nutritional Supplements in Preparing for IVF
    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • Amelie - July 20, 2017 reply

    Dear Dr. Sher,
    I am 40, with DOR, undergoing 5th IVF attempt (Day 9). I know that you advise to use a Pituitary down-Regulation Protocol in cases like mine, but my doctor decided to use the microflare protocol. I only have 3 antral follicles in this cycle.

    My hormones on Day 2:
    FSH 19.53 IU/l,
    LH 10.52 IU/l
    Estradiol 25.84 pg/mL
    Progesterone 0.16 ng/mL

    Day 6, lead follicle 10 mm
    LH 12.25 IU/l
    Estradiol 339.14 pg/mL
    Progesterone 0.29 ng/mL

    Day 8, lead follicle 13 mm
    LH 7.17 IU/l
    Estradiol 744.48 pg/mL
    Progesterone 0.41 ng/mL

    1. Is it possible that I have had an LH peak between Day 2 and Day 6 (value has slightly increased, instead of decreasing) or is it too early in the cycle for that? Can I safely assume that LH is decreasing as it should?

    2. Is it possible that my FSH and LH have increased because of birth control pills taken the previous month (I took them for 19 days and have never been on BCP in my life)? So far, my highest FSH has been 12.7 and LH goes as high as 5-6. Will this ruin my eggs in this cycle?

    3. Do I have any chance of competent eggs with FSH as high as 19.5? Would you recommend cancelling this cycle?

    I am stimulated with Decapeptyl 0.1 on Day 2 and Decapeptyl 0.1 and FSHr of 300U each subsequent day.

    I would really appreciate your opinion, because this is probably going to be my last attempt.
    Thank you and best regards!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 20, 2017 reply

    1. Is it possible that I have had an LH peak between Day 2 and Day 6 (value has slightly increased, instead of decreasing) or is it too early in the cycle for that? Can I safely assume that LH is decreasing as it should?

    A: It is likely that the flare effect of the agonist caused the increase in LH early on but now it seems to be coming down. I cannot comment on the effect of the initial rise, because I just do not know. What would be telling is what happens with the E2 as the stimulation proceeds and egg/embryo quality in the final analysis.

    2. Is it possible that my FSH and LH have increased because of birth control pills taken the previous month (I took them for 19 days and have never been on BCP in my life)? So far, my highest FSH has been 12.7 and LH goes as high as 5-6. Will this ruin my eggs in this cycle?

    A: In my opinion ..no!

    3. Do I have any chance of competent eggs with FSH as high as 19.5? Would you recommend cancelling this cycle?

    A: At this stage I would simply proceed as planned

    Good luck!

    Geoff her

  • Sharon Howard - July 20, 2017 reply

    Dear Dr Sher, Sir I am not sure if you might wish to assist me by a reply but it would be so very appreciated. Very briefly not sure my clinic hasn’t missed something but they get a bit defensive if we question: Me 32yrs, husband 35. 2yrs TTC, so far diagnosis unexplained. Good AMH, apparently good semen analysis, 33 day (approx.) cycle, ovulate ok (so they say) all other levels ok. Straight to first fresh cycle as nothing else suggested, we have put off our first home due to this expense, stims show roughly 16 good sized follicles (plus more smaller) then -devastatingly only 4 oocytes retrieved! No explanation just nothing. Anyway, only 1 fertilised. 5 day grade 1-2 embryo transferred, progesterone pessaries, result looking negative, HCG only 36 at first beta bloods. Understand first time success would be rare but the low egg retrieval number against so many good follicles makes me question the protocol, trigger shot, maybe even the expertise of the person aspirating. Is it reasonable to question this? We are healthy non smokers, good BMI, try very hard to do all the right things. Are there specific questions we should ask when we meet to regroup? We are not American but found you accidentally, you sound kind and we are lost. Thank you even if you only read this.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 20, 2017 reply

    All that matters here is ultimate outcome. Hopefully all will work out. That having been said, I would need to know much more about your case to advise regarding the protocol used for stimulation…but that can be addressed if this cycle is not successful.

    Here is the protocol I advise for women, <40Y who have adequate ovarian reserve.
    My advice is to use a long pituitary down regulation protocol starting on a BCP, and overlapping it with Lupron 10U daily for three (3) days and then stopping the BCP but continuing on Lupron 10u daily (in my opinion 20U daily is too much) and await a period (which should ensue within 5-7 days of stopping the BCP). At that point an US examination is done along with a baseline measurement of blood estradiol to exclude a functional ovarian cyst and simultaneously, the Lupron dosage is reduced to 5U daily to be continued until the hCG (10,000u) trigger. An FSH-dominant gonadotropin such as Follistim, Puregon or Gonal-f daily is started with the period for 2 days and then the gonadotropin dosage is reduced and a small amount of menotropin (Menopur---no more than 75U daily) is added. This is continued until US and blood estradiol levels indicate that the hCG trigger be given, whereupon an ER is done 36h later. I personally would advise against using Lupron in “flare protocol” arrangement (where the Lupron commences with the onset of gonadotropin administration.
    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation (COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas
    • Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
    • A personalized, stepwise approach to IVF
    • “Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • Amy - July 20, 2017 reply

    We were started on our first IVF cycle with a med error. We were given and told the wrong dose (wrong concentration) and they started us on 1mg Lupron instead of 40 micrograms.
    We are on day 6 of stims. We only have 10 follicles. Do you think the Lupron could have any thing to do with the low count? Should we start over?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 20, 2017 reply

    I doubt that is the reason!

    Geoff Sher

  • Anna - July 20, 2017 reply

    Hello,
    I will be having a FET in 6 days and my lining was checked today. I was told its 12 mm. I’m wondering is it possible that it will get too thick in 6 days by the time I have the transfer? The transfer will be a 5 day embryo. Thank you.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 20, 2017 reply

    In the absence of endometrial pathology (rare), there is in my opinion, no such thing as an over-thick lining!

    Geoff Sher

    Anna - July 20, 2017 reply

    Thank you! I appreciate it. I have 2 embryos that I can transfer from a recent Ivf cycle that I completed. Will see how it goes.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 20, 2017 reply

    Good luck Anna,

    Geoff Sher

  • Nancy - July 19, 2017 reply

    Hello Dr Sher, I am 43 years of age and had embryo transfer yesterday (3 day 3 transfers). After laying down in the clinic after the procedure for about 45 minutes, I walked to the car and drove home (about 20 minutes drive). It was very hot and sunny here yesterday. Until the air conditioning started cooling the car, the temperature in the car was about 110 F given the car was parked in the sun. I am a bit worried – does walking shortly after embryo transfer, driving and most importantly, outside heat (while walking to the car and inside the car), hurt the embryos? I have been a couch potato since I got home yesterday.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 20, 2017 reply

    Should not have any adverse effect Nancy!

    Good luck!

    Geoff Sher

  • Lynn Collins - July 19, 2017 reply

    Hi Dr Sher, A face book member asks? What causes an Amh test to change so differently in one year? Last year my amh was 5.21ml and I got my results back from the other day and it’s 3.20ml

    thanks lynn

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 20, 2017 reply

    There are natural variations that occur. Also ovarian cysts and possibly even hormonal therapy such as a BCP can do this too!

    Geoff Sher

  • Eleanore - July 18, 2017 reply

    Hi dr. Sher,
    What do you think about a Decapeptyl depot 3.75mg as a attempt to get more mature eggs in a cycle?
    My AMH is 3.29 ng/ml, FSH 4,7 mIU/ml, LH3,30 mU/ml. Looking forward to hearing from you.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 18, 2017 reply

    It could be fine, but my preference would be daily shots of regular agonist starting about 5 days prior to the period.

    Two main factors determine the quality of a woman’s eggs at ovulation or egg retrieval. First is her age and second is the protocol used for ovarian stimulation. With the possible the exception of cases where there is severe sperm dysfunction, it is the chromosomal integrity of the egg rather than the sperm that will ultimately determine the chromosomal integrity of the embryo (i.e. its “competency”, or its potential to propagate a healthy babies). It therefore follows that the only way by which to influence embryo “competence” is through the selection and implementation of an optimal protocol for ovarian stimulation. Since older women (≥35 years) and those who have diminished ovarian reserve (DOR) are at greatest risk of yielding “incompetent” eggs, they are the ones that require special attention. This article will highlight the reasons why such women are the ones most prone to produce poor quality eggs and embryos and how best to address ovarian stimulation in an attempt to minimize this risk.

    Cells that have a full chromosomal component are termed euploid while those that do not, are aneuploid. Most euploid eggs are “competent”, that is, they are the one’s that are most likely to propagate euploid, “competent” embryos. Aneuploid, “incompetent” eggs will invariably develop into aneuploid, “incompetent” embryos. There is a progressive increase in the incidence in egg/embryo aneuploidy with advancing age. To put numbers to the equation; by time a woman reaches 35 yrs; approximately 60% of her eggs are likely to be aneuploid. By the time she reaches her mid 40’s the incidence will be greater than 85%.

