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.
Hello dr. Sher,
I am 28 yo, 5ft5inch, 119pounds. I have a diagnosis of hypothalamic amenorrhea. I have been on birth control from the age of 15 until 20. Before BC i had normal periods. After stopping BC, I had my first period after 7 months, then I had it every 3-4 months until 2015, when it completely stopped. My weight fluctuated from 114(2012) pounds to 136(2013) pounds and then back to 114 pounds in 2015 when my period completely stopped. I always excercised regularly (3-5 times a week, 40 min). I also started tracking my food in 2014 and became a bit obsessed with my intake. I also have had some stressful events with my mother in 2015 right after I had my last period.
My OB-GYN put me on HRT for 6m every year because of my bone health. Last year we decided we wanted to start a family and we went through one IVF procedure which resulted in 4 blastocysts, which were said to be perfect, but we got a BFN after a fresh transfer (I had to take a higher dose of medications, because at first I did not react to them) . We then had another FET last month which also resulted in a BFN. I was put on Letrozole, but did not react to it, so I had to take Menopur. We have two more blastocysts frozen.
Any ideas what is going on or how to handle my situation?
perhaps you have an implantation dysfunction due to an anatomical cause. It is not uncommon for women with prolonged absence of menstruation (amenorrhea) (whether due to prolonged menopause or hypothalamic (central) dysfunction) to have chronic estrogen deprivation. In many such cases this causes the uterus to shrink (involute) and/or renders the uterine lining (endometrium) relatively refractory (unresponsive) to subsequent estrogen therapy, increases the risk of miscarriage, and potentially compromises fetal development. All these sequelae are potentially avoidable if women who have prolonged amenorrhea ( >6 months) associated with hypoestrogenism, first have their blood gonadotropins (FSH and LH) and blood estradiol (E2) levels measured to differentiate between menopause (ovarian failure) and hypothalamic hypoestrogenism (where the low estrogen is due to under-stimulation of the ovaries. Thereupon they should be evaluated for physical evidence of uterine involution (shrinkage) and/or the ability of the uterine lining to thicken beyond 8mm in response to a therapeutic trial with supplementary estrogen. This should be followed by several months of cyclical estrogen therapy in an attempt to restore uterine size and endometrial responsiveness to estrogen, prior to their undergoing embryo transfer.
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ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.
Patients are encouraged to share the information I provide, with their treating Physicians and/or to avail themselves of my personal hands-on services, provided through batched IVF cycles that I conduct every 3 months at Los Angeles IVF (LAIVF) Clinic, Century City, Los Angeles, CA.
If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).
PLEASE SPREAD THE WORD ABOUT SFS!
Geoff Sher
I had a natural complete miscarriage on 9/19/19. I never got an ultrasound after just a physical exam. Ever since I have had pain in my lower right abdomen whenever I ovulate. It feels like my abdomen is going to explode and I have a sharp pain in one particular spot I think where my ovary is. I have also been spotting 5-7 days before getting my full flow period. My periods have been about 27–28 day’s apart if you don’t count the spotting. I am 35 years old and TTC and I’m worried this spotting could be a hormonal imbalance and is preventing me from becoming pregnant again. What should I do? The soonest drs appt I can get is six weeks away and this is so distressing. I’m worried I will never be able to have a baby. We have been trying for one year and have had one loss. Please help!
You need to be evaluated ASAP to rule out pathology. If you cannot get a GYN appointment, go to the ER.
Geoff Sher
Dear doctor
What causes follicles to grow too fast? I did the protocol that starts with birth control then overlap Lupron. The long protocol. I used this in two cycles. By cycle day 8 both times I had follicles that were 19mm. I read it’s bad for follicles to grow so fast. What’s your opinion?
It is not too fast if after 8 days of stimulation you are ready for a “trigger”.
Geoff Sher
Hi Dr. Sher. Thank you so much for this blog and all the valuable information you provide for couples dealing with fertility issues. I am 37 years old and want to bank embryos. How many should I bank if I want to have 3 kids given some of my blastocysts may be abnormal due to my age?
