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Dear Patients,

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

– Geoffrey Sher, MD

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26,379 Comments

S. King

Dr. Sher,

What are your thoughts on Embryo Glue and HCG infusion? Does it increase live births and reduce miscarriage?

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Dr. Geoffrey Sher

I know of no convincing data that proves a benefit from using embryo glue!

Geoff Sher

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Cassidy

Hi!

I’ve just completed a cycle and today they froze 4x 5 day blasts and there are several other growing and are expected to made it blastocyst on day 6. I’m considering doing a fresh transfer tomorrow with the 6 day blasts, it seems unlikely that they’ll work (given I’m 42) but I feel it won’t hurt reaching the envitable sooner (I’ve not attempted any transfers yet). I’ve got several Euploid embryos that I can try – just wondering, however, can a failed embryo transfer impact the outcome of future embryo transfer?

Many thanks – your help is truly appreciated!

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Dr. Geoffrey Sher

No! A failed embryo transfer now should not impact a future ET.

Geoff Sher

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Victoria

Dear Dr Sher,

I was wondering if you could review my HCG rise. I have had two previous miscarriages and am nervous.
4 weeks 4 days 1001
5 weeks 3084
5 weeks 2 days 5712

Doubling time has slowed from 45 hours to 54 hours. Is this normal?

Thank you.

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Dr. Geoffrey Sher

At this stage of pregnancy it is not abnormal to see a slow down in the hCG rise.

Geoff Sher

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Victoria

My question seems to have not gone through;
Hi,
I’ve had 2 previous miscarriages and am now getting my HCG checked. My HCG at 4 weeks 4 days was 1001, at 5 weeks was 3084 (doubling time 45 hours) but at 5 weeks 2 days HCG is 5712 (doubling time 54 hours). My doubling time seems to have slowed dramatically. Is this a cause for concern? Do I prepare for another miscarriage? Or a normal finding given the levels are now higher? I have an ultrasound booked but would like some advice in the mean time?

Thanks!

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Stephanie

I am 30 years old. I had a FET on 5/19 with PGT-A testing. I had my first Hcg test done on 5/27 and it was 98. I had a second Hcg draw on 6/1 and it was 1120. Everything was looking great.

I had my first ultrasound on 6/14 and all that was visible was a gestational sac (11.7 mm) and a yolk sac (4.5 mm). My doctor was please with the ultrasound and assumed I was just a little earlier than expected. This does not make sense to me because the dates are exact with IVF. He wants to see me next week for another scan. I feel that she should have at least been a fetal pole at this point. Is it possible for this to be a normal pregnancy and a just a little behind?

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Dr. Geoffrey Sher

Yes! It is possible that this could turn out to be a normal pregnancy!

Good luck!

Geoff Sher

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Katie

I don’t think my question went through- What are your thoughts on the covid vaccine for pregnant women who had immune-related subfertility? I have Hashimotos and celiac disease with positive ANA. I am 21 weeks pregnant. Would you recommend the covid shot or could that cause some kind of immune flare up that could harm the baby?

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Dr. Geoffrey Sher

It probably wont do any harm. But personally, I would delay the vaccination until after the baby is born. But discuss with your personal OB!

Good luck!

Geoff Sher

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Raj

Hi Dr.

We did a FET of a PGT tested euploid embryo on 5/27.

Got a home hcg test positive on 6/6 at 10dpt. Day 11 initial beta HCG was 54, day 13 -94, day 15-150, day 16-207,and day 19-587.

After 15dpt result of 150, our doctor advised to stop meds (prior to ultrasound confirmation, which we did for 1.5 days out of fear of complications explained to us). Had an independent beta HCG drawn following morning 6/12 (16dpt) which showed 207 HCG. No symptoms of cramping or bleeding. We decided to resume meds (estrogen TID and PIO IM at bedtime) pending repeat beta and ultrasound on 6/15.

Based on day 19 (6/15) beta HCG of 587 and ultrasound done same day ( which showed no sign of sac or embryo), our doctor is telling us that this is not a viable pregnancy and we should stop estrogen/progesterone as at this point it’s either a pregnancy of unknown origin or an ectopic pregnancy not yet seen.

We have read that in 15% of pregnancies, slow rising HCG could be normal and that rise does not necessarily need to be every 48 hours and/or 100% to be considered viable. If we were to go by those metrics, the sudden increase to 587 could indicate we would be over 1,000 in 2 days at 5w6d. And which is the lowest beta HCG the doctor told us is something would be visible on ultrasound with anyway. Also, we were under impression sometimes nothing is visible on u/s until 6 weeks gestation. Through this entire time, at home urine pregnancy tests have been consistently coming back positive, with darkening test lines. Finally, the doctor mentioned to us that there’s no such thing as late implantation with IVF, which we understand – but my wife felt like her implantation cramps occurred and continued later.

Between those facts and questions, we are left wondering if it’s actually too early to call it, confused about the facts and circumstances, and feeling like it’s too early to stop but of course not wanting to prolong the inevitable and cause greater harm to my wife and her health.

Any feedback would be helpful! Thank you in advance!

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Dr. Geoffrey Sher

It could be too early still. I would continue meds, give it 10 days and do an US for a definitive answer. Your OB should however, be watching for the unlikely event of an ectopic (tubal) pregnancy.

Geoff Sher

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Katie K

What are your thoughts on pregnant women who have immune-related infertility getting the covid shot?

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Dr. Geoffrey Sher

I have no problem with it, but I personally advise against taking the shot during pregnancy and would wait at least 1 month after the vaccination before trying to conceive.

Geoff sher

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Simone Campbell

I am 39 years old and in the mist of my 1st IVF cycle due to SIN of my tube and MFI. I started BCP on April 19th, had a hysteroscopy on May 20th . Stopped BC on 6/7 and went in for my first baseline u/s on 6/9. RE said several small follicles on both ovaries and we was clear to push forward with IVF. I have regular cycles every 28 days and my protocol is as follows : Lupron 5 units, Follistim 350 +1 and Menopur 1 vial. I went in today for my 2nd U/S and no follicles on left ovaries and 5 follicles on right ovaries. My RE was disappointed and stated that this was not what he expected and asked was I giving my injections correctly. They want me back in 3 days and also awaiting bloodwork from today. My bloodwork from 6/9 was Total Estradiol- 23.63 pg/mL and Progesterone Level- 0.32 ng/mL. The only thing I can think of that I did out of the ordinary was get acupuncture yesterday for the 1st time. Any suggestions? He kept me at the same dosage until I return on Friday and stated that he may have to call in another prescription for me.

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Dr. Geoffrey Sher

It sounds as if you might have severely diminished ovarian reserve and if so, you would in my opinion need a an aggressive but individualized protocol for ovarian stimulation.

It is primarily the egg (rather than the sperm) that determines the chromosomal integrity (karyotype) of the embryo, the most important determinant of egg/embryo competency”. A “competent” egg is therefore one that has a normal karyotype and has the best potential to propagate a “competent” embryo. In turn, a “competent embryo is one that possesses the highest potential to implant and develop into a normal, healthy, baby.
When it comes to reproductive performance, humans are the least efficient of all mammals. Even in young women under 35y, at best only 1 out of 2 eggs are chromosomally numerically normal (euploid). The remained have an irregular number of chromosomes (aneuploid) and are thus “incompetent”. The incidence of egg aneuploidy increases with age such by age 39 years, 3 in 4 are competent, and by the mid-forties, less 8 to 9 out of 10 are aneuploid. The fertilization of an aneuploid egg will inevitably lead to embryo aneuploid and an aneuploid embryo cannot propagate a normal pregnancy
Within hours of the spontaneous pre-ovulatory luteinizing hormone (LH) surge, and also following administration of the human chorionic gonadotropin (hCG) “trigger” shot (given to induce ovulation after ovarian stimulation with fertility drugs), the egg embarks on a rapid maturational process that involves halving of its 46 chromosomes to 23. During this process, (known as meiosis) 23 chromosomes are retained within the nucleus of the egg while the remaining (now redundant) 23are expelled, enveloped by a thin membrane. This small structure comes to lie immediately below the “shell” of the egg (the zona pellucida) and is known as the 1st polar body or PB-1. The spermatozoon, in the process of its maturation also undergoes meiosis at which time it too reduces its chromosomes by half. Thus in the process of fertilization the sperm divides into two separate functional gametes, each containing 23 chromosomes such that with subsequent fertilization, the 23 chromosomes in the egg, fuse with the 23 chromosomes of the mature sperm resulting in the development of an embryo that has 46 chromosomes (the normal human genome) comprising a combination of the genetic material from both partners. For the embryo to have exactly 46 chromosomes (the euploid number), both the mature egg and mature spermatozoon must contain exactly 23 chromosomes. Only euploid embryos are “competent” (capable of developing into healthy babies). Those with an irregular number of chromosomes (aneuploid embryos) are “incompetent” and are incapable of developing into healthy babies. While embryo “incompetence” can result from either egg or sperm aneuploidy, it usually stems from egg aneuploidy. However, in cases of moderate or severe male factor infertility, the sperm’s contribution to aneuploidy of the embryo increases significantly.
While embryo ploidy (numerical chromosomal integrity) is not the only determinant of its “competency, it is by far the most important and in fact is rate-limiting factor in human reproduction. It is causal in most cases of “failed implantation” which in turn is responsible for most cases of failed IVF. It causes early miscarriages and is responsible for many chromosomal birth defects such as X-monosomy and Down’s syndrome. . In most cases, embryos that develop too slowly as well as those that grow too fast (i.e. ones that by day 3 post-fertilization comprise fewer than 6 cells or more than 9 cells) and/or embryos that contain a large amount of cell debris or “fragments” are usually aneuploid and are thus “incompetent”. Additionally, embryos that fail to survive in culture to the blastocyst stage are also almost always aneuploid/”incompetent”. At a certain point in the later stage of a woman’s reproductive career, the number of remaining eggs in her ovaries falls below a certain threshold, upon which she is unable to respond optimally to fertility drugs. Often times this is signaled by a rising day 3 blood follicle stimulating hormone (FSH) level. Such women with diminishing ovarian reserve produce fewer eggs in response to ovarian stimulation. While diminished ovarian reserve is most commonly encountered in women over 40 years of age it can and indeed sometimes does occur in much younger women. A few important (but often overlooked concepts should be considered in this regard: 1. Age: It is advancing chronologic age and NOT declining ovarian reserve (as evidenced by abnormal blood AMH or FSH that results in an increased incidence of egg/embryo “incompetence” due to aneuploidy 2. DOR: The ovaries and developing eggs of women with diminished ovarian reserve (regardless of age) are highly susceptible to the adverse effect of excessive Luteinizing Hormone (LH)-induced overproduction of male hormones (mainly testosterone). A little testosterone produced by the ovary promotes normal follicle growth and orderly egg development but too much testosterone has the opposite effect. That is why (especially in women with diminished ovarian reserve who often have high LH and increased ovarian testosterone production , the use of ovarian stimulation protocols that fail to down-regulate LH production prior to initiating stimulation with gonadotropins, often prejudices egg/embryo quality and IVF outcome. Simply stated, while age is certainly the most important factor in determining the incidence of egg/embryo aneuploidy, women with diminished ovarian reserve (regardless of their age), unless they receive customized/individualized protocols of ovarian stimulation are less likely to propagate euploid (competent) eggs/embryos.
Selection of the ideal protocol for controlled ovarian stimulation: While NOTHING can be done to lower the incidence of age related aneuploidy, it is indeed possible to avoid a further increase in egg/embryo aneuploidy by individualizing the protocols of ovarian stimulation used.
• My preferred protocols for women who have relatively normal ovarian reserve:
a) The conventional long pituitary down regulation protocol: BCP are commenced early in the cycle and continued for at least 10 days. Starting 3 days before the BCP is to be discontinued, it is overlapped with an agonist such as Lupron 10U daily for three (3) days and continued until menstruation begins (which should ensue within 5-7 days of stopping the BCP). At that point an US examination is done along with a baseline measurement of blood estradiol to exclude a functional ovarian cyst. Simultaneously, the Lupron dosage is reduced to 5U daily and an FSH-dominant gonadotropin such as Follistim, Puregon or Gonal-f daily is commenced for 2 days. On the 3rd day the gonadotropin dosage is reduced and a small amount of daily menotropin (Menopur 75U daily) is added. Daily ultrasound and blood estradiol measurements are done starting on the 7th or 8th day of gonadotropin administration and continued until daily ultrasound follicle assessments indicate that most follicles have fully developed. At this point egg maturation is “triggered” using an intramuscular injection of 10,000U hCG. And an egg retrieval is scheduled for 36h later.
b) The agonist/antagonist conversion protocol (A/ACOP): This is essentially the same as the conventional long down regulation protocol (as above), except that with the onset of post-BCP menstruation, the agonist is supplanted by daily administration of a GnRH antagonist (e.g. Ganirelix, Cetrotide or Orgalutron) at a dosage of 125mcg daily until the day of the hCG trigger
• My preferred protocol for women who have relatively diminished ovarian reserve (DOR):
When it comes to women who have DOR I favor the use of the A/ACP, adding supplementary human growth hormone (HGH). In some cases where the DOR is regarded as severe, I also augment the process with estrogen priming, preferring twice weekly intramuscular administration of estradiol valerate (Delestrogen), starting with the commencement of antagonist injection and continuing for 1 week before commencing gonadotropins and continued until the hCG “trigger. I further recommend that such women be offered access to preimplantation genetic screening (PGS) for4 embryo selection and in some cases, for embryo banking (stockpiling). This is followed in a later hormone replacement cycle with the selective transfer of up to two (2) PGS-normal, euploid blastocysts. In this way we are able to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” , significantly enhancing the opportunity to achieve a viable pregnancy
• The following Ovarian stimulation protocols are in my opinion best avoided in women with DOR:
a) Microdose agonist (e.g. Lupron) “flare” protocols
b) High doses of LH/hCG-containing fertility drugs (E.G. Menopur).
c) Protocols that incorporate supplementation with male hormones (e.g. testosterone)
d) Supplementation with DHEA
e) Clomiphene citrate or Letrozole which cause an elevation in LH and thus increase ovarian male hormone (testosterone and androstenedione output.
f) “Triggering” egg maturation using too low a dosage of hCG (e.g. 5,000U rather than 10,000U) or Ovidrel e.g. 250mcg of Ovidrel rather than 500mcg)
g) “Triggering” women who have large numbers of follicles using an agonist such as Lupron, Superfact or Buserelin.
• Preimplantation Genetic Screening (PGS):
The introduction of preimplantation genetic screening (PGS) for the first time permits identification of all the chromosomes in the egg and embryo such that we can now far better identify “competent” (euploid) embryos for selective transfer to the uterus. This vastly improves the efficiency and success of the IVF process. This additional tool has better equipped us to manage cases with DOR. In my opinion, next generation gene sequencing (NGS), currently represents the most reliable method for performing PGS

