Ask Our Doctors – Archive
Our Medical Directors are outstanding physicians that you will find to be very personable and compassionate, who take care to ensure that you have the most cutting-edge fertility treatments at your disposal. This is your outlet to ask your questions to the doctors.
Dear Dr. Sher.
I have a quick question regarding our situation. I’m 42 yrs old and just went through my 4th IVF cycle. My first IVF cycle (at 41) ended in an ectopic. Second and Third one failed (all day 3 transfers upto the 3rd IVF cycle). In general I respond very well the the treatment and my numbers are good for my age (AMH level about 5 ng/ml, day 3 FSH ranges between 6.5 – 8.5). For our 4th (most recent) cycle, we opted for Day 5 PGD/FET so that we get a better idea about my egg quality. This cycle, they retrieved 10 matured eggs, 8 fertilized with ICSI. Only one of them made it to day 6 (grade 3BC). PGD revealed that it was 45 XX, -19.
I learned that there is this phenomenon called mosaicism where each and every genetically abnormal embryo may go through “self-correction” at some point, be it at the preimplantation, or prenatal, or postnatal period.
Does it make any sense to cryopreserve that embryo and use it as a last resort?
Is it possible that the biopsied cells have shown chromosomal abnormalities but may be there are overwhelming number of good cells and the embryo might autocorrect later?
You are correct. Your one embryo is a monosomy 19 and if that is due to meiotic aneuploidy (which is the most likely scenario) it is NOT reversible. However if it is due to a mitotic aneuploidy it is potentially able to autocorrect and therefore should be vitribanked and kept, in my opinion.
Human embryo development occurs through a process that encompasses reprogramming, sequential cleavage divisions and mitotic chromosome segregation and embryonic genome activation. Chromosomal abnormalities may arise during germ cell and/or pre-implantation embryo development, and represents a major cause of early pregnancy loss. About a decade ago, I and an associate, Levent Keskintepe Ph.D. were the first to introduce full embryo karyotyping (identification of all 46 chromosomes) through preimplantation genetic sampling (PGS) as a method by which to selectively transfer only euploid embryos (i.e. those that have a full component of chromosomes) to the uterus. We subsequently reported on a 2-3 fold improvement in implantation and birth rates as well as a significant reduction in early pregnancy loss, following IVF. Since then PGS has grown dramatically in popularity such that it is now widely used throughout the world.
Most IVF programs that offer PGS services, require that all participating patients consent to all their aneuploid embryos (i.e. those with an irregular quota of chromosomes) be disposed of. However, there is now growing evidence to suggest that following embryo transfer, some aneuploid embryos will in the process of ongoing development, convert to the euploid state (i.e. “auto correction”) and then go on to develop into chromosomally normal offspring. In fact, I am personally aware of several such cases occurring within our IVF network. So clearly, by summarily discarding all aneuploid embryos as a matter of routine we are sometimes destroying some embryos that might otherwise have “autocorrected” and gone on to develop into normal offspring.
Thus by discarding all aneuploid embryos we, in so doing, might be denying some women the opportunity of having a baby. This creates a major ethical and moral dilemma for those of us that provide the option of PGS to our patients. On the one hand, we strive “to avoid knowingly doing harm” (the Hippocratic Oath) and as such would prefer to avoid or minimize the risk of miscarriage and/or chromosomal birth defects and on the other hand we would not wish to deny patients with aneuploid embryos, the opportunity to have a baby.