    For example, a woman of 43 years would be fortunate if six (6) or eight (8), of her eggs would upon being fertilized, result in one (1) “competent” embryo. As the woman gets older, the inevitable decline in egg/embryo quality results in her having a reduced ability to conceive naturally, a declining IVF success rates, an increase in miscarriages, and a rising incidence of having her baby affected by chromosomal birth defects such as Trisomy 21 (Down’s syndrome). This is why for such a woman, the anticipated IVF birth rate per egg retrieval is less than 10% (i.e. >70% lower than at age 35), the miscarriage rate increases from about 15% at 35y to >40% at age above 40y.and why her risk of having a baby with Down’s syndrome is about 0 2% at 35y as compared to 2% at 44y).

    The anticipation of poor IVF outcome statistics for women in their mid-40’s makes IVF with ovum donation the most rational approach. Yet, in spite of this, many older women still elect to use their own eggs as long as there is even the slightest chance of having their own genetic offspring.

    As a woman approaches and then engages her 40’s, her ability to produce “competent” eggs progressively declines. At the same time she experiences diminishing ovarian reserve that results in a progressive fall-off in the number of eggs she is likely to produce at egg retrieval. As a result, there will be a commensurate drop of in the number of “competent” embryos available for transfer to her uterus.

    The following IVF stimulation protocols are the ones most commonly used for COS in older women and those with DOR:

    1.GnRHa Flare (“Short”) protocol: Some IVF physicians advocate the use of gonadotropin releasing hormone-agonist (GnRHa)- flare protocols in which the administration of GnRHa (e.g. Lupron, Buserelin, Nafarelin, Synarel) therapy begins at the same time that ovarian stimulation with gonadotropins is started (usually with the onset of menstruation). The proposed benefit of such an approach is that the GnRHa will cause the woman’s pituitary gland to release large amounts of follicle stimulating hormone (FSH), which would augment the administered dosage of FSH and thereby synergizing the growth of ovarian follicles.

    The problem associated with this “flare” approach is that concurrent with the GnRHa-induced FSH luteinizing hormone (LH) also surges. In older women and those who have diminished ovarian reserve, the out-pouring of LH can cause the ovarian connective tissue (stroma or theca) which produces excessive male hormones (predominantly, testosterone). While some testosterone is essential for optimal follicle growth, too much testosterone can compromise its development as well as egg/embryo quality. Since older women and women with diminished ovarian reserve often have increased LH production as well as an overgrown of ovarian stroma/theca (i.e. hyperthecosis), a further GnRHa-induced increase in LH can so elevate local ovarian testosterone levels as to severely compromise egg/ embryo “competency”.

    2.Combined Clomiphene or Letrazole) /Gonadotropin Stimulation: This approach when used in older women and women with diminished ovarian reserve is also potentially harmful to egg/embryo quality. The reason is that like GnRHa, clomiphene and Letrazole also cause LH to be released in large amounts. Since these medications are given at the start of ovarian stimulation they, as with “flare protocols” can elicit ovarian over-production of testosterone. As such this approach is in my opinion far less than ideal for older women and women who have diminished ovarian reserve.

    3.Mid-follicular GnRH-antagonist protocol: With this approach, stimulation with gonadotropins is commenced with the onset of the cycle. Then, several days later, once the majority of follicles have reached about 12mm in size, GnRH antagonist (e.g. Ganirelix, Cetrotide, Cetrorelix, and Orgalutron) is added. The intent in adding the antagonist is to abruptly block pituitary LH release and so prevent a “premature LH surge” with its effect of causing increased ovarian testosterone and impaired follicle and egg development.

    The problem with such a regime is that women with diminished ovarian reserve already have too much of their own LH around at the beginning of the cycle. Accordingly, blocking LH release only 6-7 days into the stimulation does nothing to prevent the early adverse effects of too much LH-induced ovarian testosterone on early egg/embryo development. It should be borne in mind that eggs are often at their most vulnerable, early on in the cycle. Thus, in my opinion such protocols are also less than optimal for older women and for those with diminished ovarian reserve.

    4.GnRHa (“Long”) Pituitary down-Regulation Protocol:

    a) The “Standard” Long Protocol Approach: This protocol, which is the mainstay of ovarian stimulation for IVF, is either initiated about 1 week after natural ovulation (a “luteal phase start”) or is launched off a monophasic birth control pill (a “BCP start”). In the case of the latter, the BCP is taken for at least 8 days before, GnRHa (e.g. Lupron/Superfact/Buserelin) is added daily. Two days after starting the GnRHa, the BCP is stopped. Menstruation usually ensues within 3-5 days. GnRHa administration is continued and gonadotropin (Follistim/Gonal-F/Puregon, Bravelle, and Menopur) stimulation is initiated. Both daily Gonadotropin stimulation and GnRHa are continued until the day of the “hCG trigger”.

    The initial administration of agonist serves to rapidly expunge pituitary FSH and LH causing an immediate rise in the blood levels of both hormones. Then, within a few days, having virtually exhausted/depleted pituitary gonadotropin stores, the blood levels of FSH and LH both rapidly decline, such that by the time menstruation occurs, the levels are very low. The initial premenstrual GnRHa-induced rise in FSH helps recruit ovarian antral follicles for the upcoming cycle, while the ultimate virtual depletion of LH serves to prevent excessive ovarian testosterone production and protects egg quality.

    I prefer to use pure FSHr (Folistim, Puregon, Gonal F) for ovarian stimulation for IVF with the initial dosage being reduced by about 25% within a few days. Thereupon 75U Menopur is added daily, up until the hCG trigger.

    b) Modified Long Protocols:
    i. Agonist/Antagonist Conversion protocol (A/ACP): Agonists might competitively inhibit follicle response to FSH. Therefore, in an attempt to improve follicle response to FSH we modified the “standard approach” (a- above) as follows: Rather than continuing to give GnRHa throughout the stimulation protocol, we here supplant GnRHa with low dosage GnRH antagonist starting with the initiation of menstruation, continuing throughout stimulation until the day of the “hCG trigger” at which point both the antagonist and gonadotropins are discontinued. We have had very good results using the A/ACP modification of the “standard long pituitary down-regulation protocol”. In fact it has become my preferred approach for most women with a normal ovarian reserve, who undergo ovarian stimulation for IVF.

    ii. Agonist/Antagonist Conversion Protocol (A/ACP) +“Estrogen Priming” (LA10-E2V): Estrogen primes follicle FSH receptors, thereby enhancing response to FSH. This forms the basis of the “estrogen priming” approach in women with diminished ovarian response. The approach involves administering estradiol by daily injection, or by skin patch starting about 10 days prior to initiating high dosage gonadotropin stimulation. As with the standard A/ACP, the estrogen priming protocol is initiated a week post-ovulation (luteal phase start) or is launched off a birth control pill regime of at least 10 days. It also starts with GnRHa administration for about 5 days whereupon menstruation ensues and the agonist is supplanted by an antagonist. But this is where things change slightly such that instead of directly initiating FSHr (Follistim/Gonal-F/Puregon) injections, the patient, while continuing to take the GnRH antagonist now receives twice weekly estradiol valerate injections or daily estradiol skin patches (I prefer the former) for a period of about 10 days. Thereupon, daily high dosage FSHr (750U) is administered once daily. Four to five days later, 75U Menopur daily is added. “Estrogen priming” is continued until more than 50% of the follicles are at least 12mm in size whereupon it is discontinued.

    5. Mini-IVF or Natural Cycle IVF for women with DOR? It is quite understandable that many women with DOR are easily persuaded that less (or no) ovarian stimulation offers a more “natural” and less “stressful” approach on eggs than a robust, high gonadotropin-based, long-pituitary down regulation approach. This, in my opinion is a fallacy and can compromise rather than benefit IVF outcome in such cases. Even in young women in their early or mid-30’s, the IVF success rate per fresh “natural” or “mini” IVF cycle is much lower (<15%) than that which can be achieved through the use of conventional long down-regulation protocols, where the anticipated success is at least double this rate (30%). Mini-IVF is usually conducted using clomiphene or Femara, alone or in combination with Menopur, all of which is associated with the production of excessive LH-induced ovarian testosterone. Furthermore, low dosage stimulation will result in fewer eggs being available, thus further reducing the odds of IVF success per egg retrieval conducted. Natural cycle IVF is in my opinion also not in the best interest of women with DOR, because with such an approach, nothing is done to control the exaggerated production of LH by the woman’s own pituitary gland.

