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.
We are planning a frozen embryo transfer in August, I am on the contraceptive pill now (embryos are from an ivf cycle 2 years ago and this is for a potential sibling!) I’ve just finished menstruating and die to start my pill again tomorrow, should I stay off it now or stay on the pill until my nurses consultation end of July? I’d heard it could effect the lining of my womb?
In my opinion, it will NOT affect the lining of your uterus and I would remain on the BCP until receiving a directive from your treating RE.
Geoff Sher
Hi Dr. Sher,
I have been trying to get pregnant for three months now, I am 28 years old with one full term pregnancy 8 years ago and one abortion 6 years ago. I received a hysterscopy two days ago and the Dr. found scar tissue and said on a scale from 1-10 its a 3-4 in the amount that can be stopping me from getting pregnant. Also he said other than that everything with me is completely healthy. He does recommend to remove the scar tissue to better my chances of getting pregnant. My only issue you is I fear further scarring. I am prone to Keloids and scarring and don’t want even more scarring in my uterus to form. Should I keep trying for a few more months before this procedure or just get it over with and remove this scar tissue?
Thank you
Lena
Hi Yelena,
The intrauterine scarring was most likely the effect of intrauterine inflammation (endometritis) that resulted from infection of some retained products of conception after your most recent pregnancy. The scar tissue needs to be removed and hopefully you will be able to conceive thereafter. However, if the germinal (basal) layer of the endometrium was intractably damaged, it might not be that easy to correct itself after the surgery and you miight still have problems conceiving.
A normal uterine cavity and endometrial lining are essential in order to conceive and maintain a pregnancy. Scar tissue in the uterine cavity (Asherman’s syndrome) can interfere with conception, or increase the risk of miscarriage. The condition is often so severe that it destroys most of the basal (germinal) layer of the endometrium from which the uterine lining (endometrium) develops each month. When most of the basal endometrium is incapacitated, no regeneration of the endometrium can take place and amenorrhea (cessation of menstruation) or infertility can follow. The condition often results in fusion/adhesion of the opposing endometrial surfaces, but can also simply destroy the basal layer of endometrium without resulting in adhesions (non-adhesive Asherman’s).
Asherman’s syndrome most commonly results from post-partum or post-abortal inflammation involving the uterine lining (endometritis), but it can also occur (although infrequently) following uterine surgery such as removal of fibroid tumors (myomectomy) that encroach upon (or penetrate into) the uterine cavity.
The treatment of adhesive Asherman’s syndrome is resection of scar tissue by hysteroscopy. A hysteroscope is a telescope-like instrument that is introduced via the vagina and cervix into the uterine cavity allowing visualization of and access to the entire uterine cavity, enabling surgical resection of scar tissue. The objective is to remove as much scar tissue as possible and to free adhesions that fuse the walls of the uterine cavity together, so as to enable viable basal endometrium to resume growth and progressively cover as much of the surface of the uterine cavity as possible. Post-operatively, a small balloon is often placed in the uterine cavity for a day or two, to keep the opposing surfaces separated in the hope of preventing recurrence of adhesion formation. The woman usually receives supplemental estrogen to encourage endometrial growth.
Endometritis of a severity sufficient to produce Asherman’s Syndrome often scars and blocks the uterine entrances into the Fallopian tubes. However it is not always the case. The lining can be damaged while the tubes remain open. In such cases, if the uterine lining cannot support proper embryo implantation, a pregnancy could still implant in a Fallopian tube leading to an ectopic (tubal) pregnancy. Unless it is diagnosed early (by blood testing in combination with ultrasound examination) and treated medically or surgically, the ectopic pregnancy will rupture with serious and potentially life endangering consequences.
About 8 years ago, we reported on the use of Viagra vaginal suppositories to improve blood flow and hence enhanced delivery of estrogen to the endometrium. In this manner, we have been able to improve endometrial development in about 75% of women who otherwise were unable to develop an “adequate” uterine lining. Most of these women had undergone several failed IVF attempts. Many of the women who were successfully treated with Viagra subsequently conceived following IVF and went on to deliver healthy babies. One such case immediately comes to mind. It involved a woman who was from Singapore and who following 15 failed IVF attempts due to poor endometrial development conceived on her first IVF-Viagra attempt with us following Viagra therapy.
But Viagra is often ineffective in thickening the uterine lining in women with Asherman’s syndrome. The reason is that with Asherman’s there is often such widespread destruction of the basal endometrium (from which fresh endometrial cells must be generated), that regardless of the improvement in uterine blood flow and improved estrogen delivery, the endometrium just can’t respond. In such cases, the woman should consider using a gestational surrogate or pursuing adoption.
Feel free to call 800-780-7437 if you would like to have a Skype consultation with me to discuss.
Geoff Sher
Good luck!
Geoff Sher
Dear Dr. Sher,
I am 30 years old with DOR (AFC 1-3) and just failed my first IVF cycle. We used an Estrogen Priming Protocol and I retrieved 2 mature eggs, 1 fertilized, and at day 3 we transferred a 9 cell with minimal fragmentation. I am considering another cycle but adding in Human Growth Hormone. Do you think that HGH could help with my egg quality or egg quantity? Or do you think we should move to donor eggs?