The basis for such embryo “auto correction” lies in the fact that some embryos found through PGS-karyotyping to harbor one or more aneuploid cells (blastomeres) will often also harbor chromosomally normal (euploid) cells (blastomeres). The coexistence of both aneuploid and euploid cells coexisting in the same embryo is referred to as “mosaicism.” Many such mosaic embryos will In the process of subsequent cell replication convert to the normal euploid state (i.e. autocorrect)
It is against this background, that an ever increasing number of IVF practitioners, rather than summarily discard PGS-identified aneuploid embryos are now choosing to cryobanking (freeze-store) certain of them, to leave open the possibility of ultimately transferring them to the uterus. In order to best understand the complexity of the factors involved in such decision making, it is essential to understand the causes of embryo aneuploidy of which there are two varieties:
1.Meiotic aneuploidy” results from aberrations in chromosomal numerical configuration that originate in either the egg (most commonly) and/or in sperm, during preconceptual maturational division (meiosis). Since meiosis occurs in the pre-fertilized egg or in and sperm, it follows that when aneuploidy occurs due to defective meiosis, all subsequent cells in the developing embryo/blastocyst/conceptus inevitably will be aneuploid, precluding subsequent “auto correction”. Meiotic aneuploidy will thus invariably be perpetuated in all the cells of the embryo as they replicate. It is a permanent phenomenon and is irreversible. All embryos so affected are thus fatally damaged. Most will fail to implant and those that do implant will either be lost in early pregnancy or develop into chromosomally defective offspring (e.g. Down syndrome, Edward syndrome, Turner syndrome).
2.“Mitotic aneuploidy” occurs when following fertilization and subsequent cell replication (cleavage), some cells (blastomeres) of a meiotically euploid early embryo mutate and become aneuploid. This is referred to as mosaicism. Thereupon, with continued subsequent cell replication (mitosis) the chromosomal make-up (karyotype) of the embryo might either comprise of predominantly aneuploid cells or euploid cells. The subsequent viability or competency of the conceptus will thereupon depend on whether euploid or aneuploid cells predominate. If in such mosaic embryos aneuploid cells predominate, the embryo will be “incompetent”). If (as is frequently the case) euploid cells prevail, the mosaic embryo will be “competent” and capable of propagating a normal conceptus.
Since some mitotically aneuploid (“mosaic”) embryos can and indeed do “autocorrect’ while meiotically aneuploid embryos cannot, it follows that an ability to differentiate between these two varieties of aneuploidy would be of enormous clinical value. Since some mosaic embryos can “autocorrect” and even go on to propagate a viable baby, the ability to confirm that aneuploidy is mitotic (potentially reversible) would provide a strong argument in favor of preserving certain aneuploid embryos for future dispensation. Unfortunately however, there is presently no microscopic or genetic test that can reliable differentiate between meiotic and mitotic aneuploidy.
Aneuploidy, whether meiotic or mitotic in origin involves the addition of one or more chromosomes to a given pair in human embryos. Certain aneuploidies involve only a single, chromosome pair (simple aneuploidy) while others involve more than a single pair (i.e. complex aneuploidy). Evidence suggests that complex aneuploidy, whether meiotic or mitotic in origin is almost always lethal while all forms of meiotic aneuploidy are permanent. Some aneuploidies, especially those that involve addition of a chromosome to any pair (trisomy) will at times progress to clinical pregnancies (e.g. trisomy 15, 18, 21 or when the sex chromosomes are involve). And as stated previously, most aneuploid embryos, should they attach, will miscarry or result in a chromosomally defective offspring.
On the other hand, some aneuploid embryos have one chromosome (in a given pair) missing (i.e. monosomy). Aside from monosomy involving absence of the Y-sex chromosome (i.e. XO) which can resulting in a live birth (Turner syndrome) all other monosomies involving autosomes (non-sex chromosomes) are lethal and will not result in viable offspring.