    Addendum:
    Human Growth Hormone (HGH) Supplementation. Recently, I began selectively adding human growth hormone (HGH) supplementation to simulation protocols in women with DOR, in cases where there is a history of the woman repeatedly producing poor quality eggs and in older women (>38Y) undergoing IVF. There is evidence that this might enhance mitochondrial activity and thus improve egg maturational division (meiosis).

    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • 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?
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas
    • Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
    • A personalized, stepwise approach to IVF
    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • nicole - July 18, 2017 reply

    Hi Dr. Sher,
    I am in the middle of an FET cycle. I’m triggering tonight with ovidrel.
    I have to have 2 moles removed on my upper abdomen on Thursday. They will use lidocaine injected into the site of the moles.
    Do you think I should wait for the mole removal until after I get pregnant and have the baby? I’m worried that the lidocaine will linger in my system or cause my uterine lining to change and the egg not implant.
    The mole removal and the day of transfer will be 5 days apart.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 18, 2017 reply

    I do not think it matters either way!

    Geoff Sher

  • Jyoti - July 18, 2017 reply

    Dear Dr. Sher, I am 34 years old and trying to conceive for last 2 years with one failed IUI. My HSG report says ‘The uterus is anteverted, normal in shape and size. No abnormal filling defect or adhesion is noted.’ and there are no abnormalities found in ovaries/uterus during ultrasound. Would you recommend laproscopy and hysteroscopy in my case? Thanks a lot!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 18, 2017 reply

    I personally would not necessarily do the laparoscopy or hysteroscopy if you are <40y, have have normal ovarian reserve and there is no significant male factor. Instead would do a hysterosonogram to check the regularity of the uterine cavity and if still unsuccessful, would do IVF.

    Geoff Sher

    Geoff Sher

  • ANNE KALLUS - July 18, 2017 reply

    Should I be concerned about my RE’s plan to delay my FET transfer day by 1-2 weeks because he’s out of town? Should I ask that his partner do it?
    Background:
    I’ve been building my lining for 21 days already. On CD 16, my RE said that my lining was ready, but that we’d to delay progesterone by ~1.5 weeks, so that we can transfer once he’s back in the office. Note: I have Asherman’s & have only recently been cleared to conceive, so there’s some chance that my lining will get slightly better?? But I’m concerned that if could get worse if I wait until CD 34 to transfer, as planned. I could ask that his partner to do it, but the partner may be less familiar with my case. Many Thanks!!

    AK - July 18, 2017 reply

    (00ps, didn’t mean to post my full name if it’s possible to redact it?)

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 18, 2017 reply

    Sorry, I am abroad until the 28th and cannot effect…but I would not be overly concerned.

    Geoff Sher

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 18, 2017 reply

    In my opinion, it would be far better not to delay unnecessarily if all else is progressing normally. Why take the risk?

    Geoff Sher

  • Angela - July 17, 2017 reply

    Dr Sher Would you recommend taking acyclovir 400 twice daily to suppress the virus during this cycle? Many thanks

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 17, 2017 reply

    You can use it …in my opinion, but not after stimulation begins.

    Geoff Sher

  • Angela - July 17, 2017 reply

    Thank you for replying Dr Sher, would you take preventative medical to stop another outbreak during this current cycle?
    Thank you

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 17, 2017 reply

    No!

    Geoff Sher

  • Susan - July 16, 2017 reply

    Hi Dr. Sher, I am 44 and recently underwent a donor egg cycle where we transferred 1- 5day blast rated 3AA. They used ICSI, assisted hatching, and embryo glue. The evening of 14dp5dt my hcg was 4635! That seems very high even pretending it was closer to 15dp5dt. My home satellite clinic didn’t seem concerned and my donor clinic hasn’t gotten back to me with feedback on that number. I am concerned it seems high especially with a SET. I previously had a high-ish hcg of 3900 at 16dp5dt with my own eggs and had a blighted ovum at 8wk ultrasound. They don’t do repeat betas or ultrasounds before 8wks so I’m destined to have a painfully slowly remaining 2.5 wks trying to stay away from the underbelly of the Internet :o) Does that number concern you and should I be trying to advocate for earlier follow up in your opinion? Thank you in advance.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 17, 2017 reply

    It is possible that the embryo split in two. Have an US in 1 week!

    Geoff Sher

    Susan - July 17, 2017 reply

    Thank you for your quick response :o) Unfortunately they will not do an ultrasound sooner than 8 weeks. From your response though it doesn’t sound like you would have particular concerns about anything nefarious other than a split with that high of an hcg? Thanks again!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 18, 2017 reply

    Correct!

    Good luck!

    Geoff Sher

  • Angela - July 16, 2017 reply

    Dear Dr Sher, I am currently on day 2 of stimms. My last fresh cycle ended up being a blighted ovum. I had a herpes outbreak just before egg collection and it was extremely painful. I didn’t take any medication to suppress the virus. Do you think the blighted ovum was caused by the infection? Do you think I should take medication now to suppress the virus to prevent another outbreak during this cycle? I am worried about taking the medication and reducing egg quality as I am over 40.
    Thank you

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 16, 2017 reply

    While possible, I doubt that the herpes caused the blighted ovum.

    Geoff Sher

  • Kate - July 15, 2017 reply

    Dear Dr. Sher, I am a 38 year old woman, and my history includes lap for stage 4 endo last year and an ectopic pregnancy (natural) right before that lap. After taking BCP for 3 months to “quiet my endo”, I finished my 1st ivf cycle at NYU. Resulted in retrieval of 5 eggs, icsi fertilization of 4 eggs, and 2 embryos which made it to blast – one was mosaic and the other had several abnormalities. My protocol was 300 gonal f and 300 menopur daily. NYU’s recommendation is to just do the same thing next month. I am concerned they might not be offering me the best choices – is there anything special to do in light of my endo, or another protocol to consider? Many thanks for your ear and any suggestions.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 15, 2017 reply

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

    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
    • The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
    • Blastocyst Embryo Transfers Should be the Standard of Care in IVF
    • IVF: How Many Attempts should be considered before Stopping?
    • “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
    • IVF Failure and Implantation Dysfunction:
    • The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
    • Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
    • Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
    • Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
    • Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
    • Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
    • Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
    • Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
    • Endometrial Thickness, Uterine Pathology and Immunologic Factors
    • Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
    • A personalized, stepwise approach to IVF
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    • The Role of Nutritional Supplements in Preparing for IVF
    • Endometriosis and Infertily
    • Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF
    • Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
    • Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
    • Treating Ovarian Endometriomas with Sclerotherapy.

    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • Annie - July 14, 2017 reply

    On my 3rd round of Ivf I had 14 embryos at day 5, at day 6 they were still compact morulas and didn’t develop further. They have said it’s the sperm factor. Can you suggest anything to change next time? Or advice why such a high number all stopped developing at the stage? Thanks

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 15, 2017 reply

    It could be a sperm factor, but it could (and based non statistical probability) could likely also be a stimulation issue!

    Here is the protocol I advise for women, <40Y who have adequate ovarian reserve.
    My advice is to use a long pituitary down regulation protocol starting on a BCP, and overlapping it with Lupron 10U daily for three (3) days and then stopping the BCP but continuing on Lupron 10u daily (in my opinion 20U daily is too much) and await a period (which should ensue within 5-7 days of stopping the BCP). At that point an US examination is done along with a baseline measurement of blood estradiol to exclude a functional ovarian cyst and simultaneously, the Lupron dosage is reduced to 5U daily to be continued until the hCG (10,000u) trigger. An FSH-dominant gonadotropin such as Follistim, Puregon or Gonal-f daily is started with the period for 2 days and then the gonadotropin dosage is reduced and a small amount of menotropin (Menopur---no more than 75U daily) is added. This is continued until US and blood estradiol levels indicate that the hCG trigger be given, whereupon an ER is done 36h later. I personally would advise against using Lupron in “flare protocol” arrangement (where the Lupron commences with the onset of gonadotropin administration.
    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation (COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas
    • Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
    • A personalized, stepwise approach to IVF
    • “Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
    • Diagnosis and treatment of Male Factor Infertility
    • Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in Favor
    • Hormonal Treatment of Male Infertility
    • Hormonal Treatment of Male Infertility
    • Antisperm Antibodies, Infertility and the Role of IVF with Intracytoplasmic Sperm Injection (ICSI)
    • Testicular Sperm Extraction (TESE) and Testicular Sperm Aspiration (TESA): Surgical Approaches for Accessing Sperm from men who have no sperm in their ejaculates (Azoospermia)
    • Varicocele and Male Infertility: When and how should it be treated?
    • The Sperm Chromatin Structure Assay (SCSA): A Measure of the Potential of Sperm to Help Propagate a Viable Pregnancy

    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • Sarah - July 14, 2017 reply

    Dear Dr Sher.