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

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

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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.

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

reply
Jamie

Is it alarming I’m not very nauseated or puking at 7w4d? I’m worried of having mild symptoms, just sore breasts and fatigue really. I had some nausea yesterday but today I feel totally normal. My first ultrasound was 6w2d and baby measured perfectly with HB 125bpm. So nervous for my ultrasound this weekend.

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Dr. Geoffrey Sher

Not everyone has strong symptoms of pregnancy. Consider yourself fortunate.

Good luck!

Geoff Sher

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Cassidy

Hello Dr Sher!

I’m due to have my 1st IVF transfer in couple of days time, at 42 yrs old. I’ve followed the banking approach, so have several Euploid embryos stored from previous IVF cycles (started the process at 41). I went to a new clinic this time, one that is highly rated for older/more difficult patients. I noted that the IVF protocol was more in-line with the one you favour, i.e. with respect to lower doses of LH etc. The cycle was intensely monitored with daily/sometimes twice daily blood tests to check various hormone levels and this cycle appears to have produced the best result, i.e. 16 eggs, 13 fertilised and 12 growing on day 3 (8 more optimally than the others), however we’ve not reached day 5 and there could be more attrition. But judging by my last cycles a reasonable number should reach blastocyst stage.

I was talked out of doing PGT-A testing (on hindsight, not sensible approach) so I’m going to be transferring embryos blind. They allow you to transfer 3 at a time, usually they transfer the best quality. However, I’m thinking given I don’t know if I’ve got any implantation issues, is it sensible to transfer the best quality now? Should I transfer lower quality and see how I get on?

Given my age, as far as I understand maybe 1 in 10 are genetically normal, so it could be the case that I transfer the only “good” embryo from this cycle and it fails to implant because I’ve got NK cells/undiagnosed endometriosis/some of implantation issue. Is it sensible to transfer lower quality now and if it fails have all the relevant tests, hysteroscopy (to check for polyps), NK killer cell test etc.

As an FYI: my hormones are well balanced, I ovulate, respond well to IVF stimulation and have a good uterine lining (age appears to be the only limiting factor!)
Many thanks for help in advance…. MOST APPRECIATED!!!
Kind regards,
Cassidy

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Dr. Geoffrey Sher

To be honest, you need to be evaluated for an anatomical or immunologic implantation dysfunction before doing an FET. Frankly, at your age, you cannot afford an errorv of omission. Time is not on your side.

Implantation dysfunction is unfortunately often overlooked as an important cause of IVF failure. In the pursuit of optimizing outcome with IVF, the clinician has a profound responsibility to meticulously assess and address this important issue if IVF success is to be optimized. This is especially relevant in cases of “unexplained IVF failure, Recurrent Pregnancy Loss (RPL) and in women suspected of having underlying anatomical and immunologic factors. Doing so will not only maximize the chance of a viable pregnancy but enhancing placentation, will at the same time promote the noble objective of optimizing the quality of life after birth.”
IVF success rates have been improving over the last decade. The average live birth rate per embryo transfer in the U.S.A for women under 40y using their own eggs , is currently better than 1:3 women. However, there is still a wide variation from program to program for IVF live birth rates, ranging from 20% to near 50%. Based upon these statistics, the majority of women undergoing IVF in the United States require two or more attempts to have a baby. IVF practitioners in the United States commonly attribute the wide dichotomy in IVF success rates to variability in expertise of the various embryology laboratories. This is far from accurate. In fact, other factors such as wide variations in patient selection and the failure to develop individualized protocols for ovarian stimulation or to address those infective, anatomical and immunologic factors that influence embryo implantation are at least equally important.
About 80% of IVF failures are due to “embryo incompetency” that is largely due to an irregular quota of chromosomes (aneuploidy) which is usually related to advancing age of the woman and is further influenced by other factors such as the protocol selected for ovarian stimulation, diminished ovarian reserve (DOR)m and severe male factor infertility. However in about 20% of dysfunctional cases embryo implantation is the cause of failure.
Anatomical Endo-uterine Lesions: This blog article will focus on implantation dysfunction and IVF failure due to:
• Anatomical abnormalities in the uterine cavity (e.g. scarring, polyps and encroaching fibroid tumors)
• A thin endometrial lining
• Immunologic rejection of the embryos
Several studies performed both in the United States and abroad have confirmed that a dye X-Ray or hysterosalpingogram (HSG) will fail to identify small endouterine surface lesions in >20% of cases. This is significant because even small uterine lesions have the potential to adversely affect implantation. Hysteroscopy is the traditional method for evaluating the integrity of the uterine cavity in preparation for IVF. It also permits resection of most uterine surface lesions, such as submucous uterine fibroids (myomas), intrauterine adhesions and endometrial or placental polyps. All of these can interfere with implantation by producing a local “inflammatory- type” response similar in nature to that which is caused by an intrauterine contraceptive device. Hysterosonography (syn; HSN/ saline ultrasound examination) and hysteroscopy have all but supplanted HSG to assess the uterine cavity in preparation for IVF. HSN which is less invasive and far less expensive than is than hysteroscopy involves a small amount of a sterile saline solution is injected into the uterine cavity, whereupon a vaginal ultrasound examination is performed to assess the contour of the uterine cavity.
Endometrial Thickness: As far back as in 1989 I first reported on the finding that ultrasound assessment of the late proliferative phase endometrium following ovarian stimulation in preparation for IVF, permits better identification of those candidates who are least likely to conceive. We noted that the ideal thickness of the endometrium at the time of ovulation or egg retrieval is >9 mm and that a thickness of less than 8 mm bodes poorly for a successful outcome following IVF.
Then in 1993, I demonstrated that sildenafil (Viagra) introduced into the vagina prior to hCG administration can improve endometrial growth in many women with poor endometrial development. Viagra’s mechanism of action is improvement in uterine blood flow with improved estrogen delivery…thereby enhancing endometrial development.
Immunologic factors: These also play a role in IVF failure. Some women develop antibodies to components of their own cells. This “autoimmune” process involves the production of antiphospholipid, antithyroid, and/or anti-ovarian antibodies – all of which may be associated with activation of Natural Killer (NK) cells in the uterine lining. Activated NK cells (NKa) release certain cytokines (TH-I) that if present in excess, often damage the trophoblast (the embryo’s root system) resulting in immunologic implantation dysfunction (IID). This can manifest as “infertility” or as early miscarriages). In other cases (though less common), the problem is due to “alloimmune” dysfunction. Here the genetic contribution by the male partner renders the embryo “too similar” to the mother. This in turn activates NK cells leading to implantation dysfunction. These IID’s are treated using combinations of medications such as heparin, Clexane, Lovenox, corticosteroids and intralipid (IL).

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

• A Fresh Look at the Indications for IVF
• The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• IVF and the use of Supplementary Human Growth Hormone (HGH) : Is it Worth Trying and who needs it?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• IVF: Approach to Selecting the Best Embryos for Transfer to the Uterus.
• Fresh versus Frozen Embryo Transfers (FET) Enhance IVF Outcome
• Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
• Genetically Testing Embryos for IVF
• Staggered IVF
• Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
• Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
• IVF: Selecting the Best Quality Embryos to Transfer
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
• PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
• PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
• Endometrial Receptivity Array (ERA): Is There an actual “There, There”?
• IVF Failure and Implantation Dysfunction:
• Diagnosing and Treating Immunologic Implantation Dysfunction (IID)
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• A Thin Uterine Lining: Vaginal Viagra is Often the Answer (update)
• Cervical Ureaplasma Urealyticum Infection: How can it Affect IUI/IVF Outcome?
• The Role of Nutritional Supplements in Preparing for IVF
• The Basic Infertility Work-Up
• Defining and Addressing an Abnormal Luteal Phase
• Male Factor Infertility
• Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in Favor
• Hormonal Treatment of Male Infertility
• Hormonal Treatment of Male Infertility
• Antisperm Antibodies, Infertility and the Role of IVF with Intracytoplasmic Sperm Injection (ICSI)
• Endometriosis and Infertily
• Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF
• Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
• Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
• Early -Endometriosis-related Infertility: Ovulation Induction (with or without Intrauterine Insemination) and Reproductive Surgery Versus IVF
• Deciding Between Intrauterine Insemination (IUI) and In Vitro Fertilization (IVF).
• Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & Con’s!IUI-Reflecting upon its Use and Misuse: Time for a Serious “Reality Check
• Mode of Action, Indications, Benefits, Limitations and Contraindications for its ue
• Clomiphene Induction of Ovulation: Its Use and Misuse!
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.

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

reply
Dr. Geoffrey Sher

To be honest, you need to be evaluated for an anatomical or immunologic implantation dysfunction before doing an FET. Frankly, at your age, you cannot afford an errorv of omission. Time is not on your side.