Since it is presently not possible, without removing more than 1 cell from an embryo (a very traumatic event) to differentiate between meiotic and mitotic aneuploidy, it follows that making a diagnosis of embryo aneuploidy does not allow for identification of mosaic embryos for transfer. This is especially true when it comes to trisomic embryos that can and sometimes do, propagate chromosomal birth defects such as Down syndrome. It is important to bear in mind that the transfer of trisomic embryos (whether due to meiotic or mitotic aneuploidy) can result in miscarriage or a birth defect. This makes any attempt to transfer such embryos to the uterus fraught with risk and in my opinion, ill advised. Conversely, since true meiotic autosomal monosomic embryos cannot propagate viable pregnancies, performing embryo transfer in such cases in the hope that the aneuploidy is mitotic (mosaic) in origin and will spontaneously “ auto correct”, is a rational consideration. Needless to say, such action would require full disclosure, and the execution of a detailed, informed consent agreement which would include an expressed commitment to undergo prenatal genetic testing aimed at excluding a chromosomal defect in the developing baby and/or a willingness to terminate the pregnancy should a serious birth defect be diagnosed.
Since it is meiotic rather than mitotic aneuploidy that is invariably lethal and given that meiotic aneuploidy originates in the egg, it is my belief that the closer to fertilization that embryo biopsy is done for PGS, the more likely it is that any aneuploidy detected, will be meiotic in origin. The longer you wait thereafter, the greater the likelihood that with repeated mitotic division, mutational changes will result in mitotic aneuploidy (mosaicism). This is why I strongly believe embryo biopsies should be performed on day 2-3 post fertilization rather on day 5-6 days (the blastocyst stage).”
Clearly with advancing age the percentage of chromosomally abnormal (aneuploid) embryos increases. At 42Y only about 1/10 will be normal. However you have excellent ovarian reserve so with the ideal stimulation, you should produce more than an average amount for your age, thereby increasing your potential to have one or two that are euploid and “competent” to propagate a normal pregnancy. I strongly urge that if PGS is done, that in this day and age next generation gene sequencing (NGS), rather than array CGH be used for PGS.You should also consider embryo banking to make hay while the sun still shines (see below).
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
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•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.
•IVF and Use of The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Secondary Infertility: Addressing the Root Causes
•Recurrent Pregnancy Loss (RPL): Why do I keep losing my Pregnancies?
•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)
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•The Role of Nutritional Supplements in Preparing for IVF
I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoff Sher
Hi
I have a question.
I am freaking out.
I had my 5 days fet blast transfer last friday (x2) today is sturday (8 days) after. I have been on progesterone. And i got my first pregnancy test positive thursday night, with wondfo stick and friday morning( yesterday).
Today i have a lot of cramping ( not constant)test was darker in the morning compared to yesterday and i have some spotting ( dark red, brown) The test is still positive… even after the spotting
Can it still be viable.? Can women have bleeding that early or late implantation bleeding?
Also my period is due today, but i feel the cramps are different…
Thank you
(The embryos passed pgs)
Spotting is very common especially when vaginal hormonal insertions are done as these can irritate the cervix and cause local bleeding. The fact that it is brown spotting is also a sign of minimal bleeding. As llong as the bleeding does not increase and the cramping get worse, you should be OK!
Good luck!
Geoff Sher
Hello,
My husband and I (both 27) have been ttc since July 2014. We have a 2 year old that was conceived naturally and spontaneously while on bcp (and antibiotics). I’ve had my tubes checked, my uterus checked for retained placenta and blood work and all was great. My husbands sperm is “one of the best sperm analysis I’ve ever seen”. We’ve done 2 months of Clomid/femara and 2 months of follistim. 3 IUI (2 failed and negative hpt at 11dpiui). Assuming this cycle is out-do we continue wasting money on IUI or do we pursue ivf? We have fertility coverage with our insurance but between copays etc were at almost 7k for IUI meds and monitoring. I’d rather put the money in a place where it might actually work. What protocol would you recommend next?
This is secondary infertility so it is vital that before you doIVF you examine for a possible implantation dysfunction (anatomical (uterine lining/contour of uterine cavity & immmunologic (alloimmune and autoimmune implantation dysfunction). I amparticulary concerned about the possibility of an alloimmune factor because this is a relatively important cause of 2ndary infertility….see below.