Women should not delay trying to have a baby, thinking that as long as they are ovulating regularly the biological clock can simply be put on hold or that they can simply to freeze their eggs and then later decide if/when to thaw them for use. The truth is that as a woman progresses to and beyond her mid thirties, there is a steady and ever accelerating decline in the quality of their eggs that will inevitably impact her chance of having a baby. Not only will her chances decline over time, but so will the chance of a successful, healthy pregnancy. This is regardless of whether she tries to conceive without medical assistance, or following assisted reproduction (intrauterine insemination-IUI, in vitro fertilization-IVF, or following egg freezing. You see….as a woman ages beyond her mid thirties the chance of any ovulated or harvested egg being chromosomally normal declines with the process accelerating rapidly as she advances to and beyond her 40’s. The result is a rapid reduction in conception rate and a rise in both miscarriages and chromosomal birth defects such as Down syndrome.
Consider the following statistics: At 30 years of age the natural conception rate per ovulation cycle is approximately 15-20%, the miscarriage rate…10-15% and the chance of a baby being affected by Down syndrome is but 1:1000 . The comparable best case scenario following a woman of the same age undergoing IVF rates is a 50-60% conception rate, an unaltered (10-15%) miscarriage rate and 1:100 chance of Down syndrome. Conversely, at age 45years, the chance of natural conception per month of trying is probably 1- 2%, the chance of miscarriage 50-60% and the risk of a baby having Down syndrome is at least 1:40. Following conventional IVF, the same woman would have about a 3-5% chance of having a baby with IVF center of excellence and should she conceive her risk of miscarrying or having a baby with Down syndrome would again be would again be 50-60% and 1:1000 respectively. But using conventional IVF this would be the best-case scenario.
In fact, as recently reported from Australia, (and is probably similar for other 1st world counties too) where about 3-5 per cent of babies are born annually through IVF, one out of three cycles initiated in women 25-34 years of age resulted in a live birth while at 45 years and above, < 1:100 initiated IVF cycles resulted in a live birth. PREIMPLANTATION GENETIC SCREENING (PGS)- EMBRYO/EGG SELECTION: Embryo karyotyping using PGS identifies all the chromosomes and allows identification of the most “competent” embryos (i.e., those that are highly likely to: a) propagate a viable pregnancy so improvers the efficiency of IVF that it can be considered to be a virtual “game changer”. Not only does it vastly improve the baby rate per embryo transferred, but regardless of the woman’s age it dramatically reduces the risk of both miscarriages and chromosomal birth defects... Who really benefits from PGS? PGS by allowing for thorough embryo evaluation, offers major diagnostic and therapeutic advantages, especially in cases of “unexplained” recurrent IVF failure “unexplained” infertility”, recurrent pregnancy loss (RPL) and in older women who not only produce fewer eggs per stimulated IVF cycle, but also whose eggs have a very much reduced chance of being chromosomally normal. Embryo Banking in older women: It is especially in women over 35 years and those with diminished ovarian reserve (DOR) that pre-implantation biopsy and selective banking (stock-piling) of PGS- normal embryos over several cycles, that the real benefit of this advanced break-through technology can be realized. Such selective embryo storage, in essence diminishes the impact of a rapidly advancing biological clock, allowing such women to capitalize on whatever time is left.......so to say, to “make hay while the sun still shines”. Egg freezing: An egg is a single cell, and as such no matter how good the freezing process, it is far more vulnerable to being damaged than is a multi-cellular embryo. Further more, even in young women, only about 1 in 3 eggs are chromosomally normal and this will inevitably steadily decline to less than 1 in 10 eggs by the time they reach their mid-40’s. Combine the difficulty in safely freezing a single cell(egg) with the fact that chromosomally abnormal eggs cannot propagate a healthy baby and you will readily understand why even today, the best one can hope for in a younger woman (<35y) is that each frozen egg will ultimately only propagate a normal live baby, is <8% . And, the older a woman becomes, the lower the chance of success, such that by age 40y and above it is <3%. Contrast this with embryo/blastocyst freezing where the comparable success rate per embryo is is about three (3) times greater. And when it comes to selectively freezing PGS-normal blastocysts, the success rate is between 40% and 50% per transferred blastocyst, regardless of the age of the woman. Given the adverse effect of advancing age on reproductive potential, women/couples seeking to initiate or expand their families should examine their reproductive options before reaching 35 years of age. These should include adopting a more aggressive stance such as moving actively and preferentially to assisted reproduction and IVF with fresh embryo transfer- versus freezing their embryos or eggs. In both cases, timing is everything and when embryo freezing is done, blastocyst (advanced embryo) selection using PGS, should be considered. When it comes to the choice of egg freezing/banking, I would caution that currently the methods of egg selection currently in use, do not include karyotyping and thus subsequent results remain so poor and imprecise as mandate careful deliberation. In my opinion, women over 35y should be cautioned and women over 40Y should be counseled against egg banking. I suggest that for such women embryo banking is a preferred approach. ___________________________________________________ ADDENDUM: PLEASE READ!! INTRODUCING SHER FERTILITY SOLUTIONS (SFS) Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.
Patients are encouraged to share the information I provide, with their treating Physicians and/or to avail themselves of my personal hands-on services, provided through batched IVF cycles that I conduct every 3 months at Los Angeles IVF (LAIVF) Clinic, Century City, Los Angeles, CA.
If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).
PLEASE SPREAD THE WORD ABOUT SFS!
Geoff Sher
Hi Dr Sher,
My husband and I tried to conceive for 15 months without success. I had many tests and was diagnosed with “unexplained infertility” however it was noted that the number of follicles I had was high (one scan showed a total of 20 follicles).
I began IVF stimulation and before egg collection I had at least 12 good-sized follicles. At egg collection they only retrieved 2 eggs. Fortunately one fertilised as an A-grade embryo and successfully implanted, I am now 12 weeks pregnant!
My fertility specialist never explained why I only retrieved 2 eggs, and never gave me a diagnosis. I would love to know why this happened and what I can do next time!
Also to note; during IVF stimulation I developed a small 6mm polyp in my uterus. Before conceiving, my menstrual cycles were long (avg. 35 days) and I had some acne (not so bad now at age 33) and some excess hair growth on face, breasts, chest.
Thank you,
Emma
In my opinion, the reason your egg number fell was the protocol used for ovarian stimulation and/or its implementation.
The importance of the IVF stimulation protocol on egg/embryo quality cannot be overstated. This factor seems often to be overlooked or discounted by t IVF practitioners who use a “one-size-fits-all” approach to ovarian stimulation. My experience is that the use of individualized/customized COS protocols can greatly improve IVF outcome. While no one can influence underlying genetics or turn back the clock on a woman’s age, any competent IVF specialist should be able to tailor the protocol for COS to meet the individual needs of the patient.
Gonadotropins (LH and FSH), whether produced by the pituitary gland or administered by way of fertility drugs, have different “targeted” sites of action in the ovary. FSH targets cells that line the inner wall of the follicle (granulosa cells) and also form the cumulus cells that bind the egg to the inner surface of the follicle. Granulosa cells are responsible for estrogen production.
LH, on the other hand, targets the ovarian connective tissue (stroma/theca) that surrounds ovarian follicles resulting in the production of male hormones such as testosterone (predominantly), androstenedione and DHEA. These androgens are then transported to the granulosa cells of the adjacent follicles in a “bucket brigade fashion”. There FSH converts testosterone to estradiol, causing granulosa cells to multiply (proliferate) and produce estradiol, follicles to grows and eggs to develop (ovogenesis) It follows that ovarian androgens (mainly testosterone) is absolutely indispensable to follicle/ egg growth and development.