Implantation dysfunction is unfortunately often overlooked as an important cause of IVF failure. In the pursuit of optimizing outcome with IVF, the clinician has a profound responsibility to meticulously assess and address this important issue if IVF success is to be optimized. This is especially relevant in cases of “unexplained IVF failure, Recurrent Pregnancy Loss (RPL) and in women suspected of having underlying anatomical and immunologic factors. Doing so will not only maximize the chance of a viable pregnancy but enhancing placentation, will at the same time promote the noble objective of optimizing the quality of life after birth.”
IVF success rates have been improving over the last decade. The average live birth rate per embryo transfer in the U.S.A for women under 40y using their own eggs , is currently better than 1:3 women. However, there is still a wide variation from program to program for IVF live birth rates, ranging from 20% to near 50%. Based upon these statistics, the majority of women undergoing IVF in the United States require two or more attempts to have a baby. IVF practitioners in the United States commonly attribute the wide dichotomy in IVF success rates to variability in expertise of the various embryology laboratories. This is far from accurate. In fact, other factors such as wide variations in patient selection and the failure to develop individualized protocols for ovarian stimulation or to address those infective, anatomical and immunologic factors that influence embryo implantation are at least equally important.
About 80% of IVF failures are due to “embryo incompetency” that is largely due to an irregular quota of chromosomes (aneuploidy) which is usually related to advancing age of the woman and is further influenced by other factors such as the protocol selected for ovarian stimulation, diminished ovarian reserve (DOR)m and severe male factor infertility. However in about 20% of dysfunctional cases embryo implantation is the cause of failure.
Anatomical Endo-uterine Lesions: This blog article will focus on implantation dysfunction and IVF failure due to:
• Anatomical abnormalities in the uterine cavity (e.g. scarring, polyps and encroaching fibroid tumors)
• A thin endometrial lining
• Immunologic rejection of the embryos
Several studies performed both in the United States and abroad have confirmed that a dye X-Ray or hysterosalpingogram (HSG) will fail to identify small endouterine surface lesions in >20% of cases. This is significant because even small uterine lesions have the potential to adversely affect implantation. Hysteroscopy is the traditional method for evaluating the integrity of the uterine cavity in preparation for IVF. It also permits resection of most uterine surface lesions, such as submucous uterine fibroids (myomas), intrauterine adhesions and endometrial or placental polyps. All of these can interfere with implantation by producing a local “inflammatory- type” response similar in nature to that which is caused by an intrauterine contraceptive device. Hysterosonography (syn; HSN/ saline ultrasound examination) and hysteroscopy have all but supplanted HSG to assess the uterine cavity in preparation for IVF. HSN which is less invasive and far less expensive than is than hysteroscopy involves a small amount of a sterile saline solution is injected into the uterine cavity, whereupon a vaginal ultrasound examination is performed to assess the contour of the uterine cavity.
Endometrial Thickness: As far back as in 1989 I first reported on the finding that ultrasound assessment of the late proliferative phase endometrium following ovarian stimulation in preparation for IVF, permits better identification of those candidates who are least likely to conceive. We noted that the ideal thickness of the endometrium at the time of ovulation or egg retrieval is >9 mm and that a thickness of less than 8 mm bodes poorly for a successful outcome following IVF.
Then in 1993, I demonstrated that sildenafil (Viagra) introduced into the vagina prior to hCG administration can improve endometrial growth in many women with poor endometrial development. Viagra’s mechanism of action is improvement in uterine blood flow with improved estrogen delivery…thereby enhancing endometrial development.
Immunologic factors: These also play a role in IVF failure. Some women develop antibodies to components of their own cells. This “autoimmune” process involves the production of antiphospholipid, antithyroid, and/or anti-ovarian antibodies – all of which may be associated with activation of Natural Killer (NK) cells in the uterine lining. Activated NK cells (NKa) release certain cytokines (TH-I) that if present in excess, often damage the trophoblast (the embryo’s root system) resulting in immunologic implantation dysfunction (IID). This can manifest as “infertility” or as early miscarriages). In other cases (though less common), the problem is due to “alloimmune” dysfunction. Here the genetic contribution by the male partner renders the embryo “too similar” to the mother. This in turn activates NK cells leading to implantation dysfunction. These IID’s are treated using combinations of medications such as heparin, Clexane, Lovenox, corticosteroids and intralipid (IL).

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

• A Fresh Look at the Indications for IVF
• The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• IVF and the use of Supplementary Human Growth Hormone (HGH) : Is it Worth Trying and who needs it?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• IVF: Approach to Selecting the Best Embryos for Transfer to the Uterus.
• Fresh versus Frozen Embryo Transfers (FET) Enhance IVF Outcome
• Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
• Genetically Testing Embryos for IVF
• Staggered IVF
• Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
• Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
• IVF: Selecting the Best Quality Embryos to Transfer
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
• PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
• PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
• Endometrial Receptivity Array (ERA): Is There an actual “There, There”?
• IVF Failure and Implantation Dysfunction:
• Diagnosing and Treating Immunologic Implantation Dysfunction (IID)
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• A Thin Uterine Lining: Vaginal Viagra is Often the Answer (update)
• Cervical Ureaplasma Urealyticum Infection: How can it Affect IUI/IVF Outcome?
• The Role of Nutritional Supplements in Preparing for IVF
• The Basic Infertility Work-Up
• Defining and Addressing an Abnormal Luteal Phase
• Male Factor Infertility
• Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in Favor
• Hormonal Treatment of Male Infertility
• Hormonal Treatment of Male Infertility
• Antisperm Antibodies, Infertility and the Role of IVF with Intracytoplasmic Sperm Injection (ICSI)
• Endometriosis and Infertily
• Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF
• Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
• Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
• Early -Endometriosis-related Infertility: Ovulation Induction (with or without Intrauterine Insemination) and Reproductive Surgery Versus IVF
• Deciding Between Intrauterine Insemination (IUI) and In Vitro Fertilization (IVF).
• Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & Con’s!IUI-Reflecting upon its Use and Misuse: Time for a Serious “Reality Check
• Mode of Action, Indications, Benefits, Limitations and Contraindications for its ue
• Clomiphene Induction of Ovulation: Its Use and Misuse!
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.

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

reply
diana L.

Sehr geehrter Dr Sher,
mein erster ICSI brachte 6 Eizellen, von denen 4 befruchtet eingefroren werden konnten.
IVF weil Ehemann vasektomiert, mit eingefrorenen Spermien.
Ich F 40, Endometriose, AMH 0,3 (vor 6 Monaten in den USA war der AMH 1,4 – wird morgen erneut getestet – Messfehler??)

Dies war mein erster IVF /ICSI Versuch. Vorher nie versucht, anderweitig schwanger zu werden (IUI o.Ä.):
Langes Protokoll, ZT 16 Profact, dann nächster Zyklus Tag 6 Menopur zusätzliche (300 Einheiten).
Triggershot Brevactit and ZT20, Punktion 2 Tage später.

Jetzt “vergass” die Klinik, dass ich back-to-back einen zweiten ALL Freeze Zyklus machen wollte. Bzw ging man davon aus, ich sollte meine Regel abwarten, dann wieder gleiches Protokoll, Tag 16 Profakt, später Menopur. Alles scheint sehr unorganisiert dort.
Nun rief mich die Ärztin an mit einem Alternativvorschlag :
kurzes Protokoll mit Menopur 300 und Pergoveris im Wechsel, kein Profakt sondern etwas anderes zur Eisprung Unterdrückung.

Sie sagt, es müsse nicht unbedingt weniger Eier bedeuten, wenn ich ein kurzes Protokoll mache. Nach Ihren Erfahrungen hatte ich dieses erste Mal 6 Eier, weil meine Eierstöcke sich “noch einmal aufbäumten”. Ich müsse jetzt sowieso mit weniger Eiern rechnen.

Jetzt meine Fragen:
Welches Protokoll würden Sie empfehlen für mein Alter, mein AMH und die Endometriose?
Macht es Sinn, den Zyklus zu retten(heute kam meine Periode) und diesmal ein kurzes Protokoll zu machen oder werden das voraussichtlich weniger Eier (weil zu nah dran und jetzt kurzes Protokoll)?
Macht es Sinn, eher eine Pause zu machen und dann wieder ein langes Protokoll? Oder ist das ganze Protokoll falsch?
Gibt es dieses “Aufbäumen” der Eierstöcke, wenn man eine erste IVF im “Alter”(40) macht?
War es sinnvoll eine ICSI zu machen, wenn doch mein Mann sehr gute Spermien ( wenn auch eingefrorene) hat? Sollten wir es nächstes Mal ohne ICSI versuchen?
Würden Sie ein ganz anderes Protokoll nehmen?
Wie stehen Sie zu DHEA?
Macht es Sinn, dass die Klinik an Tag 1 eingefroren hat? Die Ärztin sagte, es gebe eine höhere Auftau-Überlebensrate als bei eingefrorenen Blastozysten.
Gibt es zufällig eine Klinik in Berlin, die Sie empfehlen? Oder macht es Sinn, ins europäische Ausland zu gehen, weil es dort mehr medizinische Möglichkeiten (Medikamente) gibt?
Tausend Dank für Ihre informative Webseite! Ich werde gleich Ihr Buch bestellen!
Mit herzlichen Grüßen
Diana L.

reply
Dr. Geoffrey Sher

Please post this question in English and` I will respond promptly.

Geoff Sher

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Christine

Hello,

LMP started 5/12.
Took pregnancy test 6/8 = negative.
Took pregnancy test around 4pm 6/9 = positive
Around 7pm on 6/9 I started spotting
6/10, 6/11 and 6/12 bled with clots present
6/13 spotting and 6/14 spotted in morning but has since stopped.
Took blood test at Dr’s office today and hcg =29.8

Does this sound like a miscarriage?
Have repeat blood test on 6/17

Thanks

reply
Dr. Geoffrey Sher

I am afraid, this does not look good! Repeat the test in 2 days tom see if it doubles as it should.

Good luck!

Geoff Sher

reply
Tina

Hello, I’m 43 years old. I’m doing the ivf journey. My doctor told me I need to quit my medicine I’m on day 5 she said my estrogen level is only a 11. Medicine not working and I only measuring 0.8cm on follicle. Left and fight She said I have several small one but . I’m so hurt I paid all this money. Now she said I have to go with donor eggs. My husband don’t want to

reply
Dr. Geoffrey Sher

I agree that egg donation will give the best chance for success , by far. However, before you do this, , perhaps we should talk first. Call my assistant Patti at 702-533-2691 for an online consultation.

Geoff Sher

reply
Natalie

Hi Dr Sher

I was hoping you could help me with a few queries.

I am 40 years old and considering doing medicated IUI inbetween ivf cycles (I am single and using donor sperm). I generally have an endometrial thickness of 65-70mm in a natural cycle.

What drug would you recommend to use?

I also have 3 aneuploid embryos from prior ivf cycles which are all -22. Have you ever transferred monosomy 22 and had success ?

Many thanks for taking the time to answer.

Natalie

reply
Dr. Geoffrey Sher

You should not do IUI at 40y , in my opinion. The chance of success is only about 1:40. You don’t have the time to waste on such a poor chance. IVF is by far your best option.

In my opinion, your monosomy 22 embryos could be mosaics…but because of your age this is highly unlikely. Again, time is your enemy.

Perhaps we should talk first. Call my assistant Patti at 702-533-2691 for an online consultation.

Geoff Sher

reply
Natalie

Thank you for your reply.

I would love to talk to you but I am based in the UK?

reply
Dr. Geoffrey Sher

That does not matter. Sixty percent of my patients are from abroad. And because we consult does not mean that I would have treat you in the USA.

Geoff Sher

reply
Shae Kamara

Good evening,

I am gearing up for my third IVF cycle. Kaiser Permanente would like me to have their typical fertility work up done. I have endometriosis and endometrial hyperplasia. My concern is that they would like me to have another HSG. I’ve had 4 in my lifetime. Each time led to a bad reaction. Immediately after the 3rd time I developed a cyst that continued to grow and leak in my POD. I have imaging that shows it wasn’t there prior to this procedure. Imaging immediately after shows it grew to 10 times the volume of my left ovary. I had difficulty walking/intercourse. They said not was wrong and ignored my complaints of pain. It finally burst a few months later and I immediately gained 10 lbs in less than a week, stretch marks on the front of my thighs, and looked pregnant. It has been hard to maintain my weight since. My weight has never fluctuated prior at the time I was 33. I am now approaching 35. My inflammation/endometriosis was controlled at this point as I had excision surgery in 1 year prior in October 2018. After this procedure I could feel inflammation traveling up my abdominal wall and up my back. I developed back acne that traveled down to my waist for the first time. They also stated that my fallopian tubes appeared closed. I had another HSG 4 months later Dec 2019 to confirm this diagnosis. The 4th time my menstruation and inflammation became so bad. I begin vomiting uncontrollably during the first day prior and during menstruation. The pain was always bad, but I never vomited from it prior to this. I would vomit from the pain of gas trapped/traveling through my intestine every 30 mins at times. At this time I did not undergo any IVF treatment or change in medication. My IVF cycles were the following year in 2020.

My question – Is endometriosis or endometrial hyperplasia a counterindication for HSG? Why would any doctor advise an HSG for a woman that already has endometriosis? I didn’t voice my concern the last two times. However, I am very hesistant to undergo an HSG a 5th time. Isn’t a diagnostic hysteroscopy and vaginal ultrasound a better alternative? I could not find any information for this online.

reply
Dr. Geoffrey Sher

In my opinion, If you do not have a hydrosalpinx(which is not common with endometriosis , unless you had concomitant pelvic inflammatory disease, your tubal status is irrelevant and an HSG is of no value. You need IVF. However, endometriosis affects IVF outcome (see below).