    I am soon to embark on my first round of IVF for gender selection. I have previously had 2 quick conceptions resulting in two healthy babies.

    My pretesting results are as follows on day 1 of my cycle;

    35 nearly 36 yo
    AMH 1.9
    AFC 12
    Prolactin 41.7
    FT4 13.1
    TSH 0.795

    This is all I was tested for, no LH.

    My clinic (not a US one) says they have had good results with Menopur only cycles and so have suggested the following protocol for me

    Day 2-4 Menopur 300
    Day 5-7 Menopur 225
    Day 6 Scan

    Scan on day 6 after which results will be reviewed and stims adjusted if necessary.

    I know from your blog, you don’t recommend Menopur only cycles.

    Based on your comments, I have queried the Menopur only protocol and the Dr has said I could have Gonal and Menopur cycle or Gonal and Luveris if I prefer

    From those with experience of this, what are your thoughts on my choices?

    I understand my results are at the lower end for my age.

    Thank you…

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 15, 2017 reply

    Here is the protocol I advise for women, <40Y who have adequate ovarian reserve.
    My advice is to use a long pituitary down regulation protocol starting on a BCP, and overlapping it with Lupron 10U daily for three (3) days and then stopping the BCP but continuing on Lupron 10u daily (in my opinion 20U daily is too much) and await a period (which should ensue within 5-7 days of stopping the BCP). At that point an US examination is done along with a baseline measurement of blood estradiol to exclude a functional ovarian cyst and simultaneously, the Lupron dosage is reduced to 5U daily to be continued until the hCG (10,000u) trigger. An FSH-dominant gonadotropin such as Follistim, Puregon or Gonal-f daily is started with the period for 2 days and then the gonadotropin dosage is reduced and a small amount of menotropin (Menopur---no more than 75U daily) is added. This is continued until US and blood estradiol levels indicate that the hCG trigger be given, whereupon an ER is done 36h later. I personally would advise against using Lupron in “flare protocol” arrangement (where the Lupron commences with the onset of gonadotropin administration.
    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation (COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas
    • Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
    • A personalized, stepwise approach to IVF
    • “Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

    Sarah - July 15, 2017 reply

    Thanks Dr Sher for your usual protocol for ladies in their mid 30s whom do not have DOR.

    What goes better with Gonal? Menopur or luveris? Those are the two options by clinic has given me.

    Thanks

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 15, 2017 reply

    Gonal-F,Follistim or Puregon + Menopur or Luveris.

    Geoff Sher

  • Tarah - July 14, 2017 reply

    Good evening I’ve been going through ivf since 2014 and I’ve had multiple cycles. I’ve had 2 miscarriages between 6-8 weeks, and then I’ve had 2 chemicals and between then I’ve had implantation failure. I was wondering if you could educate me on what protocol would better suit me. I’ve taken 300 follistim and 2 vials menapur during stim, along with 20 mg of prednisone. And hgh makes me over stimulate. I just was wondering if there was something you would recommend for stims and transfer protocols. I get quite a few follicles usually like 10-12 but I get like 4-6 mature. My husband has two kids of his own previous marriage. Thank you so much

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 15, 2017 reply

    Hi tarah,

    So sorry to hear of your tribulations, but while the the protocol for stimulation could explain the reason for your losses, it could very easily also be due to an implantation dysfunction.

    When it comes to reproduction, humans are the poorest performers of all mammals. In fact we are so inefficient that up to 75% of fertilized eggs do not produce live births, and up to 30% of pregnancies end up being lost within 10 weeks of conception (in the first trimester). RPL is defined as two (2) or more failed pregnancies. Less than 5% of women will experience two (2) consecutive miscarriages, and only 1% experience three or more.
    Pregnancy loss can be classified by the stage of pregnancy when the loss occurs:
    • Early pregnancy loss (first trimester)
    • Late pregnancy loss (after the first trimester)
    • Occult “hidden” and not clinically recognized, (chemical) pregnancy loss (occurs prior to ultrasound confirmation of pregnancy)
    • Early pregnancy losses usually occur sporadically (are not repetitive).
    In more than 70% of cases the loss is due to embryo aneuploidy (where there are more or less than the normal quota of 46 chromosomes). Conversely, repeated losses (RPL), with isolated exceptions where the cause is structural (e.g., unbalanced translocations), are seldom attributable to numerical chromosomal abnormalities (aneuploidy). In fact, the vast majority of cases of RPL are attributable to non-chromosomal causes such as anatomical uterine abnormalities or Immunologic Implantation Dysfunction (IID).
    Since most sporadic early pregnancy losses are induced by chromosomal factors and thus are non-repetitive, having had a single miscarriage the likelihood of a second one occurring is no greater than average. However, once having had two losses the chance of a third one occurring is double (35-40%) and after having had three losses the chance of a fourth miscarriage increases to about 60%. The reason for this is that the more miscarriages a woman has, the greater is the likelihood of this being due to a non-chromosomal (repetitive) cause such as IID. It follows that if numerical chromosomal analysis (karyotyping) of embryonic/fetal products derived from a miscarriage tests karyotypically normal, then by a process of elimination, there would be a strong likelihood of a miscarriage repeating in subsequent pregnancies and one would not have to wait for the disaster to recur before taking action. This is precisely why we strongly advocate that all miscarriage specimens be karyotyped.
    There is however one caveat to be taken into consideration. That is that the laboratory performing the karyotyping might unwittingly be testing the mother’s cells rather than that of the conceptus. That is why it is not possible to confidently exclude aneuploidy in cases where karyotyping of products suggests a “chromosomally normal” (euploid) female.
    Late pregnancy losses (occurring after completion of the 1st trimester/12th week) occur far less frequently (1%) than early pregnancy losses. They are most commonly due to anatomical abnormalities of the uterus and/or cervix. Weakness of the neck of the cervix rendering it able to act as an effective valve that retains the pregnancy (i.e., cervical incompetence) is in fact one of the commonest causes of late pregnancy loss. So also are developmental (congenital) abnormalities of the uterus (e.g., a uterine septum) and uterine fibroid tumors. In some cases intrauterine growth retardation, premature separation of the placenta (placental abruption), premature rupture of the membranes and premature labor can also causes of late pregnancy loss.
    Much progress has been made in understanding the mechanisms involved in RPL. There are two broad categories:
    1. Problems involving the uterine environment in which a normal embryo is prohibited from properly implanting and developing. Possible causes include:
    • Inadequate thickening of the uterine lining
    • Irregularity in the contour of the uterine cavity (polyps, fibroid tumors in the uterine wall, intra-uterine scarring and adenomyosis)
    • Hormonal imbalances (progesterone deficiency or luteal phase defects). This most commonly results in occult RPL.
    • Deficient blood flow to the uterine lining (thin uterine lining).
    • Immunologic implantation dysfunction (IID). A major cause of RPL. Plays a role in 75% of cases where chromosomally normal preimplantation embryos fail to implant.
    • Interference of blood supply to the developing conceptus can occur due to a hereditary clotting disorder known as Thrombophilia.
    2. Genetic and/or structural chromosomal abnormality of the embryo.Genetic abnormalities are rare causes of RPL. Structural chromosomal abnormalities are slightly more common but are also occur infrequently (1%). These are referred to as unbalanced translocation and they result from part of one chromosome detaching and then fusing with another chromosome. Additionally, a number of studies suggest the existence of paternal (sperm derived) effect on human embryo quality and pregnancy outcome that are not reflected as a chromosomal abnormality. Damaged sperm DNA can have a negative impact on fetal development and present clinically as occult or early clinical miscarriage. The Sperm Chromatin Structure Assay (SCSA) which measures the same endpoints are newer and possibly improved methods for evaluating.

    IMMUNOLOGIC IMPLANTATION DYSFUNCTION
    Autoimmune IID: Here an immunologic reaction is produced by the individual to his/her body’s own cellular components. The most common antibodies that form in such situations are APA and antithyroid antibodies (ATA).
    But it is only when specialized immune cells in the uterine lining, known as cytotoxic lymphocytes (CTL) and natural killer (NK) cells, become activated and start to release an excessive/disproportionate amount of TH-1 cytokines that attack the root system of the embryo, that implantation potential is jeopardized. Diagnosis of such activation requires highly specialized blood test for cytokine activity that can only be performed by a handful of reproductive immunology reference laboratories in the United States.
    Alloimmune IID, i.e., where antibodies are formed against antigens derived from another member of the same species, is believed to be a relatively common immunologic cause of recurrent pregnancy loss.
    Autoimmune IID is often genetically transmitted. Thus it should not be surprising to learn that it is more likely to exist in women who have a family (or personal) history of primary autoimmune diseases such as lupus erythematosus (LE), scleroderma or autoimmune hypothyroidism (Hashimoto’s disease), autoimmune hyperthyroidism (Grave’s disease), rheumatoid arthritis, etc. Reactionary (secondary) autoimmunity can occur in conjunction with any medical condition associated with widespread tissue damage. One such gynecologic condition is endometriosis. Since autoimmune IID is usually associated with activated NK and T-cells from the outset, it usually results in such very early destruction of the embryo’s root system that the patient does not even recognize that she is pregnant. Accordingly the condition usually presents as “unexplained infertility” or “unexplained IVF failure” rather than as a miscarriage.