Thanks very much!
Women and less “competent” eggs, the main reason for reduced IVF success in such cases. The compromised outcome is largely due to the fact that such women tend to have increased LH biological activity which often results in excessive LH-induced ovarian testosterone production which in turn can have a deleterious effect on egg/embryo “competency”.
Certain ovarian stimulation regimes either promote excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), augment LH/hCG delivered through additional administration (e.g. high dosage menotropins such as Menopur), or fail to protect against body’s own/self-produced LH (e.g. late antagonist protocols where drugs such as Ganirelix/Cetrotide/Orgalutron that are first administered 6-7 days after ovarian stimulation has commenced).
I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of a modified, long pituitary down-regulation protocol (the agonist/antagonist conversion protocol-A/ACP) augmented by adding supplementary human growth hormone (HGH). I further recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing/NGS)-normal blastocysts in such cases. This type of approach will in my opinion, optimize the chance of a viable pregnancy per embryo transfer procedure and provide an opportunity to capitalize on whatever residual ovarian reserve and egg quality still exists, allowing the chance to “make hay while the sun still shines”.
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
•Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
•Preimplantation Genetic Testing (PGS) in IVF: It Should be Used Selectively and NOT be Routine.
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
•PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
•Implications of “Empty Follicle Syndrome and “Premature Luteinization”
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Hi Dr. Sher,
I am 27 yrs old, had 2 failed IVF cycles, every cycle I have immature eggs. (I have AMH 7.5)
I read your post about empty follicle syndrome and I was wondering if the trigger that I had during the cycles was wrong or I need selective protocol to let my eggs mature. First cycle trigger was ovidrel 250 and second cycle was pregnyl 10,000. I would be gratful if you can guide me.
Regards,
Salma
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.
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•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
•Blastocyst Embryo Transfers Done 5-6 Days Following Fertilization are Fast Replacing Earlier day 2-3 Transfers of Cleaved Embryos.
•Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
•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)
•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:
•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
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
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.
Reposting, just in case:
Dear Dr. Sher
I am 40 years old. My husband is 65, diabetic (using insulin), not living very healthy lifestyle. Due to ED the ART is our only way to try to have baby.
We conceived thru second medicated IUI cycle in September 2014 with one opened fallopian tube and motile 5 mil. Unfortunately I lost the baby in wk 16 of the pregnancy. High possibility was that it happened due to incompetent cervix (painless contractions and no bleeding) and maybe an overseas flight contributed to the loss as well. No abnormalities were noticed on the baby, the prenatal tests were fine too.
We started to try to get pregnant again in March 2015. All of the attempts were the IUIs (7 or 8 from March 2015 to Feb.2016). I just couldn’t get over the fact, that it has to work, if it worked before so fast. Unfortunately that was not the case this time.
In October 2015 I had a tubal cannulation done to open the left fallopian tube.
In January 2016 I had a hormonal profile done. The numbers were: AMH 3.76, FSH 5.97. I always reacted well to the medication. Unfortunately the age is my enemy and I understand that.
My concern is about my husband’s sperm as well. I learned online, that sperm DNA fragmentation increases with the age and also diabetic patients have increased sperm DNA fragmentation too. I believe, that the combination of the two is even worse. Test of sperm DNA fragmentation was not done in our case. ICSI was recommended to us as a best option. I am very nervous about using it. My worries are that the sperm with highly fragmented DNA would be chosen. I know, that clinics in Europe and Australia use PICSI and MACS for the selection of the best sperm, that would be used with ICSI. I couldn’t find any clinic that would be offering these two methods in NJ, where I live. Why isn’t it standard in the US? According to publications these two methods increase success of pregnancy, not only success of fertilization. If that’s true, it would save couples so much heartache. I would like to know your opinion about using ICSI in our case. I read some study online comparing natural conception, conventional IVF and ICSI. Pregnancy that followed ICSI in this study had the highest risk of developmental problems of embryos and babies and also highest miscarriage rate. Is it too risky to use it without PICSI and MACS in our case? Would you recommend ICSI without these two methods and without sperm DNA fragmentation test? Would it be ok to use conventional IVF for us? We will do also PGS (NGS) It’s our first IVF.
Thank you
Hi Bibi,
I realize that having had one baby with IUI, you felt it would happen quickly again, but alas that is not so. As the person that 1st introduced IUI >30y ago and having a large experience with the procedure, I can tell you authoritatively that the success rate per cycle in women >40Y is <3%. You simply cannot afford wasting time on IUI. You need IVF and preferentially using Embryo Banking of PGS-normal embryos to make hay while the sun still shines. Given your husband's male factor, ICSI is mandatory. However, there is no convincing evidence in my opinion, that PICSI is beneficial. Wetried it and it made no difference. SCSA (DNA fragmentation testing), can be used but again, I am not sure it will change much even if DNA-FI is elevated.
Intracytoplasmic Sperm Injection ICSI which began in 1992 as a treatment for severe male factor infertility, involves the direct injection of a single sperm into each egg under direct microscopic vision.