When women with infertility due to endometriosis seek treatment, they are all too often advised to first try ovarian stimulation (ovulation Induction) with intrauterine insemination (IUI) ………as if to say that this would be just as likely to result in a baby as would in vitro fertilization (IVF). Nothing could be further from reality It is time to set the record straight. And hence this communication!
Bear in mind that the cost of treatment comprises both financial and emotional components and that it is the cost of having a baby rather than cost of a procedure. Then consider the fact that regardless of her age or the severity of the condition, women with infertility due to endometriosis are several fold more likely to have a baby per treatment cycle of IVF than with IUI. It follows that there is a distinct advantage in doing IVF first, rather than as a last resort.
So then, why is it that ovulation induction with or without IUI is routinely offered proposed preferentially to women with mild to moderately severe endometriosis? Could it in part be due to the fact that most practicing doctors do not provide IVF services but are indeed remunerated for ovarian stimulation and IUI services and are thus economically incentivized to offer IUI as a first line approach? Or is because of the often erroneous belief that the use of fertility drugs will in all cases induce the release (ovulation) of multiple eggs at a time and thereby increase the chance of a pregnancy. The truth however is that while normally ovulating women (the majority of women who have mild to moderately severe endometriosis) respond to ovarian stimulation with fertility drugs by forming multiple follicles, they rarely ovulate > 1 (or at most 2) egg at a time. This is because such women usually only develop a single dominant follicle which upon ovulating leaves the others intact. This is the reason why normally ovulating women who undergo ovulation induction usually will not experience improved pregnancy potential, nor will they have a marked increase in multiple pregnancies. Conversely, non-ovulating women (as well as those with dysfunctional ovulation) who undergo ovulation induction, almost always develop multiple large follicles that tend to ovulate in unison. This increases the potential to conceive along with an increased risk multiple pregnancies.

So let me take a stab at explaining why IVF is more successful than IUI or surgical correction in the treatment of endometriosis-related infertility:
1. The toxic pelvic factor: Endometriosis is a condition where the lining of the uterus (the endometrium) grows outside the uterus. While this process begins early in the reproductive life of a woman, with notable exceptions, it only becomes manifest in the 2ndhalf of her reproductive life. After some time, these deposits bleed and when the blood absorbs it leaves a visible pigment that can be identified upon surgical exposure of the pelvis. Such endometriotic deposits invariably produce and release toxins” into the pelvic secretions that coat the surface of the membrane (the peritoneum) that envelops all abdominal and pelvic organs, including the uterus, tubes and ovaries. These toxins are referred to as “the peritoneal factor”. Following ovulation, the egg(s) must pass from the ovary (ies), through these toxic secretions to reach the sperm lying in wait in the outer part the fallopian tube (s) tube(s) where, the sperm lie in waiting. In the process of going from the ovary(ies) to the Fallopian tube(s) these eggs become exposed to the “peritoneal toxins” which alter s the envelopment of the egg (i.e. zona pellucida) making it much less receptive to being fertilized by sperm. As a consequence, if they are chromosomally normal such eggs are rendered much less likely to be successfully fertilized. Since almost all women with endometriosis have this problem, it is not difficult to understand why they are far less likely to conceive following ovulation (whether natural or induced through ovulation induction). This “toxic peritoneal factor impacts on eggs that are ovulated whether spontaneously (as in natural cycles) or following the use of fertility drugs and serves to explain why the chance of pregnancy is so significantly reduced in normally ovulating women with endometriosis.
2. The Immunologic Factor: About one third of women who have endometriosis will also have an immunologic implantation dysfunction (IID) linked to activation of uterine natural killer cells (NKa). This will require selective immunotherapy with Intralipid infusions, and/or heparinoids (e.g. Clexane/Lovenox) that is much more effectively implemented in combination with IVF.
3. Surgical treatment of mild to moderate endometriosis does not usually improve pregnancy potential:. The reason is that endometriosis can be considered to be a “work in progress”. New lesions are constantly developing. So it is that for every endometriotic seen there are usually many non-pigmented deposits that are in the process of evolving but are not yet visible to the naked eye and such evolving (non-visible) lesions can also release the same “toxins that compromise fertilization. Accordingly, even after surgical removal of all visible lesions the invisible ones continue to release “toxins” and retain the ability to compromise natural fertilization. It also explains why surgery to remove endometriotic deposits in women with mild to moderate endometriosis usually will fail to significantly improve pregnancy generating potential. In contrast, IVF, by removing eggs from the ovaries prior to ovulation, fertilizing these outside of the body and then transferring the resulting embryo(s) to the uterus, bypasses the toxic pelvic environment and is therefore is the treatment of choice in cases of endometriosis-related infertility.
4. Ovarian Endometriomas: Women, who have advanced endometriosis, often have endometriotic ovarian cysts, known as endometriomas. These cysts contain decomposed menstrual blood that looks like melted chocolate…hence the name “chocolate cysts”. These space occupying lesions can activate ovarian connective tissue (stroma or theca) resulting in an overproduction of male hormones (especially testosterone). An excess of ovarian testosterone can severely compromise follicle and egg development in the affected ovary. Thus there are two reasons for treating endometriomas. The first is to alleviate symptoms and the second is to optimize egg and embryo quality. Conventional treatment of endometriomas involves surgical drainage of the cyst contents with subsequent removal of the cyst wall (usually by laparoscopy), increasing the risk of surgical complications. We recently reported on a new, effective and safe outpatient approach to treating endometriomas in women planning to undergo IVF. We termed the treatment ovarian Sclerotherapy. The process involves; needle aspiration of the “chocolate colored liquid content of the endometriotic cyst, followed by the injection of 5% tetracycline hydrochloride into the cyst cavity. Such treatment will, more than 75% of the time result in disappearance of the lesion within 6-8 weeks. Ovarian sclerotherapy can be performed under local anesthesia or under conscious sedation. It is a safe and effective alternative to surgery for definitive treatment of recurrent ovarian endometriomas in a select group of patients planning to undergo IVF

I am not suggesting that all women with infertility-related endometriosis should automatically resort to IVF. Quite to the contrary…. In spite of having reduced fertility potential, many women with mild to moderate endometriosis can and do go on to conceive on their own (without treatment). It is just that the chance of this happening is so is much lower than normal.

IN SUMMARY: For young ovulating women (< 35 years of age ) with endometriosis, who have normal reproductive anatomy and have fertile male partners, expectant treatment is often preferable to IUI or IVF. However, for older women, women who (regardless of their age) have any additional factor (e.g. pelvic adhesions, ovarian endometriomas, male infertility, IID or diminished ovarian reserve-DOR) IVF should be the primary treatment of choice. I strongly recommend that you visit www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly. • The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride” • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation (COS) • The Fundamental Requirements For Achieving Optimal IVF Success • Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols. • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF: • The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID): PART 1-Background • Immunologic Implantation Dysfunction (IID) & Infertility (IID): PART 2- Making a Diagnosis • Immunologic Dysfunction (IID) & Infertility (IID): PART 3-Treatment • Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID) • Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management: (Case Report) • Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID) • Intralipid (IL) Administration in IVF: It’s Composition; how it Works; Administration; Side-effects; Reactions and Precautions • Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy! • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas • Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year • A personalized, stepwise approach to IVF • How Many Embryos should be transferred: A Critical Decision in IVF? • Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF • Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice. • Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options • Early -Endometriosis-related Infertility: Ovulation Induction (with or without Intrauterine Insemination) and Reproductive Surgery Versus IVF • Treating Ovarian Endometriomas with Sclerotherapy. • Effect of Advanced Endometriosis with Endometriotic cysts (Endometriomas) on IVF Outcome & Treatment Options. • Deciding Between Intrauterine Insemination (IUI) and In Vitro Fertilization (IVF). • Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & • Induction of Ovulation with Clomiphene Citrate: Mode of Action, Indications, Benefits, Limitations and Contraindications for its use • Clomiphene Induction of Ovulation: Its Use and Misuse! ______________________________________________________ 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.

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

reply
Jessie perez

I’m 36 years old with pcos. I have 3 daughters. 1st was concieved with clomid and iui. 2nd was concieved 8 years later on 3rd round of letrozole. 3rd was concieved 2 months after my second was born. Naturally. Pregnancy 4 was also Naturally but ended in miscarriage due to trisomy 16. Pregnancy 5 was Naturally as well. Healthy baby boy we lost him at 14 weeks gestation. Pregnancy 6.. 100 mg of clomid..another healthy boy.. we lost him at 12 weeks. Pregnancy 7. 7.5 mg of letrozole.. a baby girl ended in miscarriage as well. Cause was triploid at 7 weeks.
I am starting letrozole again and just had cycle day 3 labs done. Total testosterone came back high at 86.6 ng/dl and dheas came back low at 44 ug/dl.
My dr wants me to take a dhea supplement.. wouldn’t this increase my testosterone that is already high, and hinder my chances of conception.. is it safe to take this cycle that I’ve taken letrozole. Today is cycle day 8…
What could cause dheas to be low and testosterone to be high.. this doesn’t make sense to me.

reply
Dr. Geoffrey Sher

My preference would be to avoid DHEA.

Dehydroepiandrosterone (DHEA), is steroid hormone produced by the adrenal glands and ovary. It is involved in producing the male hormones, androstenedione testosterone and also estrogen. DHEA blood levels tend to decline naturally with age.
Under the effect if luteinizing hormone (LH), DHEA is metabolized to testosterone in ovarian connective tissue (theca/stroma). Thereupon the testosterone is transported to the granulosa cells that form the innermost layer of the ovarian follicles where, under the influence of follicle stimulating hormone (FSH)-induced desmolase and aromatase enzymatic activity the testosterone is converted to estradiol. As this happens, granulosa cells multiply, follicle fluid volume increases along with estrogen output and egg development is promoted.
It is recognition of the essential/indispensable role that male hormones (mainly testosterone) play in follicle and egg development that prompted the belief that by giving DHEA and boosting ovarian testosterone production might benefit follicle/egg development. This belief was given some credence by an Israeli study that in 2010 reported on improved fertility when a group of infertile women were given the administration of 75mg of oral DHEA for 5 months. However, this study was seriously flawed by the fact that it did not separate out women who had diminished ovarian reserve, older women and those with PCOS, all of whom have increased LH-induced production of testosterone. In fact, we recently completed a study (currently being processed for publication) where we conclusively showed that when follicular fluid testosterone levels exceeded a certain threshold, egg quality was seriously prejudiced as evidenced by a marked increase in the incidence of egg chromosomal defects (aneuploidy).
Consider the following: Ovarian testosterone is needed for follicular development. However, the amount required is small. Too much ovarian testosterone spills over into the follicular fluid and has a deleterious effect on egg/follicle development. Some women (women with diminished ovarian reserve –DOR, older women and those with polycystic ovarian syndrome-PCOS) who tend to have increased LH biological activity, already over-produce testosterone. To such women, the administration of DHEA to such women, by “adding fuel to the fire” can be decidedly prejudicial, in my opinion. Young women with normal ovarian reserve do not over produce LH-induced ovarian testosterone, and are thus probably not at significant risk from DHEA supplementation. It is noteworthy that to date, none of the studies that suggest a benefit from DHEA therapy have differentiated between young healthy normal women with normal ovarian reserve on the one hand and older women, those with DOR and women with PCOS on the other hand.

In Some countries DHEA treatment requires a medical prescription and medical supervision. Not so in the U.S.A where it can be bought over the counter. Since DHEA is involved in sex hormone production, including testosterone and estrogen, individuals with malignant conditions that may be hormone dependent (certain types of breast cancer or testicular cancer) should not receive DHEA supplementation. Also, if overdosed with DHEA some “sensitive women” might so increase their blood concentrations of testosterone that they develop increased aggressive tendencies or male characteristics such as hirsuites (increased hair growth) and a deepening voice. DHEA can also interact other medications, such as barbiturates, corticosteroids, insulin and with other oral diabetic medications.
BUT the strongest argument against the use of routine DHEA supplementation is the potential risk of compromising egg quality in certain categories of women and since there is presently no convincing evidence of any benefit, why take the risk in using it on anyone.
Finally, for those who in spite of the above, still feel compelled to take DHEA, the best advice I can give is to consult their health care providers before starting the process.

Addendum: One potential advantage of DHEA therapy if used appropriately came from a study conducted by Washington University School of Medicine in St. Louis, MI and reported in the November 2004 issue of the “Journal of the American Medical Association” which showed that judicious (selective) administration of 50mg DHEA daily for 6 months resulted in a significant reduction of abdominal fat and blood insulin in elderly women.

Geoff Sher
.

reply
Dr. Geoffrey Sher

My preference would be to avoid DHEA.