    Alloimmune IID, on the other hand, usually starts off presenting as unexplained miscarriages (often manifesting as RPL). Over time as NK/T cell activation builds and eventually becomes permanently established the patient often goes from RPL to “infertility” due to failed implantation. RPL is more commonly the consequence of alloimmune rather than autoimmune implantation dysfunction.
    However, regardless, of whether miscarriage is due to autoimmune or alloimmune implantation dysfunction the final blow to the pregnancy is the result of activated NK cells and CTL in the uterine lining that damage the developing embryo’s “root system” (trophoblast) so that it can no longer sustain the growing conceptus. This having been said, it is important to note that autoimmune IID is readily amenable to reversal through timely, appropriately administered, selective immunotherapy, and alloimmune IID is not. It is much more difficult to treat successfully, even with the use of immunotherapy. In fact, in some cases the only solution will be to revert to selective immunotherapy plus using donor sperm (provided there is no “match” between the donor’s DQa profile and that of the female recipient) or alternatively to resort to gestational surrogacy.
    DIAGNOSING THE CAUSE OF RPL
    In the past, women who miscarried were not evaluated thoroughly until they had lost several pregnancies in a row. This was because sporadic miscarriages are most commonly the result of embryo numerical chromosomal irregularities (aneuploidy) and thus not treatable. However, a consecutive series of miscarriages points to a repetitive cause that is non-chromosomal and is potentially remediable. Since RPL is most commonly due to a uterine pathology or immunologic causes that are potentially treatable, it follows that early chromosomal evaluation of products of conception could point to a potentially treatable situation. Thus I strongly recommend that such testing be done in most cases of miscarriage. Doing so will avoid a great deal of unnecessary heartache for many patients.
    Establishing the correct diagnosis is the first step toward determining effective treatment for couples with RPL. It results from a problem within the pregnancy itself or within the uterine environment where the pregnancy implants and grows. Diagnostic tests useful in identifying individuals at greater risk for a problem within the pregnancy itself include:

    • Karyotyping (chromosome analysis) both prospective parents
    • Assessment of the karyotype of products of conception derived from previous miscarriage specimens
    • Ultrasound examination of the uterine cavity after sterile water is injected or sonohysterogram, fluid ultrasound, etc.)
    • Hysterosalpingogram (dye X-ray test)
    • Hysteroscopic evaluation of the uterine cavity
    • Full hormonal evaluation (estrogen, progesterone, adrenal steroid hormones, thyroid hormones, FSH/LH, etc.)
    • Immunologic testing to include:
    a) Antiphospholipid antibody (APA) panel
    b) Antinuclear antibody (ANA) panel
    c) Antithyroid antibody panel (i.e., antithyroglobulin and antimicrosomal antibodies)
    d) Reproductive immunophenotype
    e) Natural killer cell activity (NKa) assay (i.e., K562 target cell test)
    f) Alloimmune testing of both the male and female partners
    TREATMENT OF RPL
    Treatment for Anatomic Abnormalities of the Uterus: This involves restoration through removal of local lesions such as fibroids, scar tissue, and endometrial polyps or timely insertion of a cervical cerclage (a stitch placed around the neck of the weakened cervix) or the excision of a uterine septum when indicated.
    Treatment of Thin Uterine Lining: A thin uterine lining has been shown to correlate with compromised pregnancy outcome. Often this will be associated with reduced blood flow to the endometrium. Such decreased blood flow to the uterus can be improved through treatment with sildenafil and possibly aspirin.
    Sildenafil (Viagra) Therapy. Viagra has been used successfully to increase uterine blood flow. However, to be effective it must be administered starting as soon as the period stops up until the day of ovulation and it must be administered vaginally (not orally). Viagra in the form of vaginal suppositories given in the dosage of 25 mg four times a day has been shown to increase uterine blood flow as well as thickness of the uterine lining. To date, we have seen significant improvement of the thickness of the uterine lining in about 70% of women treated. Successful pregnancy resulted in 42% of women who responded to the Viagra. It should be remembered that most of these women had previously experienced repeated IVF failures.

    Use of Aspirin: This is an anti-prostaglandin that improves blood flow to the endometrium. It is administered at a dosage of 81 mg orally, daily from the beginning of the cycle until ovulation.
    Treating Immunologic Implantation Dysfunction with Selective Immunotherapy: Modalities such as IL/IVIg, heparinoids (Lovenox/Clexane), and corticosteroids (dexamethasone, prednisone, prednisolone) can be used in select cases depending on autoimmune or alloimmune dysfunction.
    The Use of IVF in the Treatment of RPL
    In the following circumstances, IVF is the preferred option:
    1. When in addition to a history of RPL, another standard indication for IVF (e.g., tubal factor, endometriosis, and male factor infertility) is superimposed.
    2. In cases where selective immunotherapy is needed to treat an immunologic implantation dysfunction.
    The reason for IVF being a preferred approach in such cases is that in order to be effective, the immunotherapy needs to be initiated well before spontaneous or induced ovulation. Given the fact that the anticipated birthrate per cycle of COS with or without IUI is at best about 15%, it follows that short of IVF, to have even a reasonable chance of a live birth, most women with immunologic causes of RPL would need to undergo immunotherapy repeatedly, over consecutive cycles. Conversely, with IVF, the chance of a successful outcome in a single cycle of treatment is several times greater and, because of the attenuated and concentrated time period required for treatment, IVF is far safer and thus represents a more practicable alternative
    Since embryo aneuploidy is a common cause of miscarriage, the use of preimplantation genetic diagnosis (PGD), with tests such as CGH, can provide a valuable diagnostic and therapeutic advantage in cases of RPL. PGD requires IVF to provide access to embryos for testing.
    There are a few cases of intractable alloimmune dysfunction due to absolute DQ alpha matching where Gestational Surrogacy or use of donor sperm could represent the only viable recourse, other than abandoning treatment altogether and/or resorting to adoption. Other non-immunologic factors such as an intractably thin uterine lining or severe uterine pathology might also warrant that last resort consideration be given to gestational surrogacy.
    The good news is that if a couple with RPL is open to all of the diagnostic and treatment options referred to above, a live birthrate of 70%–80% is ultimately achievable.

    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
    • Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
    • Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
    • The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
    • Blastocyst Embryo Transfers Should be the Standard of Care in IVF
    • IVF: How Many Attempts should be considered before Stopping?
    • “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
    • IVF Failure and Implantation Dysfunction:
    • The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
    • Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
    • Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
    • Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
    • Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
    • Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
    • Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
    • Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
    • Endometrial Thickness, Uterine Pathology and Immunologic Factors
    • Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
    • A personalized, stepwise approach to IVF
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    • The Role of Nutritional Supplements in Preparing for IVF

    ANNOUNCEMENTS:
    1. About my Retirement by mid-2018:
    After > 30 years in the field of Assisted Reproduction (AR), the time is approaching for my retirement. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.
    If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

    .

  • Brandi - July 14, 2017 reply

    If I set up a Skype Consultation with you and give you all of my information, would you be willing to help me come up with a protocol for a stim cycle? I’m DOR, my clinic had me on 225 gonal 75 Menopur with cetrotide starting after day 4-5 of stims. I just do not feel that was the right protocol for me.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 15, 2017 reply

    Hi Brandi,

    I could advise but I would not dictate a specific protocol for those I personally would not be treating. Your RE could contact me at any time should he/she so desire and I would again offer my opinion, but that, for ethical and legal reasons, is as far as I could go.