However, the emphasis is on a “small” amount of testosterone. Over-exposure of the follicle to testosterone can compromise egg development and lead to an increased likelihood of chromosomal irregularities (aneuploid) following LH/hCG-induced egg maturational division (meiosis) and compromise embryo “competency/quality.
Ovarian androgens can also reach the uterine lining where they sometimes will compromise estrogen receptor -induced endometrial growth and development.
Many older women and those who have diminished ovarian reserve (DOR) have increased LH activity is increased. Such women either over-produce LH and/or the LH produced is far more biologically active. Chronically increased LH activity leads to overgrowth of ovarian connective tissue (stroma/theca). This condition, which is often referred to as Stromal Hyperplasia or hyperthecosis can result in excessive ovarian androgen/testosterone production and poorer egg-embryo quality/competency, Similarly, women with polycystic ovarian syndrome (PCOS), also characteristically have Stromal hyperplasia/hyperthecosis due to chronically increased LH activity. Thus they too often manifest with increased ovarian androgen production. It is therefore not surprising that “poor egg/embryo quality” is often also a feature of PCOS.
In my opinion, the over-administration of LH-containing menotropins such as Menopur, [which is comprised of roughly equal amount of FSH and hCG ,which acts similar to LH)], to older women, women with DOR and those who have PCOS can also lead to reduced egg/embryo competency . Similarly, drugs such as clomiphene or Letrozole that cause the pituitary gland to release excessive amounts of LH, are also potentially harmful to egg development and in my opinion, are best omitted from IVF COS protocols. This is especially the case when it comes to older women and those with DOR, who in my opinion should preferably be stimulated using FSH-dominant products such as Follistim, Puregon, Fostimon and Gonal-F.
Gonadotropin releasing hormone agonists (GnRHa): GnRHa such as Lupron, Buserelin, Superfact, Gonopeptyl etc. are often used to launch ovarian stimulation cycles. They act by causing an initial outpouring followed by a depletion of pituitary gonadotropins. This results in LH levels falling to low concentrations, within 4-7 days, thereby establishing a relatively “LH-free environment”. When GnRHa are administered for about 7 days prior to initiating gonadotropin stimulation (“long” pituitary down-regulation”), the LH depletion that will exist when COS is initiated, will usually be protective of subsequent egg development. In contrast, when the GnRHa administration commences along with the initiation of gonadotropin therapy, there will be a resultant immediate surge in the release of pituitary LH with the potential to increase ovarian testosterone to egg-compromising levels , from the outset of COS. This, in my opinion could be particularly harmful when undertaken in older women and those who have DOR.
GnRH-antagonists such as Ganirelix, Cetrotide and Orgalutron, on the other hand, act very rapidly (within hours) to block pituitary LH release. The purpose in using GnRH antagonists is to prevent the release of LH during COS. In contrast, the LH-lowering effect of GnRH agonists develops over a number of days.
GnRH antagonists are traditionally given, starting after 5th -7th day of gonadotropin stimulation. However, when this is done in older women and those (regardless of age) who have DOR, LH-suppression might be reached too late to prevent the deleterious effect of excessive ovarian androgen production on egg development in the early stage of ovarian stimulation. This is why, it is my preference to administer GnRH-antagonists, starting at the initiation of gonadotropin administration.
My preferred Protocols for Controlled Ovarian Stimulation (COS):
1.“Long” GnRHa (Lupron/Buserelin/Superfact/Gonopeptyl) Pituitary Down-regulation Protocol: The most commonly prescribed protocol for GnRHa/gonadotropin administration is the so-called “long protocol”. Here, GnRHa is given, starting a week or so prior to menstruation. This results in an initial rise in FSH and LH , which is rapidly followed by a precipitous fall to near zero. It is followed by a withdrawal bleed (menstruation), whereupon gonadotropin treatment should commence, while daily Lupron injections continue, to ensure a “low LH” environment. A modification to the “long protocol” which I prefer prescribing for older women and in cases of DOR, is the Agonist/Antagonist Conversion Protocol (A/ACP) where, upon the onset of a GnRHa-induced bleed, the agonist is supplanted by an antagonist (Ganirelix/Cetrotide/Orgalutron) and this is continued until the hCG trigger. In many such cases I often supplement with human growth hormone (HGH) in such cases in an attempt to enhance egg mitochondrial activity and so enhance egg development. This approach is often augmented with preimplantation genetic screening (PGS) of all embryos that reach the expanded blastocyst stage of development by day 5-6 post-fertilization. I also commonly recommend blastocyst banking to many such patients.