Dehydroepiandrosterone (DHEA), is steroid hormone produced by the adrenal glands and ovary. It is involved in producing the male hormones, androstenedione testosterone and also estrogen. DHEA blood levels tend to decline naturally with age.
Under the effect if luteinizing hormone (LH), DHEA is metabolized to testosterone in ovarian connective tissue (theca/stroma). Thereupon the testosterone is transported to the granulosa cells that form the innermost layer of the ovarian follicles where, under the influence of follicle stimulating hormone (FSH)-induced desmolase and aromatase enzymatic activity the testosterone is converted to estradiol. As this happens, granulosa cells multiply, follicle fluid volume increases along with estrogen output and egg development is promoted.
It is recognition of the essential/indispensable role that male hormones (mainly testosterone) play in follicle and egg development that prompted the belief that by giving DHEA and boosting ovarian testosterone production might benefit follicle/egg development. This belief was given some credence by an Israeli study that in 2010 reported on improved fertility when a group of infertile women were given the administration of 75mg of oral DHEA for 5 months. However, this study was seriously flawed by the fact that it did not separate out women who had diminished ovarian reserve, older women and those with PCOS, all of whom have increased LH-induced production of testosterone. In fact, we recently completed a study (currently being processed for publication) where we conclusively showed that when follicular fluid testosterone levels exceeded a certain threshold, egg quality was seriously prejudiced as evidenced by a marked increase in the incidence of egg chromosomal defects (aneuploidy).
Consider the following: Ovarian testosterone is needed for follicular development. However, the amount required is small. Too much ovarian testosterone spills over into the follicular fluid and has a deleterious effect on egg/follicle development. Some women (women with diminished ovarian reserve –DOR, older women and those with polycystic ovarian syndrome-PCOS) who tend to have increased LH biological activity, already over-produce testosterone. To such women, the administration of DHEA to such women, by “adding fuel to the fire” can be decidedly prejudicial, in my opinion. Young women with normal ovarian reserve do not over produce LH-induced ovarian testosterone, and are thus probably not at significant risk from DHEA supplementation. It is noteworthy that to date, none of the studies that suggest a benefit from DHEA therapy have differentiated between young healthy normal women with normal ovarian reserve on the one hand and older women, those with DOR and women with PCOS on the other hand.

In Some countries DHEA treatment requires a medical prescription and medical supervision. Not so in the U.S.A where it can be bought over the counter. Since DHEA is involved in sex hormone production, including testosterone and estrogen, individuals with malignant conditions that may be hormone dependent (certain types of breast cancer or testicular cancer) should not receive DHEA supplementation. Also, if overdosed with DHEA some “sensitive women” might so increase their blood concentrations of testosterone that they develop increased aggressive tendencies or male characteristics such as hirsuites (increased hair growth) and a deepening voice. DHEA can also interact other medications, such as barbiturates, corticosteroids, insulin and with other oral diabetic medications.
BUT the strongest argument against the use of routine DHEA supplementation is the potential risk of compromising egg quality in certain categories of women and since there is presently no convincing evidence of any benefit, why take the risk in using it on anyone.
Finally, for those who in spite of the above, still feel compelled to take DHEA, the best advice I can give is to consult their health care providers before starting the process.

Addendum: One potential advantage of DHEA therapy if used appropriately came from a study conducted by Washington University School of Medicine in St. Louis, MI and reported in the November 2004 issue of the “Journal of the American Medical Association” which showed that judicious (selective) administration of 50mg DHEA daily for 6 months resulted in a significant reduction of abdominal fat and blood insulin in elderly women.

Geoff Sher
.

reply
Jessie

What would cause dheas to be low and testosterone to be high? Will this affect me being able to concieve this cycle ?

reply
Dr. Geoffrey Sher

There are many causes. The commonest is a higher than normal LH associated with polycystic ovarian syndrome.

Perhaps we should talk. If you are interested in my input though an online Face-Time or Skype consultation, please call my assistant, Patti Converse at all 702-533-2691 .

Geoff Sher

reply
Jessie perez

With a low dheas level and high testosterone level.. do you think I could still conceive this cycle with the letrozole?

reply
Autumn

I have had 2 miscarriages in the past so I do worry but I am pregnant. My first hcg level was 148 and 2 days late it is 342. Does this sound okay? I am just so worried. I don’t have an ultrasound until July 12.

reply
Dr. Geoffrey Sher

I think this could turn out to be na keeper!

Good luck!

Geoff Sher

reply
Andrew

Hi Dr Sher!

We recently got our results back from the HLA DQ panel screen but no one is able to tell us if we are a DQ Alpha gene match or not. Do you take consults for people wanting results explained? Thank you

reply
Dr. Geoffrey Sher

Yes…but it also depends on which laboratory performed the tests and whether/where/how you had NK cell activation assessed.

Central to making a diagnosis of an immunologic implantation dysfunction (IID) is a need for the appropriate interpretation of Natural Killer Cell Activity (NKa). In this regard, one of the commonest and most serious errors, is interpret the blood concentration of natural killer cells as being relevant. Rather it is the activity (toxicity) of NK cells that matters as mentioned. This activity can best be measured using the blood, K-562 target cell test (the gold standard). and/ or endometrial biopsy for cytokine activity.
With the K-562 test, the most important consideration is the percentage of target cells “killed” in the “native state”. In most cases a level of >10% killing should be regarded with suspicion and >12% overtly abnormal. In addition to reporting the result of the K-562 test, in the “native state” (without adding, Immunoglobulin-G (IVIG) or Intralipid (IL) which many Laboratories erroneously do to try and determine whether either or both of these immune therapies would have a therapeutic benefit or is/are unlikely to be of clinical value. The entire premise upon which this assertion is based, is in my opinion flawed. Clinically such NK cell deactivation can only be significantly affected in vivo as it takes more than a week following infusion to occur. Thus, what happens to the percentage of target cells killed with the K-562 test, by adding IVIG or IL is in my opinion irrelevant
Another way to assess endometrial NKa is by measuring TH-1 and TH-2 cytokines in endometrial tissue derived through biopsy.TH-1 cytokines kill the trophoblast (the root system of the embryo). Thus if is an excess of TH-1 cytokine activity is found with/without a disruption in the TH-1: TH-2 ratio, this points to NK cell activation.
There are basically two causes of immunologic implantation dysfunction (IID), a) Autoimmune (85%) & , b) Alloimmune (15%). The former occurs when the body reacts to its own tissue and the latter (far less common) when the male and female partners share certain genotypic similarities involving DQ alpha and HLA genes. In both cases IID results in rejection of the pregnancy due to uterine Natural Killer (NK) Cell and T-cell activation leading to the release of an excessive amount of TH-1 cytokines. These, “toxins” attack the embryo’s root system (trophoblast), killing the cells and causing implantation to fail.
Autoimmune Implantation Dysfunction: Autoimmune implantation dysfunction, most commonly presents with presumed “infertility” due to such early pregnancy losses that the woman did not even know she was pregnant in the first place. Sometimes there as an early miscarriage. Tests required are: a) blood levels of all IgA, IgG and IgM-related antiphospholipid antibodies (APA’s) directed against six or seven specific phospholipids, b) both antithyroid antibodies (antithyroid and antimicrosomal antibodies), c) a comprehensive reproductive immunophenotype (RIP) and, c) most importantly, assessment of Natural Killer (NK) cell activity (rather than concentration) by measuring by their killing, using the K-562 target cell test and/or endometrial cytokine activity tests.
It is important to recognize that currently there are only about 3 or 4 Reproductive Immunology Reference Laboratories in the U.S.A that, are capable of reliably analyzing the required elements with a sufficient degree of sensitivity and specificity. I use a Reprosource, a laboratory located in Boston,MA.
Patients with Alloimmune implantation Dysfunction usually present with a history of unexplained (usually repeated) miscarriages or secondary infertility (where the woman conceived initially and thereupon was either unable to conceive again or started having repeated early miscarriages. However, it can also present as “presumed” primary infertility. Alloimmune dysfunction is diagnosed by testing the blood of both the male and female partners for matching DQ alpha genes and NK/CTL activation. It is important to note that any DQ alpha match (partial or complete) will only result in an IID when there both a DQa/HLA match exists along with NK cell activation. With the exception of cases where both partners have a total (absolute DQa match and treatment requires the use of sperm from a non-matching sperm donor, about 90% of cases alloimmune implantation will have a partial match where 1: 2 embryos will match the woman’s DQa genotype and half will not. In cases of an alloimmune dysfunction (with associated NKa), treatment with IL or IVIG will in my opinion, will not protect against a matching embryo being rejected. It can only clear the NK environment for an embryo that does not match the woman’s DQa genotype. For this reason, it is my opinion that only 1 embryo should be transferred at a time because, given the fact that i:2 embryos will match, transferring >1 embryo at a time creates a risk that the matching embryo will evoke a local NKa/’cytokine response that will “muddy the water” for both. Thus, in cases of a “partial” DQa match I recommend against transferring more than a single embryo at a time.
.
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.

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

• The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation (COS)
• The Fundamental Requirements for Achieving Optimal IVF Success
• Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
• 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) Why did my IVF Fail
• Recurrent Pregnancy Loss (RPL): Why do I keep losing my Pregnancies
• Genetically Testing Embryos for IVF
• Staggered IVF
• Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
• 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?
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management 🙁 Case Report)
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; how it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year.
• A personalized, stepwise approach to IVF
• Nutritional supplements in IVF
______________________________________________________
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.

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

reply
Raja

I have been watching your youtube videos and would like to thank you for your education. I have had 2 failed IVF cycles with 3 failed transfers. We deal with male factor (vasectomy) and endometriosis. We never achieve good-quality embryos. Our last cycle was slightly better with good grade embryos until day 3 and a loss of all but 1 on day 5. The one that was left was a slow-growing morula. My first protocol was the long down-regulation with birth control, then suprefact and stim with gonal f and luveris, HCG trigger (Ovidrel), We got severely fragmented embryos from day 1. I had a hysteroscopy and laparoscopy after. Mild endo was discovered and a cyst on my left ovary. Everything was removed and we started our next cycle 3 months later. I was given Zoladex for 1 month, then stim with gonal and menopur with orgalutran on day 4 until trigger. Double trigger with suprefact and Pregnyl. Our day 3 embryos were good quality but as I said we lost all but one by day 5. I will start my last stim cycle in a few months but I am wondering which protocol we should use? We also will use donor sperm this time.
Any advice would be much appreciated! Thank you!

reply
Dr. Geoffrey Sher

Thank you!

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 15y ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3. The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.

4. Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:

a. A“ thin uterine lining”
b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c. Immunologic implantation dysfunction (IID)
d. Endocrine/molecular endometrial receptivity issues
e. Ureaplasma Urealyticum (UU) Infection of cervical mucous and the endometrial lining of the uterus, can sometimes present as unexplained early pregnancy loss or unexplained failure following intrauterine insemination or IVF. The infection can also occur in the man, (prostatitis) and thus can go back and forth between partners, with sexual intercourse. This is the reason why both partners must be tested and if positive, should be treated contemporaneously.
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.

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

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

reply
Raja

Thank you for your reply. I think my main question would be what protocol you would use for someone with endometriosis considering birth control is not recommended?

reply
Dr. Geoffrey Sher

Please call Patti (702-533-2691) and set up an online consultation with me to discuss!

Geoff Sher

reply
Ashley

Hi there – I just had an FET on Tuesday and the next morning, I seemed to have an orgasm in a dream and didn’t know until I woke up and felt my uterus contract. Will this compromise implantation and the potential success of this transfer?

reply
Lisa

Hi there,

I had an embryo transfer 2 x 5aa blasts however the dr was meant to do an hcg infusion before the transfer and forgot. This has sent me into a bit of a spin and I’m convinced this means it won’t work now. Is all hope lost?

reply
Dr. Geoffrey Sher

I do NOT believe uterine Lavage with hCG has any proven benefit!

Geoff Sher

reply
MC

I am 28 years old, and my AMH is quickly declining. A year ago it was 4, a month ago it was 1.5, and today it was at 1. My RE is recommended a DuoStim cycle. I did one IVF cycle that resulted in 4 eggs and no blasts. I am concerned that I am such a poor responder that the DuoStim will be a flop. I do not naturally have a period ever, so I’m also confused how it goes off a cycle when I don’t have one. Suggestions?

reply
Dr. Geoffrey Sher

I am not a fan of DuoStim IVF.

Women who (regardless of age) have diminished ovarian reserve (DOR) have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production, and/or biological activity, of LH. This can result in excessive ovarian male hormone (predominantly testosterone) production. This in turn can have a deleterious effect on egg/embryo “competency”.
While it is presently not possible by any means, to reverse the effect of DOR, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can in my opinion, make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.
I try to avoid using such protocols/regimes (especially) in women with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy
Please visit my new Blog on this very site, www. SherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly

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

___________________________________________________
ADDENDUM: 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.

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

reply
Janelle Miller

Hello Doctor – My husband and I went through our first round of IVF (ICSI) for male factor infertility.

05/23: 5 day blastocyst transfer
06/04: HCG 386
06/08: HCG 654

My doctor would have hoped that my HCG had increased a little more. Does this seem like a viable pregnancy, or is it still too early to tell?

Thanks!

reply
Dr. Geoffrey Sher

It could well be viable. Wait 10 days and do an Ultrasound for confirmation.