    Here is the protocol I advise for women, <40Y who have adequate ovarian reserve.
    My advice is to use a long pituitary down regulation protocol starting on a BCP, and overlapping it with Lupron 10U daily for three (3) days and then stopping the BCP but continuing on Lupron 10u daily (in my opinion 20U daily is too much) and await a period (which should ensue within 5-7 days of stopping the BCP). At that point an US examination is done along with a baseline measurement of blood estradiol to exclude a functional ovarian cyst and simultaneously, the Lupron dosage is reduced to 5U daily to be continued until the hCG (10,000u) trigger. An FSH-dominant gonadotropin such as Follistim, Puregon or Gonal-f daily is started with the period for 2 days and then the gonadotropin dosage is reduced and a small amount of menotropin (Menopur---no more than 75U daily) is added. This is continued until US and blood estradiol levels indicate that the hCG trigger be given, whereupon an ER is done 36h later. I personally would advise against using Lupron in “flare protocol” arrangement (where the Lupron commences with the onset of gonadotropin administration.
    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation (COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas
    • Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
    • A personalized, stepwise approach to IVF
    • “Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • Lauren - July 14, 2017 reply

    Good afternoon, Dr. Sher —
    My first IVF cycle was cancelled two weeks ago after 3 days of stims due to poor response. Prior to starting stims, I was on 25 days of BCP while overlapping 10 units of Lupron. The Lupron was reduced to 5 units on day 1 of my Gonal F and Menopur injections. Because I have to wait for my next cycle day 1 to try again with a new protocol I’m obviously anxious for my cycle to arrive. Will it be delayed? The cancellation was two weeks ago and there have been no signs of ovulation or my period.

    thanks in advance!
    Lauren

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 14, 2017 reply

    It sounds as if you have severely diminished ovarian redserve. Thus without access to much more information, I cannot comment authoritatively.

    In my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”.
    Women who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.

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

    Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.

    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
    • A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
    • Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
    • Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
    • Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
    • The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
    • Blastocyst Embryo Transfers should be the Standard of Care in IVF
    • Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
    • Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
    • Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
    • Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
    • Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
    • Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
    • PGS in IVF: Are Some Chromosomally Abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
    • PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
    • Traveling for IVF from Out of State/Country–
    • A personalized, stepwise approach to IVF
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    • The Role of Nutritional Supplements in Preparing for IVF
    • Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
    • IVF Egg Donation: A Comprehensive Overview

    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • Tara Anderson - July 14, 2017 reply

    Hi Dr. Sher.

    I am 39 years old and just finished my 3rd ivf cycle. We ended up with 1 embryo that made it to blast, but not until day 6. They froze the embryo which got a good, quality rating. I like the idea of doing a natural frozen transfer vs. a medicated one. What are your thoughts on this?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 14, 2017 reply

    I personally prefer FET done in hormone replacement cycles as it assures an optimally primed endometrium and allows for better pinpointing of the window of implantation.

    Geoff Sher

  • Sana - July 14, 2017 reply

    Hello Dr. Sher,
    I have had 3 failed IVF cycles starting at age 39 and I.m now 44 years old. I have been told it’s related to egg Quality and Just wanted to know your thoughts on Supplements like DHEA, COQ10 and more importantly PQQ (pyrroloquinoline quinone) which support and help Mitochondria and cell regeneration….Thanks!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 14, 2017 reply

    It is important to nurture and take care of yourself mentally and physically when preparing and going through your IVF journey. This starts with trying to have a positive attitude about what you are about to go through, creating a stress support system for yourself by using tools such as visualization, acupuncture and meditation, eating the right foods taking a few supplements (see below) and balancing exercise with sufficient rest. . Not only will it help your experience but it may also help to increase your chances for IVF success
    This article will focus on the role of nutritional supplements in preparing for IVF. You’ve probably wondered whether commercially available fertility supplements could help you achieve your goal. The answer is complex.
    Here is my take: Nutrition is indeed a vital prerequisite for optimal reproductive function. However, a well-balanced diet that meets food preferences, coupled with modest vitamin, mineral and antioxidant supplementation (as can be found in many prenatal vitamin preparations) should suffice.
    This having been said, conceiving is a delicate process, and eating the right foods is essential to optimize reproductive potential. Indeed, a balanced diet (i.e. a lot of organic and brightly colored foods) will provide most of the nutrients you need. But the truth is that most people do not have a balanced diet and are unwittingly often deficient in important nutrients.
    A balanced diet is one that is rich in good quality protein, low in sugar, salt, caffeine and industrially created trans-fats (trans-fatty acids or partially hydrogenated oils) and soy, uncontaminated by heavy metals, free of nicotine, alcohol and recreational drugs. This is why routine supplementation with the following nutrients could enhance preconception readiness:
    • Folic acid (400 micrograms daily)
    • Vitamins D-3 1,000U daily; Viamin A (2565 IU daily); B6 (6mg -10 mg daily); B12 (12-20 mcg per day); C- (2,000 mg a day for both men and women); E (both sexes should get 150-200U daily)
    • Co-enzyme Q10 (400-600mg daily )
    • Amino acids such as L-Carnitine (3 grams daily) and L-arginine (1 gram per day )
    • Omega 3 fatty acids (2,000mg per day)
    • Minerals, mainly zinc (15mg per day); selenium (70-100mcg per day); iron (up to 20mg per day ); magnesium (400mg per day )
    There are likely to be significant reproductive health benefits (including enhanced fertility and intrauterine development) associated with the use of nutritional supplements. However there are also certain potential pitfalls associated with their use. Some supplements are not as safe as they would seem. For example, excessive intake of fat-soluble vitamins (A, D, E and K) can even be dangerous to your health and may be associated with fetal malformations.
    Additionally, numerous supplements have been found to contain contaminants such as toxic plant materials, heavy metals and even prescription medications that can compromise fetal development. Prior to the passage of the Dietary Supplement Health and Education Act of 1994, supplements (vitamins, minerals, amino acids, and botanicals) were required to demonstrate safety. However, since passage of “the Act”, they are now presumed to be safe until shown otherwise, thus establishing a rather hazardous situation where a typical prenatal vitamin that will provide sufficient vitamins and minerals for a healthy early pregnancy and potentially dangerous supplements can and are being sold in the same store without product liability.
    What about the use of dehydroepiandrosterone (DHEA)? DHEA is a male hormone supplement that is metabolized to androstenedione and testosterone in the ovaries. While a small amount of ovarian testosterone is needed for optimal follicle and egg development, too much testosterone could be decidedly harmful. DHEA supplements probably won’t do harm if taken by healthy young women who have normal ovarian reserve, but they probably would not derive any benefit either. However, in my opinion, DHEA supplementation could be potentially harmful when taken by women with diminished ovarian reserve (DOR), women who have polycystic ovarian syndrome (PCOS) and older women in their 40’s as such women often already tend to have increased LH-activity, leading to increased ovarian testosterone. Additional ovarian testosterone in such women, could thus potentially compromise follicle development and egg quality/competency.
    In summary: Maximizing reproductive performance and optimizing outcome following fertility treatment requires a combined strategy involving a balanced diet (rich in protein, low in sugars, soy and trans-fats), modest nutritional supplementation, limiting/avoiding foods and contaminants that can compromise reproductive potential, and adopting disciplined lifestyle modification such as not smoking, reducing stress, minimizing alcohol intake, avoiding nicotine and recreational drug consumption, and getting down to a healthy weight through diet and exercise.

    I hope this helps!

    If interested, please contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me to discuss your case in detail. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

    Geoff Sher

  • Jyoti - July 14, 2017 reply

    Dear Dr. Sher, Do you recommend undergoing a Laparoscopy and Hysteroscopy as part of the initial fertility work-up before IVF for everyone or there are specific symptoms that should prompt such tests? Thanks a lot for your advice.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 14, 2017 reply

    Unnecessary unless there is a suspicion of a specific problem needing surgical attention (e.g. endometriotic cyst; submucous fibroid or polyp; hydrosalpinx etc.). A simple sonohysterogram done within 1 year of ET, usually suffices.

    Geoff Sher

  • Div - July 14, 2017 reply

    Hi Dr Sher. I am 27 years old. My periods for last 3 months lasts for 2 weeks. The bleeding is very very less. Me and my hubby are trying to get conceived from past one year. But no success. I got tested for ovarian cancer last year as a routine checkup and the result was negative. I am little overweight. Is there anything serious for me to consult doctor. Please suggest.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 14, 2017 reply

    You need to be evaluated carefully fo ovulation dysfunction as well as for an underlying organic reproductive problem.

    Geoff Sher

  • Siobhan - July 14, 2017 reply

    Hi Dr Sher,
    For my FET I have been given fematab? And also ovitrelle injection? I did the ovitrelle injection for my stim cycle, why would it be needed for my FET prep?
    Thank you 🙂

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 14, 2017 reply

    You have got me there…I have no clue….