Soon after the turn of the 20th century it was reported that while the diagnosis of a male factor infertility had remained static, the use of ICSI had markedly increased and that indications for ICSI had expanded from solely male infertility (for which it had primarily been developed) to a wide variety of other indications such as “unexplained infertility, unexplained IVF failure, polycystic Ovarian Syndrome (PCOS) and cases where the woman’s eggs had become more resistant to conventional fertilization. ICSI was also being used in cases where sperm was absent (or virtually absent) from the ejaculate due to congenital or traumatic or medically acquired obstruction of the main collecting ducts (vasa deferentia), testicular failure and in cases where for traumatic, neurologic, or psychologi reasons (impotency) no semen/sperm was being ejaculated. In such cases, sperm obtained through Testicular Sperm Extraction (TESE), or aspiration (TESA) was being successfully used for ICSI. Today in the United states more than 70% of all IVF fertilizations are being conducted using ICSI with high fertilization and pregnancy rates being reported, regardless of sperm concentration, motility or morphology.
Clearly ICSI is increasingly replacing conventional insemination due to its many benefits and lack of definable drawbacks. In fact, pregnancy rates achieved by this method of fertilization are at least as high as those of conventional IVF performed in cases of non-male-factor infertility. Indeed, ICSI is associated with high fertilization and pregnancy rates regardless of sperm concentration, motility or morphology.
Notwithstanding, the above, the proposition that ICSI be preferentially used as the routine method for fertilizing eggs in IVF continues to meet with resistance. Die hards argue that about 1-3% of pregnancies resulting from ICS are associated with congenital developmental and genetic defects that affect the offspring. They cite conditions such as *Beckwith-Wiedemann syndrome, *Angelman syndrome, *hypospadias, sex chromosome abnormalities, a slightly increased miscarriage rate and the fact that male offspring resulting fom ICSI pregnancies are themselves at risk of subsequently developing male infertility in later life.
What you do not often hear from nay-sayers is that those studies that site the above mentioned risks do not distinguish between cases where ICSI is/was mandated for male infertility )and cases where ICSI is/was done for other (non-male infertility) reasons. If this was done, what in my opinion would emerge is that the above mentioned birth defects and developmental conditions are largely confined to the underlying male factor for which ICSI was indicated and are not due to the ICSI process itself. In fact a relatively recent study performed in Sweden demostrated this well. Here 542 children who were conceived naturally were compared with 941 children conceived through IVF (440 by conventional IVF & 541via ICSI) The babies/children were assessed at birth and during the first 5 years of life: The findings revealed that while the incidence of birth and developmental defects was indeed higher in ICSI babies, this only applied to cases where ICSI had been done for male infertility. It did not apply to cases where ICSI was done in the absence of male factor infertility.
Another very important consideration that supports the routine fertilization of eggs by ICSI is the fact that good quality IVF relies heavily on an ability to adequately assess egg maturation immediately following egg retrieval. To do this requires removal of layers of cumulus oophoris (CO) cells that cover the egg envelopment (zona pellucida). Only after the CO is stripped can the 1st polar body (PB-1) which is located immediately under the zona pellucida be identified and it is the presence of PB-1 signifies that indicates that the egg has gone through meiosis (reproductive division) and is thus mature (M2) and overwhelmingly, successful fertilzation and viable embryo development requires that the fertilized egg was mature (M2). This assessment for the presence of PB-1 cannot be reliably done without first removing the cumulus oophoris cells attached to the outer surface of the zona pellucida. The problem is that stripping the cumulus oophoris cells away, markedly reduces natural fertilization potential, leaving ICSI as the only alternative by which to subsequently achieve viable embryo propagation. The only way by which to avoid fertilization by ICSI would be to bypass the important step of assessing egg maturation and this in my opinion would compromize IVF outcome significantly. Thus optimization of the entire IVF process virtually mandates routine ICSI in IVF.
For the above reasons, I proudly count myself among a growing majority of IVF practitioners who support the routine use of ICSI for all IVF patients
*Angelman syndrome is a complex genetic disorder characterized by delayed development, intellectual disability, speech impairment, and problems with movement and balance (ataxia). Most cases are not inherited, particularly those caused by a deletion in the maternal chromosome 15 or by paternal uniparental disomy. These genetic changes are random events that take place during the formation of reproductive cells (eggs and sperm) or in early embryonic development.
*Beckwith-Wiedemann syndrome is a congenital growth disorder that causes large body size, large organs, and other symptoms. t results from a defect in the genes on chromosome 11. About 10% of cases can be passed down through families.
*Hypospadias: Hypospadias is a condition where the opening isn't at the tip of the penis. Instead, it is located any place along the underside of the penis.
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 Aproach
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•Why did my IVF Fail
•Secondary Infertility: Addressing the Root Causes
•Blastocyst Embryo Transfers Done 5-6 Days Following Fertilization are Fast Replacing Earlier day 2-3 Transfers of Cleaved Embryos.
•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
•Male Factor 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
•IVF for Women Who Have Previously Conceived (Secondary Infertility).
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:
Email: Julied@sherivf.com
OR
Phone: 702-533-2691
800-780-7437
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
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