It is one thing for a woman who has never been able to conceive (primary infertility) to come to grips with undergoing In Vitro Fertilization. It is quite another matter for someone who has successfully achieved a pregnancy in the past having to come to terms with a subsequent inability to conceive (secondary infertility). When this happens, it raises issues of guilt, a declining sense of self-worth and ultimately self-recrimination. The ramifications often impact family relationships involving partners and siblings. The truth is that secondary infertility can be just as difficult for individuals and family to deal with as primary infertility.
There are many factors that contribute to the problem of secondary infertility. These include:
Social and marital factors: In this modern day and age where at least one in two marriages ends in divorce, it is not surprising that there would be an inevitable hiatus in childbearing. This often results in a considerable delay in re-initiating family building. Since the biological clock keeps on ticking in the interim, advancing age can, and often does, have a profound affect on a woman’s ability to subsequently conceive and successfully complete a pregnancy. In my experience, this is one of the most common reasons for secondary infertility. In addition, by the time a decision is made to enter a new relationship, many men and women will have undergone a prior sterilization procedure which now needs to be addressed. To make matters worse, many such men and women first opt for surgical reversal of their occlusive surgery, only to learn in the end that the procedures were not successful, and they now need to consider in vitro fertilization (IVF) in one form or another.
Financial factors: Here, the cost of raising a child often weighs heavily, especially in this present tough economic climate. This is becoming more of an issue as women playing an ever increasing role as a primary bread winner.
Career demands: There can be little doubt that when it comes to climbing the career ladder, women are considerably disadvantaged by the fact that pregnancy and the immediate demands of child rearing take away from their ability to compete with men. As such, many women choose to delay having another child until such time as they have been able to make up for prior lost opportunity.
Medical barriers to fertility: Certain common medical conditions, while not absolutely precluding pregnancy, make it much more difficult to conceive.
Endometriosis: It is not uncommon for women with endometriosis to achieve a pregnancy, but find difficulty in doing so again at a later date. The reason for this is that while most women with endometriosis have patent fallopian tubes, the environment surrounding their tubes is compromised due to pelvic toxins that are produced by the endometriotic implants. These toxins compromise egg fertilization potential, making it more difficult for sperm in the fallopian tube to fertilize the egg upon its arrival there. As such, endometriosis is one of the commonest causes of secondary infertility.
Tubal damage due to prior pelvic inflammatory disease: In first world countries, the early and often indiscriminate use of antibiotics for the slightest symptom has led to the point where an acute attack of pelvic inflammatory disease is often masked. As such, less than 30% of American women with tubal damage have knowledge that their tubes are compromised and that they might have subsequent difficulty in conceiving. Since, in many such cases the tubal damage will not have totally blocked both tubes, some of the women so affected might experience a pregnancy but have difficulty in conceiving again later down the line.
Dysfunctional ovulation: Since ovulation as well as normal hormonal support of the early implanting embryo are both essential for a healthy pregnancy to occur, it follows that women with irregular or dysfunctional ovulation (e.g., polycystic ovarian syndrome – PCOS, persistent follicular luteal phase deficiencies or post birth control pill ovulatory problems) might sporadically conceive and thereupon find it difficult to do achieve another pregnancy later on.
Immunologic Implantation Dysfunction (IID): has become ever more apparent that immunologic factors play an important role in achieving healthy implantation. Women with endometriosis (regardless of its severity), those with a personal or family history of autoimmune diseases such as lupus erythematosus, rheumatoid arthritis and thyroid autoimmunity (TAI), and some cases where the man and the woman share certain genetic similarities (alloimmune implantation dysfunction), will have activated CTL/NK cells that can inhibit or compromise healthy implantation. This is an often overlooked cause of secondary infertility. Most such autoimmune/alloimmune cases require selective immunotherapy and IVF.
Antisperm Antibodies: Although infrequent, some cases of secondary infertility might also be caused by the woman harboring antisperm antibodies. In such cases IVF is mandated.