    Geoff Sher

  • Tonya B - July 14, 2017 reply

    Dr. Sher,
    My 27 year old daughter had 55 eggs retrieved and 20 something fertilized back in March. Her husband had the (TESE) process done with only 10 sperm that did not survive the thaw. They had back up donor sperm which are the ones that fertilized the eggs. The RE said lining was great and 2- 5day blasts were great. It was a failed fresh possibly due to uterus being out of sorts- possibly mild ohss. Approx. 3 days after transfer, a rash/acne with tiny white pimples began to appear on her chest and face. This was a bfn. A couple of months later they had FET #1. Same thing as fresh. Lining was great, 2- 5day blasts were great. 3-4 days after transfer, rash/acne began to appear on her chest and face. FET #1 was bfn. RE seems to think rash/acne has nothing to do with failed attempts. As far as we know my daughter is as healthy as can be. Two questions: Could rash/acne have anything to do with bfns? And with 7 remaining 5 day blasts of good to great quality, should they just continue on with their next FET hoping this one will have success?
    Thank you so much for your response!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 14, 2017 reply

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

    • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
    • Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
    • The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
    • Blastocyst Embryo Transfers Should be the Standard of Care in IVF
    • IVF: How Many Attempts should be considered before Stopping?
    • “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
    • IVF Failure and Implantation Dysfunction:
    • The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
    • Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
    • Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
    • Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
    • Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
    • Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
    • Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
    • Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
    • Endometrial Thickness, Uterine Pathology and Immunologic Factors
    • Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
    • A personalized, stepwise approach to IVF
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    • The Role of Nutritional Supplements in Preparing for IVF
    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • Joanna Troccoli - July 13, 2017 reply

    Hi dr.sher!
    I just did a transfer yesterday at 1:00 pm of a PGS tested 5 day embryo and today around noon I started mildly cramping . I know it’s too early for implantation and too early for my period so what causes these mild cramps so early on??? It was a FET
    Thank you!!!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 14, 2017 reply

    That is inconsequential. It is not due to implantation.

    Geoff sher

  • Brandi - July 13, 2017 reply

    Thank you very much for your very detailed response on RPL. Greatly appreciated and will look into it.
    If you do not mind, what is your take on Repeat implantation failure. I’m talking 3+ transfers with no implantation at all after having REpeat pregnancy loss naturally.
    Thanks again for your time.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 14, 2017 reply

    It is likely immunologic…but we should talk!

    Geoff Sher

  • Brandi - July 13, 2017 reply

    What would you think would be the cause of repeat implantation failure with ivf? I have been pregnant 8 times naturally (no live births) but no implantation with ivf. I’m on my last embryo now, 5dp3dt and terrified this one may not work because I haven’t had implantation before. But holding out hope that it does.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 13, 2017 reply

    When it comes to reproduction, humans are the poorest performers of all mammals. In fact we are so inefficient that up to 75% of fertilized eggs do not produce live births, and up to 30% of pregnancies end up being lost within 10 weeks of conception (in the first trimester). RPL is defined as two (2) or more failed pregnancies. Less than 5% of women will experience two (2) consecutive miscarriages, and only 1% experience three or more.
    Pregnancy loss can be classified by the stage of pregnancy when the loss occurs:
    • Early pregnancy loss (first trimester)
    • Late pregnancy loss (after the first trimester)
    • Occult “hidden” and not clinically recognized, (chemical) pregnancy loss (occurs prior to ultrasound confirmation of pregnancy)
    • Early pregnancy losses usually occur sporadically (are not repetitive).
    In more than 70% of cases the loss is due to embryo aneuploidy (where there are more or less than the normal quota of 46 chromosomes). Conversely, repeated losses (RPL), with isolated exceptions where the cause is structural (e.g., unbalanced translocations), are seldom attributable to numerical chromosomal abnormalities (aneuploidy). In fact, the vast majority of cases of RPL are attributable to non-chromosomal causes such as anatomical uterine abnormalities or Immunologic Implantation Dysfunction (IID).
    Since most sporadic early pregnancy losses are induced by chromosomal factors and thus are non-repetitive, having had a single miscarriage the likelihood of a second one occurring is no greater than average. However, once having had two losses the chance of a third one occurring is double (35-40%) and after having had three losses the chance of a fourth miscarriage increases to about 60%. The reason for this is that the more miscarriages a woman has, the greater is the likelihood of this being due to a non-chromosomal (repetitive) cause such as IID. It follows that if numerical chromosomal analysis (karyotyping) of embryonic/fetal products derived from a miscarriage tests karyotypically normal, then by a process of elimination, there would be a strong likelihood of a miscarriage repeating in subsequent pregnancies and one would not have to wait for the disaster to recur before taking action. This is precisely why we strongly advocate that all miscarriage specimens be karyotyped.
    There is however one caveat to be taken into consideration. That is that the laboratory performing the karyotyping might unwittingly be testing the mother’s cells rather than that of the conceptus. That is why it is not possible to confidently exclude aneuploidy in cases where karyotyping of products suggests a “chromosomally normal” (euploid) female.
    Late pregnancy losses (occurring after completion of the 1st trimester/12th week) occur far less frequently (1%) than early pregnancy losses. They are most commonly due to anatomical abnormalities of the uterus and/or cervix. Weakness of the neck of the cervix rendering it able to act as an effective valve that retains the pregnancy (i.e., cervical incompetence) is in fact one of the commonest causes of late pregnancy loss. So also are developmental (congenital) abnormalities of the uterus (e.g., a uterine septum) and uterine fibroid tumors. In some cases intrauterine growth retardation, premature separation of the placenta (placental abruption), premature rupture of the membranes and premature labor can also causes of late pregnancy loss.
    Much progress has been made in understanding the mechanisms involved in RPL. There are two broad categories:
    1. Problems involving the uterine environment in which a normal embryo is prohibited from properly implanting and developing. Possible causes include:
    • Inadequate thickening of the uterine lining
    • Irregularity in the contour of the uterine cavity (polyps, fibroid tumors in the uterine wall, intra-uterine scarring and adenomyosis)
    • Hormonal imbalances (progesterone deficiency or luteal phase defects). This most commonly results in occult RPL.
    • Deficient blood flow to the uterine lining (thin uterine lining).
    • Immunologic implantation dysfunction (IID). A major cause of RPL. Plays a role in 75% of cases where chromosomally normal preimplantation embryos fail to implant.
    • Interference of blood supply to the developing conceptus can occur due to a hereditary clotting disorder known as Thrombophilia.
    2. Genetic and/or structural chromosomal abnormality of the embryo.Genetic abnormalities are rare causes of RPL. Structural chromosomal abnormalities are slightly more common but are also occur infrequently (1%). These are referred to as unbalanced translocation and they result from part of one chromosome detaching and then fusing with another chromosome. Additionally, a number of studies suggest the existence of paternal (sperm derived) effect on human embryo quality and pregnancy outcome that are not reflected as a chromosomal abnormality. Damaged sperm DNA can have a negative impact on fetal development and present clinically as occult or early clinical miscarriage. The Sperm Chromatin Structure Assay (SCSA) which measures the same endpoints are newer and possibly improved methods for evaluating.

    IMMUNOLOGIC IMPLANTATION DYSFUNCTION
    Autoimmune IID: Here an immunologic reaction is produced by the individual to his/her body’s own cellular components. The most common antibodies that form in such situations are APA and antithyroid antibodies (ATA).
    But it is only when specialized immune cells in the uterine lining, known as cytotoxic lymphocytes (CTL) and natural killer (NK) cells, become activated and start to release an excessive/disproportionate amount of TH-1 cytokines that attack the root system of the embryo, that implantation potential is jeopardized. Diagnosis of such activation requires highly specialized blood test for cytokine activity that can only be performed by a handful of reproductive immunology reference laboratories in the United States.
    Alloimmune IID, i.e., where antibodies are formed against antigens derived from another member of the same species, is believed to be a relatively common immunologic cause of recurrent pregnancy loss.
    Autoimmune IID is often genetically transmitted. Thus it should not be surprising to learn that it is more likely to exist in women who have a family (or personal) history of primary autoimmune diseases such as lupus erythematosus (LE), scleroderma or autoimmune hypothyroidism (Hashimoto’s disease), autoimmune hyperthyroidism (Grave’s disease), rheumatoid arthritis, etc. Reactionary (secondary) autoimmunity can occur in conjunction with any medical condition associated with widespread tissue damage. One such gynecologic condition is endometriosis. Since autoimmune IID is usually associated with activated NK and T-cells from the outset, it usually results in such very early destruction of the embryo’s root system that the patient does not even recognize that she is pregnant. Accordingly the condition usually presents as “unexplained infertility” or “unexplained IVF failure” rather than as a miscarriage.