Geoff Sher

reply
April

In my past I have had 3 failed pregnancies. The last being a blighted ovum. It has been 4 years and I recently learned I was pregnant. I have irregular periods however my LMP was 4/23/2021 and I should be 6wks 3 days right now. Yesterday I went for my US and was told they could only see a small gestational sac but no fetal pole or yolk sac yet. They did say the sac was small and I could be earlier than I predicted. However I know my LMP for a fact and i fear Im going to experience another blighted ovum. I love had blood work done and my numbers are doubling every 2 days as they should. 5/27 they were 1445 and today they were 64456. I’m worried there should have been a fetal pole with those HCG levels. What do you think? Is there hope?

reply
Dr. Geoffrey Sher

In order to determine the viability of this pregnancy, you need to give it 1 week and repeat the US.

Good luck!

Geoff Sher

reply
Chelsey

Hi,
I’m wondering what you recommend for an IUI with PCOS. Is there a process that’s similar to the coasting process you mentioned? I noticed the eggs won’t fertilize naturally with this method. Can Lupron or Ganirelix be used in an IUI cycle with Follistim and pregnyl?
My son was conceived using Follistim, Menopur, and Pregnyl via IUI. We had a failed IUI this year and will be doing another one soon. I’ve been slowly reading through your articles to see if there’s anything I can do differently. I read in one of your articles that you don’t recommend menopur with PCOS patients, so I’m surprised that cycle worked for me! Now that I’ve learned about LH and androgens, I’m very interested in finding a way to incorporate lower LH levels into my next IUI. I’m 29 years old. Thank you!

reply
Dr. Geoffrey Sher

It is not that I reject Menopur . However, it should be combined with Gonal-F or Follistim, both in low dosages.

I am afraid that “coasting will not work with IUI, for reasons too complex to go in to on this forum.

However, low-dosage stimulation with gonadotropins should work.

Discuss with your RE.

Good luck!

Geoff Sher

reply
Lisa M Shriver

Hi DrSherif, our recent 5/20 transfer of double donor FET with the addition of lovenox resulted in HCG dropping. This is our 5th transfer and order of results have been: 6wks no heartbeat- non tested embryo; negative non tested embryo; chemical non tested embryo; 8wks normal embryo lost heartbeat, and now probable chemical. I believe I have alloimmune or auto immune implantation disorder. Can we make an appointment to speak with you virtually? We are in Houston, Texas.
Thank you for your consideration.

reply
Dr. Geoffrey Sher

Please call my assistant, Patti at 702-533-2691and set up an online consultation with me.

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 15y ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3. The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.

4. Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:

a. A“ thin uterine lining”
b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c. Immunologic implantation dysfunction (IID)
d. Endocrine/molecular endometrial receptivity issues
e. Ureaplasma Urealyticum (UU) Infection of cervical mucous and the endometrial lining of the uterus, can sometimes present as unexplained early pregnancy loss or unexplained failure following intrauterine insemination or IVF. The infection can also occur in the man, (prostatitis) and thus can go back and forth between partners, with sexual intercourse. This is the reason why both partners must be tested and if positive, should be treated contemporaneously.
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.

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

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

reply
Elizabeth H

Hi Dr Sher,

I recently had an open myomectomy to remove fibroids Type 0 from my uterus. My periods were regular for 3 months following the procedure. My RE did a second endoscope and removed 2 small fibroids although he found no scar tissue. Since then my last two periods have been light – 3 /4 days with very light bleeding. Should I be concerned that scar tissue formed after this second endoscope or could it just be a natural period for me? Thank you

reply
Dr. Geoffrey Sher

We need to talk Elizabeth.

Please contact my assistant, Patti at 702-533-2691 and set up an online consultation with me.

Geoff Sher

reply
Vee

Hi Dr Sher,

I had poor ivf outcome for my first ivf cycle, would you be able to give your opinion on what went wrong and what to do differently next time?

Day1: I started on 150 gonal and 150 menopur

Day 5: they are increasing me to 300 gonal and staying at 150 menopur. My estrogen was 203 and they wanted it at 500.

Day 7: 15 follicles ranging from 5-10, before I started meds we saw 19. My estrogen however is lower than they want it to be today. It should be atleast 1000 but I’m in the 700s so meds are being increased again today. Gonalf is going up again to 425 for the next 2 days menopur remains at 150.

Day 13: estrogen ended up at 6400

IVF 1 results: collected 11 eggs, 10 ICSI, 9 fertilized , 4 SER, 5 nonSER, 1 3cc fresh transfer which did not result in a pregnancy

reply
Vee

By the way I’m turning 31 in June, we did ICSI due to failed vasectomy reversal.

I’m taking SISU prenatals, CoQ10 500mg daily, vitD 2000iu

reply
Dr. Geoffrey Sher

This could very well have to do with the protocol used for opvarian stimulation nand its implementation.

Perhaps we should talk!

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 15y ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3. The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.

4. Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:

a. A“ thin uterine lining”
b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c. Immunologic implantation dysfunction (IID)
d. Endocrine/molecular endometrial receptivity issues
e. Ureaplasma Urealyticum (UU) Infection of cervical mucous and the endometrial lining of the uterus, can sometimes present as unexplained early pregnancy loss or unexplained failure following intrauterine insemination or IVF. The infection can also occur in the man, (prostatitis) and thus can go back and forth between partners, with sexual intercourse. This is the reason why both partners must be tested and if positive, should be treated contemporaneously.
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.

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

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

reply
Jamie

My betas were
9dp5dt 118
13dp5dt 344
15dp5dt 730

Today I’m 6w2d and we saw a heartbeat today at 125bpm, measuring 6w1d. Should we still be cautiously optimistic based on betas or just use ultrasounds now as more of a prediction?

reply
Brittany Slater

Hi Dr Sher! Thanks for giving me your expert opinion about what possibly likely happened with my pregnancy. My d&c went very smoothly today.
Since i had such a stressful time with HCG numbers this last pregnancy not rising but 3 scans showing baby growing wonderfully- I wanted to ask a few questions just to be as equipped as i can for my next hopeful pregnancy-
D
1. how much do you like to see hcg rising every 48 hours? I realize they say “rose appropriately”. But do you personally like to see them more than double ever 48 hours? Or just at least double?
2. If hcg rises but not QUITE doubles, how likely will that pregnancy fail? Meaning, is there a percentage you can throw out?
3. At what week in the prefnancy is it acceptable for hcg to level off?
Thanks for your time and energy. This blog space is saintly!! Ha seriously thanks

reply
Dr. Geoffrey Sher

1. how much do you like to see hcg rising every 48 hours? I realize they say “rose appropriately”. But do you personally like to see them more than double ever 48 hours? Or just at least double?

A: It should at least double every 48-52h

2. If hcg rises but not QUITE doubles, how likely will that pregnancy fail? Meaning, is there a percentage you can throw out?

A: It sometimes falls short of the mark and then catches up .

3. At what week in the pregnancy is it acceptable for hcg to level off?

A: When the level rises above 4,000U.

Good luck!

Geoff Sher

reply
Brittany Slater

My level stopped rising at 5,000 -6000 at 4w1day. and my doctors told me to prepare for a miscarriage. It never rose past that number. 4 weeks later my babys heart stopped beating .
Thanks for your help doctor

reply
Dr. Geoffrey Sher

In my opinion, it is quite normal for the rise in hCG to start slowing down drastically after it rises above 4,000U.

Good luck!

Geoff Sher

reply
Sarah

Hi Dr Sher, I had a 5d frozen embryo transfer 5/7. On 5/26 my hcg was 1900 and transvaginal ultrasound showed gestational sac measuring exactly on time at 5w3d. Today at 6w5d tv ultrasound showed CRL measuring at 6w1d and hcg 7375 (had been doubling every two days prior). What are your thoughts?

reply
Sonia

Hi Dr. Sher!

I have had a total of 4 FETs 2 of which were non viable pregnancies and 2 that just failed. I conceived my daughter naturally back in 2013 with Femara. My estrogen levels always get very high but my uterine lining struggles…My current doctor just tells me my uterus is stubborn and that I may need a surrogate. I cannot help but think I have some autoimmune issues going on. (I am 32 lean pcos) All of my embryos are PGS tested and I am gearing up for my 5th. I have had 3 ERAs done and negative for endometritis and as well as endometriosis. I am at a loss! 🙁

reply
Dr. Geoffrey Sher

There clearly is an implantation issue!

Implantation dysfunction is unfortunately often overlooked as an important cause of IVF failure. In the pursuit of optimizing outcome with IVF, the clinician has a profound responsibility to meticulously assess and address this important issue if IVF success is to be optimized. This is especially relevant in cases of “unexplained IVF failure, Recurrent Pregnancy Loss (RPL) and in women suspected of having underlying anatomical and immunologic factors. Doing so will not only maximize the chance of a viable pregnancy but enhancing placentation, will at the same time promote the noble objective of optimizing the quality of life after birth.”
IVF success rates have been improving over the last decade. The average live birth rate per embryo transfer in the U.S.A for women under 40y using their own eggs , is currently better than 1:3 women. However, there is still a wide variation from program to program for IVF live birth rates, ranging from 20% to near 50%. Based upon these statistics, the majority of women undergoing IVF in the United States require two or more attempts to have a baby. IVF practitioners in the United States commonly attribute the wide dichotomy in IVF success rates to variability in expertise of the various embryology laboratories. This is far from accurate. In fact, other factors such as wide variations in patient selection and the failure to develop individualized protocols for ovarian stimulation or to address those infective, anatomical and immunologic factors that influence embryo implantation are at least equally important.
About 80% of IVF failures are due to “embryo incompetency” that is largely due to an irregular quota of chromosomes (aneuploidy) which is usually related to advancing age of the woman and is further influenced by other factors such as the protocol selected for ovarian stimulation, diminished ovarian reserve (DOR)m and severe male factor infertility. However in about 20% of dysfunctional cases embryo implantation is the cause of failure.
Anatomical Endo-uterine Lesions: This blog article will focus on implantation dysfunction and IVF failure due to:
• Anatomical abnormalities in the uterine cavity (e.g. scarring, polyps and encroaching fibroid tumors)
• A thin endometrial lining
• Immunologic rejection of the embryos
Several studies performed both in the United States and abroad have confirmed that a dye X-Ray or hysterosalpingogram (HSG) will fail to identify small endouterine surface lesions in >20% of cases. This is significant because even small uterine lesions have the potential to adversely affect implantation. Hysteroscopy is the traditional method for evaluating the integrity of the uterine cavity in preparation for IVF. It also permits resection of most uterine surface lesions, such as submucous uterine fibroids (myomas), intrauterine adhesions and endometrial or placental polyps. All of these can interfere with implantation by producing a local “inflammatory- type” response similar in nature to that which is caused by an intrauterine contraceptive device. Hysterosonography (syn; HSN/ saline ultrasound examination) and hysteroscopy have all but supplanted HSG to assess the uterine cavity in preparation for IVF. HSN which is less invasive and far less expensive than is than hysteroscopy involves a small amount of a sterile saline solution is injected into the uterine cavity, whereupon a vaginal ultrasound examination is performed to assess the contour of the uterine cavity.
Endometrial Thickness: As far back as in 1989 I first reported on the finding that ultrasound assessment of the late proliferative phase endometrium following ovarian stimulation in preparation for IVF, permits better identification of those candidates who are least likely to conceive. We noted that the ideal thickness of the endometrium at the time of ovulation or egg retrieval is >9 mm and that a thickness of less than 8 mm bodes poorly for a successful outcome following IVF.
Then in 1993, I demonstrated that sildenafil (Viagra) introduced into the vagina prior to hCG administration can improve endometrial growth in many women with poor endometrial development. Viagra’s mechanism of action is improvement in uterine blood flow with improved estrogen delivery…thereby enhancing endometrial development.
Immunologic factors: These also play a role in IVF failure. Some women develop antibodies to components of their own cells. This “autoimmune” process involves the production of antiphospholipid, antithyroid, and/or anti-ovarian antibodies – all of which may be associated with activation of Natural Killer (NK) cells in the uterine lining. Activated NK cells (NKa) release certain cytokines (TH-I) that if present in excess, often damage the trophoblast (the embryo’s root system) resulting in immunologic implantation dysfunction (IID). This can manifest as “infertility” or as early miscarriages). In other cases (though less common), the problem is due to “alloimmune” dysfunction. Here the genetic contribution by the male partner renders the embryo “too similar” to the mother. This in turn activates NK cells leading to implantation dysfunction. These IID’s are treated using combinations of medications such as heparin, Clexane, Lovenox, corticosteroids and intralipid (IL).