2.
3.Short (“Flare”) GnRHa Protocol: Another GnRHa usage for COS is the so called “(micro) flare protocol”. This involves initiating gonadotropin therapy commensurate with initiation of gonadotropin administration. The supposed objective is to deliberately allow Lupron to elicit an initial surge (“flare”) in pituitary FSH release in order to augment FSH administration by increased FSH production. Unfortunately, this “spring board effect” constitutes “a double-edged sword”. While it indeed increases the release of FSH, it at the same time causes a surge in LH release. The latter can evoke excessive ovarian stromal/thecal androgen production which could potentially compromise egg quality, especially when it comes to older women and women with DOR. I am of the opinion that by evoking an exaggerated ovarian androgen response, such “(micro) flare protocols” can harm egg/embryo quality and reduce IVF success rates, especially when it comes to COS in older women, and in women with diminished ovarian reserve. Accordingly, I do not prescribe such protocols to my IVF patients.
4.Estrogen Priming – This is the approach I sometimes prescribe for my patients who have virtually depleted ovarian reserve , as determined by very low blood anti-Mullerian hormone AMH levels (<0.2ng/ml or 2 pmol/L) and are thus likely to be very “poor responders”. It involves a modified A/ACP. We start with the birth control pill (BCP) for 10 days or longer, overlap it for 3 days with a GnRHa whereupon the BCP is stopped. Th GnRHa is continued until the onset of menstruation (usually 5-7 days later) to cause pituitary LH, down-regulation. Upon menstruation and confirmation by ultrasound and measurement of blood estradiol levels that adequate ovarian suppression has been achieved, the dosage of GnRHa is stopped and is immediately supplanted by daily administration of GnRH antagonist. The patient is given twice-weekly injections of estradiol valerate (Delestrogen) for a period of 8 days whereupon COS is initiated using a relatively high dosage FSH-(Follistim, Fostimon, Puregon or Gonal F), which is continued along with daily administration of GnRH antagonist until the “hCG “trigger.” This approach is often augmented with HGH administration throughout the process of COS and by preimplantation genetic screening (PGS) of all embryos that reach the expanded blastocyst stage of development by day 5-6 post-fertilization. I also commonly recommend blastocyst banking to many such patients.
Estrogen Priming has succeeded in significantly enhancing ovarian response to gonadotropins in many of otherwise very poor responders.
Triggering egg Maturation prior to egg Retrieval: hCG versus GnRHa
With ovulation induction using fertility drugs, the administration of 10,000U hCGu (Pregnyl; Profasi, Novarel) or 500mcg hCGr (Ovidrel/Ovitrel) “trigger”) sends the eggs (into maturational division (meiosis). This process is designed to halve the chromosome number, resulting in mature eggs (M2) that will have 23 chromosomes rather that the 46 chromosomes they had prior to the “trigger”. Such a chromosomally numerically normal (euploid), mature (MII) eggs, upon being fertilized will (hopefully) propagate euploid embryos that have 46 chromosomes and will be “: competent” to propagate viable pregnancies. In my opinion, the key is to always “trigger” with no less than 10,000U of hCGu or 500mcg hCGr (Ovidrel/Ovitrel). Any lesser dosage often will reduce the efficiency of meiosis and increase the risk of the eggs being aneuploid. I personally do not use the agonist (Lupron) “trigger”, unless it is combined with (low dosage) hCG. The supposed reason for using the agonist, (Lupron) “trigger” is that by inducing meiosis through compelling a surge in the release of LH by the pituitary gland, the risk it reduces the risk of OHSS. This may be true, but it comes at the expense of egg quality because the extent of the induced LH surge varies and if too little LH is released, meiosis can be compromised, thereby increasing the likelihood of aneuploid and immature (MI) eggs. And there are other better approaches to preventing OHSS (e.g. “prolonged coasting”), in my opinion.