    Alloimmune IID, on the other hand, usually starts off presenting as unexplained miscarriages (often manifesting as RPL). Over time as NK/T cell activation builds and eventually becomes permanently established the patient often goes from RPL to “infertility” due to failed implantation. RPL is more commonly the consequence of alloimmune rather than autoimmune implantation dysfunction.
    However, regardless, of whether miscarriage is due to autoimmune or alloimmune implantation dysfunction the final blow to the pregnancy is the result of activated NK cells and CTL in the uterine lining that damage the developing embryo’s “root system” (trophoblast) so that it can no longer sustain the growing conceptus. This having been said, it is important to note that autoimmune IID is readily amenable to reversal through timely, appropriately administered, selective immunotherapy, and alloimmune IID is not. It is much more difficult to treat successfully, even with the use of immunotherapy. In fact, in some cases the only solution will be to revert to selective immunotherapy plus using donor sperm (provided there is no “match” between the donor’s DQa profile and that of the female recipient) or alternatively to resort to gestational surrogacy.
    DIAGNOSING THE CAUSE OF RPL
    In the past, women who miscarried were not evaluated thoroughly until they had lost several pregnancies in a row. This was because sporadic miscarriages are most commonly the result of embryo numerical chromosomal irregularities (aneuploidy) and thus not treatable. However, a consecutive series of miscarriages points to a repetitive cause that is non-chromosomal and is potentially remediable. Since RPL is most commonly due to a uterine pathology or immunologic causes that are potentially treatable, it follows that early chromosomal evaluation of products of conception could point to a potentially treatable situation. Thus I strongly recommend that such testing be done in most cases of miscarriage. Doing so will avoid a great deal of unnecessary heartache for many patients.
    Establishing the correct diagnosis is the first step toward determining effective treatment for couples with RPL. It results from a problem within the pregnancy itself or within the uterine environment where the pregnancy implants and grows. Diagnostic tests useful in identifying individuals at greater risk for a problem within the pregnancy itself include:

    • Karyotyping (chromosome analysis) both prospective parents
    • Assessment of the karyotype of products of conception derived from previous miscarriage specimens
    • Ultrasound examination of the uterine cavity after sterile water is injected or sonohysterogram, fluid ultrasound, etc.)
    • Hysterosalpingogram (dye X-ray test)
    • Hysteroscopic evaluation of the uterine cavity
    • Full hormonal evaluation (estrogen, progesterone, adrenal steroid hormones, thyroid hormones, FSH/LH, etc.)
    • Immunologic testing to include:
    a) Antiphospholipid antibody (APA) panel
    b) Antinuclear antibody (ANA) panel
    c) Antithyroid antibody panel (i.e., antithyroglobulin and antimicrosomal antibodies)
    d) Reproductive immunophenotype
    e) Natural killer cell activity (NKa) assay (i.e., K562 target cell test)
    f) Alloimmune testing of both the male and female partners
    TREATMENT OF RPL
    Treatment for Anatomic Abnormalities of the Uterus: This involves restoration through removal of local lesions such as fibroids, scar tissue, and endometrial polyps or timely insertion of a cervical cerclage (a stitch placed around the neck of the weakened cervix) or the excision of a uterine septum when indicated.
    Treatment of Thin Uterine Lining: A thin uterine lining has been shown to correlate with compromised pregnancy outcome. Often this will be associated with reduced blood flow to the endometrium. Such decreased blood flow to the uterus can be improved through treatment with sildenafil and possibly aspirin.
    Sildenafil (Viagra) Therapy. Viagra has been used successfully to increase uterine blood flow. However, to be effective it must be administered starting as soon as the period stops up until the day of ovulation and it must be administered vaginally (not orally). Viagra in the form of vaginal suppositories given in the dosage of 25 mg four times a day has been shown to increase uterine blood flow as well as thickness of the uterine lining. To date, we have seen significant improvement of the thickness of the uterine lining in about 70% of women treated. Successful pregnancy resulted in 42% of women who responded to the Viagra. It should be remembered that most of these women had previously experienced repeated IVF failures.

    Use of Aspirin: This is an anti-prostaglandin that improves blood flow to the endometrium. It is administered at a dosage of 81 mg orally, daily from the beginning of the cycle until ovulation.
    Treating Immunologic Implantation Dysfunction with Selective Immunotherapy: Modalities such as IL/IVIg, heparinoids (Lovenox/Clexane), and corticosteroids (dexamethasone, prednisone, prednisolone) can be used in select cases depending on autoimmune or alloimmune dysfunction.
    The Use of IVF in the Treatment of RPL
    In the following circumstances, IVF is the preferred option:
    1. When in addition to a history of RPL, another standard indication for IVF (e.g., tubal factor, endometriosis, and male factor infertility) is superimposed.
    2. In cases where selective immunotherapy is needed to treat an immunologic implantation dysfunction.
    The reason for IVF being a preferred approach in such cases is that in order to be effective, the immunotherapy needs to be initiated well before spontaneous or induced ovulation. Given the fact that the anticipated birthrate per cycle of COS with or without IUI is at best about 15%, it follows that short of IVF, to have even a reasonable chance of a live birth, most women with immunologic causes of RPL would need to undergo immunotherapy repeatedly, over consecutive cycles. Conversely, with IVF, the chance of a successful outcome in a single cycle of treatment is several times greater and, because of the attenuated and concentrated time period required for treatment, IVF is far safer and thus represents a more practicable alternative
    Since embryo aneuploidy is a common cause of miscarriage, the use of preimplantation genetic diagnosis (PGD), with tests such as CGH, can provide a valuable diagnostic and therapeutic advantage in cases of RPL. PGD requires IVF to provide access to embryos for testing.
    There are a few cases of intractable alloimmune dysfunction due to absolute DQ alpha matching where Gestational Surrogacy or use of donor sperm could represent the only viable recourse, other than abandoning treatment altogether and/or resorting to adoption. Other non-immunologic factors such as an intractably thin uterine lining or severe uterine pathology might also warrant that last resort consideration be given to gestational surrogacy.
    The good news is that if a couple with RPL is open to all of the diagnostic and treatment options referred to above, a live birthrate of 70%–80% is ultimately achievable.

    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
    • Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
    • Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
    • The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
    • Blastocyst Embryo Transfers Should be the Standard of Care in IVF
    • IVF: How Many Attempts should be considered before Stopping?
    • “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
    • IVF Failure and Implantation Dysfunction:
    • The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
    • Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
    • Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
    • Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
    • Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
    • Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
    • Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
    • Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
    • Endometrial Thickness, Uterine Pathology and Immunologic Factors
    • Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
    • A personalized, stepwise approach to IVF
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    • The Role of Nutritional Supplements in Preparing for IVF

    ANNOUNCEMENTS:
    1. About my Retirement by mid-2018:
    After > 30 years in the field of Assisted Reproduction (AR), the time is approaching for my retirement. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.
    If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • Siobhan - July 13, 2017 reply

    Hi Dr Sher,
    In your opinion would a natural or medicated FET be best?
    Also why would an injection used during a stim cycle (ovitrelle) also be used for FET?
    Thank you!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 13, 2017 reply

    In my opinion, a hormone-replacement (Estrogen-progesterone) replacement FET cycle is best.

    Geoff Sher

  • Amelia - July 13, 2017 reply

    Dr Sher I am looking everywhere for an explanation to this and can’t find any: Why does flying on international flights make me skip a period? I am about to visit another country and I am terrified that the month after I will not ovulate and I have natural cycle IVF planned…..What is it about flying and is there anything I can do to help my body?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 13, 2017 reply

    It does not do this.

    Geoff Sher

  • Sofy - July 13, 2017 reply

    Hi Dr. Sher.
    I had a successful 3 day transfer when I was 34. I was on 225 menopur, got 7 eggs, 6 fertilised. None to freeze. I’m now 37 and going to try again. My dr has upped my menopur to 300 and 375 on alternate days. This seems high to me. I think he’s doing that as my AMH was 5.7 pmol, and is hoping to get more eggs to do PGS. What are your thoughts? My AFC was 10 when I was 34 and is still 10 now. I did not have My AMH done when I was 34.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 13, 2017 reply

    You have diminished ovarian reserve and require an individualized protocol…in my opinion.

    In my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”.
    Women who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.

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

    Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.

    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
    • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
    • The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
    • A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
    • Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
    • Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
    • Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
    • The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
    • Blastocyst Embryo Transfers should be the Standard of Care in IVF
    • Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
    • Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
    • Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
    • Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
    • Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
    • Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
    • PGS in IVF: Are Some Chromosomally Abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
    • PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
    • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
    • Traveling for IVF from Out of State/Country–
    • A personalized, stepwise approach to IVF
    • How Many Embryos should be transferred: A Critical Decision in IVF.
    • The Role of Nutritional Supplements in Preparing for IVF
    • Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
    • IVF Egg Donation: A Comprehensive Overview

    ANNOUNCEMENTS:
    1. About my Retirement
    After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to contemplate retiring from full-time clinical medicine. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.

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

    Geoffrey Sher MD

  • Jyoti - July 13, 2017 reply

    Dear Dr. Sher, I have read that even if you opt out of PGS, the success rate with a frozen ET is better than the fresh transfer. What are your views on this? Do you think waiting for a cycle to have a frozen transfer makes more sense? Thank you so much!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 13, 2017 reply

    There is little doubt that preparing the uterus through HRT for receiving an embryo usually establishes a better environment for plantation than that which can be achieved through ovarian stimulation. This plus the fact that vitrification can preserve an embryo in good condition, explains why we get slightly better results with FET.

    Geoff Sher

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