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

• A Fresh Look at the Indications for IVF
• The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• IVF and the use of Supplementary Human Growth Hormone (HGH) : Is it Worth Trying and who needs it?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• IVF: Approach to Selecting the Best Embryos for Transfer to the Uterus.
• Fresh versus Frozen Embryo Transfers (FET) Enhance IVF Outcome
• Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
• Genetically Testing Embryos for IVF
• Staggered IVF
• Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
• Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
• IVF: Selecting the Best Quality Embryos to Transfer
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
• PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
• PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
• Endometrial Receptivity Array (ERA): Is There an actual “There, There”?
• IVF Failure and Implantation Dysfunction:
• Diagnosing and Treating Immunologic Implantation Dysfunction (IID)
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• A Thin Uterine Lining: Vaginal Viagra is Often the Answer (update)
• Cervical Ureaplasma Urealyticum Infection: How can it Affect IUI/IVF Outcome?
• The Role of Nutritional Supplements in Preparing for IVF
• The Basic Infertility Work-Up
• Defining and Addressing an Abnormal Luteal Phase
• Male Factor Infertility
• Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in Favor
• Hormonal Treatment of Male Infertility
• Hormonal Treatment of Male Infertility
• Antisperm Antibodies, Infertility and the Role of IVF with Intracytoplasmic Sperm Injection (ICSI)
• Endometriosis and Infertily
• Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF
• Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
• Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
• Early -Endometriosis-related Infertility: Ovulation Induction (with or without Intrauterine Insemination) and Reproductive Surgery Versus IVF
• Deciding Between Intrauterine Insemination (IUI) and In Vitro Fertilization (IVF).
• Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & Con’s!IUI-Reflecting upon its Use and Misuse: Time for a Serious “Reality Check
• Mode of Action, Indications, Benefits, Limitations and Contraindications for its ue
• Clomiphene Induction of Ovulation: Its Use and Misuse!
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.

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

reply
Natalie

Hello Dr,
What are you thoughts on dual trigger shot: lupron + hcg. I’m 38 yo with AMH 7.18 and 27 follicular counts. I have never been diagnosed with PCOS. Thank you!

reply
Dr. Geoffrey Sher

It works, but I personally prefer to only use hCG.

Geoff Sher

reply
Lauren

Hi there,

I did a fresh transfer, tested pos, an 3 weeks pregnant. HCG rising appropriately, progesterone >600. Should I be concerned this pregnancy isn’t viable? I’ve been injecting myself with progesterone since before the transfer of course and will continue until my first OB scan at week 5. Waiting to hear from my physician but worried I won’t be able to sleep tonight. I’ve been researching for some sense that progesterone that high is normal with IVF protocol but I’ve found nothing. Please advise.

reply
Lacy

Hi Dr
First day of last period 04/30
1st hcg on 05/27 :350
2nd hcg on 05/29 : 1126
Is this normal to have such a high hcg in just a month from last period?
Please help I am anxious.

reply
Dr. Geoffrey Sher

Looks promising. Might even e twins??

Good luck!

Geoff Sher

reply
Lacy

Thank you Doctor. But when do you think I should have an US, given that my first day of last period was 04/30 and the HCG values?

reply
Tammy

Hi Dr. Sher. This is Tammy again. Sorry for all the questions! 🙂

I know you mentioned possible ectopic, but wanted to give you some more information.
I have PCOS and have no idea when my last cycle was so the guess on how far along I am is based on the size of the gestational sac.

Beta hcg Levels
5/23 – 4,000
5/28 – 13,673
6/1 – 23,706

Vaginal Ultrasounds:
5/23: gestational sac measuring 5 week 4 day (sac diam3: 1.06cm, mean sac dam .91cm).
5/28: gestational sac measuring 6 week 2 day (not sure the diameter)

At the 5/28 ultrasound they said I more than likely miscarried because they are not seeing a yolk sac, so my hcg levels will start going down, but they keep going up.

Could I be not as far along as my gestational sac (in uterus) is measuring?

reply
Dr. Geoffrey Sher

Only a repeat US in about 1-2 weeks will be able to tell with reliability!

Geoff Sher

reply
Joy

Hi doc!

I am 5 weeks and 4 days based on my chart. My 1st hcg was 23600 then after 48 hours was 37200. What is your thoughts about this? I have a mild dull pain on my left pelvic area its been 6 days now. Thank you

reply
Dr. Geoffrey Sher

Have an US in 1 week for a definitive answer.

Good luck!

Geoff Sher

reply
Joy

Thanks for your response. I am afraid of my hcg result since it did not doubled plus a left sided pain. Is there any probability of ectopic? My hcg level is high.

reply
Dr. Geoffrey Sher

Your RE needs to be on the look-out for an ectopic!

Good luck!

Geoff Sher

reply
Anecia Lamb

I would like to know if your office is open for new client? I am looking for IUI or IVF insemination to become a parent. I am a single lesbian female, 41 years of age, I have been wanting a child since I was 35 years old but my Primary doctor was concern about my diabetes so he never moved forward. I have taken tests and I have no obstacles that will prevent me in coming pregnant.

reply
Dr. Geoffrey Sher

Absolutely we are open. And you should know that I have a very large Same-Sex clientele.

Gay, lesbian, or transgender individuals experience the same fears as any individual in the world. One of these is trepidation that they might not be able to have children. In the United States of America, same-sex marriage has been legal nationwide since June 26, 2015, when the United States Supreme Court ruled that state-level bans on same-sex marriage are unconstitutional. Same sex couples now have equal right as do straight couples and do not have to fear discrimination based on their gender. Reproductive medicine is for everybody’s benefit, and should not be restricted to heterosexuals.

I have been treating infertile couples for more than three decades, having been involved in the genesis of in vitro fertilization in the US virtually from its inception. During this time, I have helped hundreds of same sex couples go from infertility to family. With very few exceptions, the medical challenges faced by such couples and the family relationships that emerged and evolved following the births of children, have hardly differed from that which affects heterosexual couples undergoing the same treatment. Many of these babies are now adults providing a real life opportunity to observe some of them as they confronted life’s challenges. Based on this experience, it is my opinion that the fact that they were born to same sex couples did not disadvantaged any of them. Furthermore, the commitment made by these same sex parents to one another and to the raising of their offspring seems to me to have been no different than in the case of sexually differing parents. I have concluded that in spite of the enormous pressures imposed on same sex couples by an often bigoted society these couples, recognize their responsibility to maintain a cohesive relationship for the well being of their offspring. Let’s face while there are indeed many enlightened people who are willing to embrace same sex families, the majority of our society is so caught up in confusion caused by entrenched religious and moral ideologies that they are not ready for this. Granted, the preservation of stable, monogamous relationships in same sex couples is subject to more pressure and scrutiny. Yet, once cemented by a profound decision to have a child together, the chance of them falling apart appears to be no greater than for heterosexual partnerships.
There are many options available to same sex couples seeking parenthood.
For female couples: In the case of female couples, the simplest approach is to undergo artificial insemination (IUI) with donor sperm. However in some cases the matter is complicated by the existence of infertility that cannot be adequately addressed through IUI with donor sperm, thus necessitating in vitro fertilization. Regardless of the approach to treatment, stringent FDA guidelines require that all sperm donors whether anonymous or known or recruited from a licensed sperm bank or independently r be tested for potentially lethal transmittable viral infections (e.g. HIV) at the time of producing the specimen and that the sperm specimen then be freeze/stored for several months at which time the sperm provider be retested before the sperm is dispatched for IUI or IVF. Once embryos are generated with donated sperm either female partner will choose to bear the child. Often times, both female partners may wish to share in the biological contribution of a pregnancy where one partner will produce the eggs necessary to be fertilized with donor sperm and the embryos will be transferred to the prepared uterus of the other partner. In some cases the couple will elect to use a gestational carrier (surrogate mother)
For male couples: Ever since the Baby M case more than 2 decades ago where a gestational carrier, who conceived after being inseminated with the sperm of the intended male partner (classical surrogacy), sued for custody and won, we have strongly advocated against the use of IUI and in favor of IVF using donated eggs and thereupon a surrogate in whose uterus the embryo(s) are implanted. In fact, in my practice I confine gestational surrogacy to situations where the carrier has no genetic link to the offspring (gestational surrogacy). Simply stated, I only conduct surrogacy when the egg provider and the carrier are different individuals. This mandates the use of in vitro fertilization rather than artificial/intrauterine insemination (IUI). Surrogacy is surrounded by legal issues, and thus a formal legal arrangement should be sought in order to prevent any future complications and can provide peace of mind. For male same sex couples, the sperm provider needs to be tested among other things for certain viral infections (including HIV, Hepatitis B and C) and the specimen must be held in quarantine for several months before being used.
In Summary: Aside from the effects of social and political pressures, same sex couples experience the same concerns as those in any other relationship. They wonder what the future holds and whether they will be able to fulfill their desire to have children and accomplish the dream of building a family. While at times this may all seem quite overwhelming, in today’s age it is easier than ever for them to experience the joy of parenthood. There is no evidence that there is any harm to anybody from same sex couples having a child. Children need to be brought up in a loving, caring environment and it is the loving care that is most important, not the sexuality of the parent.

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

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

___________________________________________________
ADDENDUM: 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.

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

reply
Dr. Geoffrey Sher

Absolutely we are open. And you should know that I have a very large Same-Sex clientele.

Gay, lesbian, or transgender individuals experience the same fears as any individual in the world. One of these is trepidation that they might not be able to have children. In the United States of America, same-sex marriage has been legal nationwide since June 26, 2015, when the United States Supreme Court ruled that state-level bans on same-sex marriage are unconstitutional. Same sex couples now have equal right as do straight couples and do not have to fear discrimination based on their gender. Reproductive medicine is for everybody’s benefit, and should not be restricted to heterosexuals.

I have been treating infertile couples for more than three decades, having been involved in the genesis of in vitro fertilization in the US virtually from its inception. During this time, I have helped hundreds of same sex couples go from infertility to family. With very few exceptions, the medical challenges faced by such couples and the family relationships that emerged and evolved following the births of children, have hardly differed from that which affects heterosexual couples undergoing the same treatment. Many of these babies are now adults providing a real life opportunity to observe some of them as they confronted life’s challenges. Based on this experience, it is my opinion that the fact that they were born to same sex couples did not disadvantaged any of them. Furthermore, the commitment made by these same sex parents to one another and to the raising of their offspring seems to me to have been no different than in the case of sexually differing parents. I have concluded that in spite of the enormous pressures imposed on same sex couples by an often bigoted society these couples, recognize their responsibility to maintain a cohesive relationship for the well being of their offspring. Let’s face while there are indeed many enlightened people who are willing to embrace same sex families, the majority of our society is so caught up in confusion caused by entrenched religious and moral ideologies that they are not ready for this. Granted, the preservation of stable, monogamous relationships in same sex couples is subject to more pressure and scrutiny. Yet, once cemented by a profound decision to have a child together, the chance of them falling apart appears to be no greater than for heterosexual partnerships.
There are many options available to same sex couples seeking parenthood.
For female couples: In the case of female couples, the simplest approach is to undergo artificial insemination (IUI) with donor sperm. However in some cases the matter is complicated by the existence of infertility that cannot be adequately addressed through IUI with donor sperm, thus necessitating in vitro fertilization. Regardless of the approach to treatment, stringent FDA guidelines require that all sperm donors whether anonymous or known or recruited from a licensed sperm bank or independently r be tested for potentially lethal transmittable viral infections (e.g. HIV) at the time of producing the specimen and that the sperm specimen then be freeze/stored for several months at which time the sperm provider be retested before the sperm is dispatched for IUI or IVF. Once embryos are generated with donated sperm either female partner will choose to bear the child. Often times, both female partners may wish to share in the biological contribution of a pregnancy where one partner will produce the eggs necessary to be fertilized with donor sperm and the embryos will be transferred to the prepared uterus of the other partner. In some cases the couple will elect to use a gestational carrier (surrogate mother)
For male couples: Ever since the Baby M case more than 2 decades ago where a gestational carrier, who conceived after being inseminated with the sperm of the intended male partner (classical surrogacy), sued for custody and won, we have strongly advocated against the use of IUI and in favor of IVF using donated eggs and thereupon a surrogate in whose uterus the embryo(s) are implanted. In fact, in my practice I confine gestational surrogacy to situations where the carrier has no genetic link to the offspring (gestational surrogacy). Simply stated, I only conduct surrogacy when the egg provider and the carrier are different individuals. This mandates the use of in vitro fertilization rather than artificial/intrauterine insemination (IUI). Surrogacy is surrounded by legal issues, and thus a formal legal arrangement should be sought in order to prevent any future complications and can provide peace of mind. For male same sex couples, the sperm provider needs to be tested among other things for certain viral infections (including HIV, Hepatitis B and C) and the specimen must be held in quarantine for several months before being used.
In Summary: Aside from the effects of social and political pressures, same sex couples experience the same concerns as those in any other relationship. They wonder what the future holds and whether they will be able to fulfill their desire to have children and accomplish the dream of building a family. While at times this may all seem quite overwhelming, in today’s age it is easier than ever for them to experience the joy of parenthood. There is no evidence that there is any harm to anybody from same sex couples having a child. Children need to be brought up in a loving, caring environment and it is the loving care that is most important, not the sexuality of the parent.