Use of the Birth Control Pill (BCP) to launch IVF-COS.
In natural (unstimulated) as well as in cycles stimulated with fertility drugs, the ability of follicles to properly respond to FSH stimulation is dependent on their having developed FSH-responsive receptors. Pre-antral follicles (PAF) do not have such primed FSH receptors and thus cannot respond properly to FSH stimulation with gonadotropins. The acquisition of FSH receptor responsivity requires that the pre-antral follicles be exposed to FSH, for a number of days (5-7) during which time they attain “FSH-responsivity” and are now known as antral follicles (AF). These AF’s are now able to respond properly to stimulation with administered FSH-gonadotropins. In regular menstrual cycles, the rising FSH output from the pituitary gland insures that PAFs convert tor AF’s. The BCP (as well as prolonged administration of estrogen/progesterone) suppresses FSH. This suppression needs to be countered by artificially causing blood FSH levels to rise in order to cause PAF to AF conversion prior to COS commencing, otherwise pre-antral-to –antral follicle conversion will not take place in an orderly fashion, the duration of ovarian stimulation will be prolonged and both follicle and egg development may be compromised. GnRH agonists cause an immediate surge in release of FSH by the pituitary gland thus causing conversion from PAF to SAF. This is why women who take a BCP to launch a cycle of COS need to have an overlap of the BCP with an agonist. By overlapping the BCP with an agonist for a few days prior to menstruation the early recruited follicles are able to complete their developmental drive to the AF stage and as such, be ready to respond appropriately to optimal ovarian stimulation. Using this approach, the timing of the initiation of the IVF treatment cycle can readily and safely be regulated and controlled by varying the length of time that the woman is on the BCP.
Since optimizing follicular response to COS requires that prior to stimulation with gonadotropins, FSH-induced conversion from PAF to AF’s first be completed and the BCP suppresses FSH, it follows when it comes to women launching COS coming off a BCP something needs to be done to cause a rise in FSH for 5-7 days prior to menstruation heralding the cycle of CO S. This is where overlapping the BCP with a GnRHa comes in. The agonist causes FSH to be released by the pituitary gland and if overlapped with the BCP for several days and this will (within 2-5 days) facilitate PAF to AF conversion…. in time to start COS with the onset of menstruation. Initiating ovarian stimulation in women taking a BCP, without doing this is suboptimal.
I strongly recommend that you visit www.SherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•The Fundamental Requirements For Achieving Optimal IVF Success
•Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
•Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
•Optimizing Response to Ovarian Stimulation in Women with Compromised Ovarian Response to Ovarian Stimulation: A Personal Approach.
•Egg Maturation in IVF: How Egg “Immaturity”, “Post-maturity” and “Dysmaturity” Influence IVF Outcome:
•Commonly Asked Question in IVF: “Why Did so Few of my Eggs Fertilize and, so Many Fail to Reach Blastocyst?”
•Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Staggered IVF
•Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation
•Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
•IVF: Selecting the Best Quality Embryos to Transfer
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
•PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
•IVF outcome: How Does Advancing Age and Diminished Ovarian Reserve (DOR) Affect Egg/Embryo “Competency” and How Should the Problem be addressed.
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ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.
Patients are encouraged to share the information I provide, with their treating Physicians and/or to avail themselves of my personal hands-on services, provided through batched IVF cycles that I conduct every 3 months at Los Angeles IVF (LAIVF) Clinic, Century City, Los Angeles, CA.
If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).
PLEASE SPREAD THE WORD ABOUT SFS!
Geoff Sher