Previous post-pregnancy uterine infection: Retention of products of conception after the birth of a child, miscarriage, or abortion can so damage the uterine lining as to result in subsequent implantation failure. Unless specifically looked for, this will usually be unknown to the patient, who will simply present with secondary infertility. Treatment is often difficult because such patients might not respond adequately to surgical removal of intrauterine scar tissue or to hormonal or Viagra therapy
Male immunologic factors: Most men who have undergone a previous vasectomy more than 10 years earlier, will have antisperm antibodies that will interfere with fertilization. Such cases require IVF with intracytoplasmic sperm injection (ICSI). Here we offer a few words of caution to men who are considering undergoing surgical reversal of vasectomy. Always first have a test done to exclude the presence of circulating antisperm antibodies, because in such cases, even if the reversal is successfully performed, they will not be able to initiate a pregnancy without IVF/ICSI.
Whatever the cause, secondary infertility often affects older couples disproportionately, creating a sense of urgency and even desperation in achieving a viable pregnancy before time runs out. It is for this reason that IVF becomes the treatment of choice in such cases. However, even IVF becomes progressively less successful with advancing age of the woman (whose eggs are being fertilized). In such cases it is important for the couple to be realistic with regard to their expectations. Here, options that include embryo banking and egg donation should be carefully considered.
Another important point is that whenever a regularly ovulating younger woman (under 36 years of age) with patent fallopian tubes is diagnosed with secondary infertility, it is essential to consider underlying endometriosis or non-obstructive tubal disease as a possible cause. In such cases, IVF is again the treatment of choice.
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
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•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)
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoff Sher
Hello dr Sher, I’ve been on long protocol. Suprecur spray and 450iui gonal f and luveris. I have low amh and high fsh. At day 7 scan I had only developed one mature folicle on my right side. There was nothing in the left. ( I had a large cyst removed from my left ovary 2 months ago). They have told me they won’t proceed with ivf on only one egg and have suggested iui and if that doesn’t work a short protocol. Can you give me any advice? Were the stimulation drugs incorrect? Thanks.
You clearly have severely diminished ovarian reserve (DOR) and probably need IVF with egg donation. However, if you feel strongly about using your own eggs, I would urge against a short protocol because in my experience this can only further compromise egg quality. I also do not advocate agonist nasal sprays. Absorption is too erratic. You need the injections. I would recommend a modified and robust (higher dosage FSHr)-long protocol coming off a BCP (the agonist/antagonist conversion protocol-A/ACP) augmented by estrogen priming and human growth hormone supplementation…see below. I would combine this with embryo banking of PGS normal blastocysts and try to make hay while the sun still shines.
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
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•IVF Egg Donation: A Comprehensive Overview
I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoff Sher
Dear Dr. Sher,
Please share your valuable inputs on the below query.
Whenever i had my IVF, during day 2 scan it would show atleast 7 to 8 follicles. But once stimulation is started, there is only doninant follicle which keeps growing in size and all of the others do not progress after a while. At the time of retrieval the one doninant follicle would be close to 18-20 mm while the rest would be at 8-10 mm.
Why does this happen and how can we address the issue of dominant follicle issue so that we are left with many more eggs at the time of collection.
Thank you Doctor.
Regards
Hi Shivani,
I need to know much more to give an authoritative response. However I can tell you that in my opinion, this is most likely to be because of premature luteinization linked to the protocol for ovarian stimulation. This is something we can often remedy after reviewing and revising the stimulation approach and its implementation.
Please visit my new Blog at http://goo.gl/4hvjoP , 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
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•Ovarian Stimulation for IVF: Comparing “conventional” use of GnRH antagonists to the Agonist/Antagonist Conversion Protocol (A/ACP)
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•Launching Ovarian Stimulation with a BCP: How Does it Affect Response?
•Frozen Embryo Transfer (FET): What Does it Involve?
•Hereditary Clotting Defects (Thrombophilia)
•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 Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•The Role of Nutritional Supplements in Preparing for IVF
•Implications of “Empty Follicle Syndrome and “Premature Luteinization”
I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoff Sher