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

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

___________________________________________________
ADDENDUM: 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.

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

reply
Michelle

I’m 41, undergoing ivf for fertility preservation before starting 5-10 years of tamoxifen. Goal is to have viable embryos to freeze (donor sperm). My first cycle resulted in 11 retrieved, 7 mature, and 2 fertilized. The embryologist recommends ICSI next round. (There were additional eggs fertilized, but abnormally.) My RE suggested HGH next cycle, and this is what I’m concerned about. My cancer was hormone receptor positive (ER+ and PR+), HER2 negative. No lymph node involvement. Would 4-5 days of HGH be horrible? I would be taking letrozole as well.
I asked RE if I can start tamoxifen now and take 2 months to improve egg quality with supplements before cycle #2. She will be asking at the big office meeting on Wednesday. Seems like a false choice to weigh immediate cycle #2 with HGH versus delaying hormone therapy in hopes of boosting egg quality naturally.

Thank you for making yourself available for questions, and for the extensive resources here!

reply
Dr. Geoffrey Sher

I do not think HGH for such a short period of time will place you at any risk!

I am not in favor of using Letrozole or clomiphene-type medications (e.e., Tamoxifin) around the time of stimulation as it increases LH-release and can cause ovarian follicular testosterone levels to increase to a level that it can compromise egg quality.

It is primarily the egg (rather than the sperm) that determines the chromosomal integrity (karyotype) of the embryo, the most important determinant of egg/embryo competency”. A “competent” egg is therefore one that has a normal karyotype and has the best potential to propagate a “competent” embryo. In turn, a “competent embryo is one that possesses the highest potential to implant and develop into a normal, healthy, baby.
When it comes to reproductive performance, humans are the least efficient of all mammals. Even in young women under 35y, at best only 1 out of 2 eggs are chromosomally numerically normal (euploid). The remained have an irregular number of chromosomes (aneuploid) and are thus “incompetent”. The incidence of egg aneuploidy increases with age such by age 39 years, 3 in 4 are competent, and by the mid-forties, less 8 to 9 out of 10 are aneuploid. The fertilization of an aneuploid egg will inevitably lead to embryo aneuploid and an aneuploid embryo cannot propagate a normal pregnancy
Within hours of the spontaneous pre-ovulatory luteinizing hormone (LH) surge, and also following administration of the human chorionic gonadotropin (hCG) “trigger” shot (given to induce ovulation after ovarian stimulation with fertility drugs), the egg embarks on a rapid maturational process that involves halving of its 46 chromosomes to 23. During this process, (known as meiosis) 23 chromosomes are retained within the nucleus of the egg while the remaining (now redundant) 23are expelled, enveloped by a thin membrane. This small structure comes to lie immediately below the “shell” of the egg (the zona pellucida) and is known as the 1st polar body or PB-1. The spermatozoon, in the process of its maturation also undergoes meiosis at which time it too reduces its chromosomes by half. Thus in the process of fertilization the sperm divides into two separate functional gametes, each containing 23 chromosomes such that with subsequent fertilization, the 23 chromosomes in the egg, fuse with the 23 chromosomes of the mature sperm resulting in the development of an embryo that has 46 chromosomes (the normal human genome) comprising a combination of the genetic material from both partners. For the embryo to have exactly 46 chromosomes (the euploid number), both the mature egg and mature spermatozoon must contain exactly 23 chromosomes. Only euploid embryos are “competent” (capable of developing into healthy babies). Those with an irregular number of chromosomes (aneuploid embryos) are “incompetent” and are incapable of developing into healthy babies. While embryo “incompetence” can result from either egg or sperm aneuploidy, it usually stems from egg aneuploidy. However, in cases of moderate or severe male factor infertility, the sperm’s contribution to aneuploidy of the embryo increases significantly.
While embryo ploidy (numerical chromosomal integrity) is not the only determinant of its “competency, it is by far the most important and in fact is rate-limiting factor in human reproduction. It is causal in most cases of “failed implantation” which in turn is responsible for most cases of failed IVF. It causes early miscarriages and is responsible for many chromosomal birth defects such as X-monosomy and Down’s syndrome. . In most cases, embryos that develop too slowly as well as those that grow too fast (i.e. ones that by day 3 post-fertilization comprise fewer than 6 cells or more than 9 cells) and/or embryos that contain a large amount of cell debris or “fragments” are usually aneuploid and are thus “incompetent”. Additionally, embryos that fail to survive in culture to the blastocyst stage are also almost always aneuploid/”incompetent”. At a certain point in the later stage of a woman’s reproductive career, the number of remaining eggs in her ovaries falls below a certain threshold, upon which she is unable to respond optimally to fertility drugs. Often times this is signaled by a rising day 3 blood follicle stimulating hormone (FSH) level. Such women with diminishing ovarian reserve produce fewer eggs in response to ovarian stimulation. While diminished ovarian reserve is most commonly encountered in women over 40 years of age it can and indeed sometimes does occur in much younger women. A few important (but often overlooked concepts should be considered in this regard: 1. Age: It is advancing chronologic age and NOT declining ovarian reserve (as evidenced by abnormal blood AMH or FSH that results in an increased incidence of egg/embryo “incompetence” due to aneuploidy 2. DOR: The ovaries and developing eggs of women with diminished ovarian reserve (regardless of age) are highly susceptible to the adverse effect of excessive Luteinizing Hormone (LH)-induced overproduction of male hormones (mainly testosterone). A little testosterone produced by the ovary promotes normal follicle growth and orderly egg development but too much testosterone has the opposite effect. That is why (especially in women with diminished ovarian reserve who often have high LH and increased ovarian testosterone production , the use of ovarian stimulation protocols that fail to down-regulate LH production prior to initiating stimulation with gonadotropins, often prejudices egg/embryo quality and IVF outcome. Simply stated, while age is certainly the most important factor in determining the incidence of egg/embryo aneuploidy, women with diminished ovarian reserve (regardless of their age), unless they receive customized/individualized protocols of ovarian stimulation are less likely to propagate euploid (competent) eggs/embryos.
Selection of the ideal protocol for controlled ovarian stimulation: While NOTHING can be done to lower the incidence of age related aneuploidy, it is indeed possible to avoid a further increase in egg/embryo aneuploidy by individualizing the protocols of ovarian stimulation used.
• My preferred protocols for women who have relatively normal ovarian reserve:
a) The conventional long pituitary down regulation protocol: BCP are commenced early in the cycle and continued for at least 10 days. Starting 3 days before the BCP is to be discontinued, it is overlapped with an agonist such as Lupron 10U daily for three (3) days and continued until menstruation begins (which should ensue within 5-7 days of stopping the BCP). At that point an US examination is done along with a baseline measurement of blood estradiol to exclude a functional ovarian cyst. Simultaneously, the Lupron dosage is reduced to 5U daily and an FSH-dominant gonadotropin such as Follistim, Puregon or Gonal-f daily is commenced for 2 days. On the 3rd day the gonadotropin dosage is reduced and a small amount of daily menotropin (Menopur 75U daily) is added. Daily ultrasound and blood estradiol measurements are done starting on the 7th or 8th day of gonadotropin administration and continued until daily ultrasound follicle assessments indicate that most follicles have fully developed. At this point egg maturation is “triggered” using an intramuscular injection of 10,000U hCG. And an egg retrieval is scheduled for 36h later.
b) The agonist/antagonist conversion protocol (A/ACOP): This is essentially the same as the conventional long down regulation protocol (as above), except that with the onset of post-BCP menstruation, the agonist is supplanted by daily administration of a GnRH antagonist (e.g. Ganirelix, Cetrotide or Orgalutron) at a dosage of 125mcg daily until the day of the hCG trigger
• My preferred protocol for women who have relatively diminished ovarian reserve (DOR):
When it comes to women who have DOR I favor the use of the A/ACP, adding supplementary human growth hormone (HGH). In some cases where the DOR is regarded as severe, I also augment the process with estrogen priming, preferring twice weekly intramuscular administration of estradiol valerate (Delestrogen), starting with the commencement of antagonist injection and continuing for 1 week before commencing gonadotropins and continued until the hCG “trigger. I further recommend that such women be offered access to preimplantation genetic screening (PGS) for4 embryo selection and in some cases, for embryo banking (stockpiling). This is followed in a later hormone replacement cycle with the selective transfer of up to two (2) PGS-normal, euploid blastocysts. In this way we are able to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” , significantly enhancing the opportunity to achieve a viable pregnancy
• The following Ovarian stimulation protocols are in my opinion best avoided in women with DOR:
a) Microdose agonist (e.g. Lupron) “flare” protocols
b) High doses of LH/hCG-containing fertility drugs (E.G. Menopur).
c) Protocols that incorporate supplementation with male hormones (e.g. testosterone)
d) Supplementation with DHEA
e) Clomiphene citrate or Letrozole which cause an elevation in LH and thus increase ovarian male hormone (testosterone and androstenedione output.
f) “Triggering” egg maturation using too low a dosage of hCG (e.g. 5,000U rather than 10,000U) or Ovidrel e.g. 250mcg of Ovidrel rather than 500mcg)
g) “Triggering” women who have large numbers of follicles using an agonist such as Lupron, Superfact or Buserelin.
• Preimplantation Genetic Screening (PGS):
The introduction of preimplantation genetic screening (PGS) for the first time permits identification of all the chromosomes in the egg and embryo such that we can now far better identify “competent” (euploid) embryos for selective transfer to the uterus. This vastly improves the efficiency and success of the IVF process. This additional tool has better equipped us to manage cases with DOR. In my opinion, next generation gene sequencing (NGS), currently represents the most reliable method for performing PGS

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

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

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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.

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

ace

reply
Gayathri

Hi Doctor.
My Hcg levels are like this

28381  – May 27th, 2021
27426 – May 23, 2021
23528 – May 20, 2021
14876 – May 13, 2021
3673 – May 6th, 2021
460 – April 30th, 2021
I booked scan on june 1st as its the latest availability. I am concerned as the numbers look indifferent. Is this a good sign? Should i wait until then or go to emergency?. Please reply.

Thanks

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Dr. Geoffrey Sher

I am a little concerned about the pattern of your hCG rise. Your upcoming ultrasound should be conclusive.

Good luck!

Geoff SDher

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Laura

Dear Dr. Sher, do you have any doctors in the UK who you have ever worked with before who would be happy to consider following one of your protocols? I would love to have a Skype consultation with you, but there is no point if I cannot then find a clinic in the UK who could carry out some of what you recommend. Thank you!

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Amy King

Do you perform IVM? I have PCOS and have a history of blood clots so less estrogen exposure in my mind would be better. Thoughts?

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Tammy

I am 32 and my husband is 36. I was actually a patient of your back in 2012 and you gave us a little miracle boy on the first IVF (using intralipid IV infusions) with you after 6 failed IVF’s prior (including an ectopic resulting in my tube being removed and preterm delivery of twins at 5 months). You did testing and found that I had an MTHFR gene mutation as well as my husband and I being a partial DQalpha match. My husband and I have been together for almost 15 years and have never used protection and have not gotten pregnant without the assistance of fertility treatment. Well, last week I was absolutely shocked to found out that as of today I am 6 weeks and 2 days pregnant. When I found out at 5 weeks and 4 days my HCG was at 4,000 (drawn at the ER). I have not had any other blood draws yet until I can get into my OB. They could see a yok sac in a stomach ultrasound (done on Wednesday), and will be going for a transvaginal ultrasound here soon. I know we had talked to you a little about if ever we got pregnant naturally what are the chances of it being a viable pregnancy that would last until term, but we also knew it was a VERY slim chance I every would get pregnant naturally. I do not remember exactly your thoughts on it, so I wanted to ask you about it. Is an HCG level of 4,000 at 5 weeks 4 days, a good sign? There was no fetal pole visible on the on the 5 week 4 day transvaginal ultra sound done at the ER. Is that normal? They could see the yok sack though, and when I went to an ultrasound place on Wednesday everything was still growing and the yok sack was visible on the stomach ultrasound. My biggest question is, what do you think the chances of the pregnancy going to term is? Do you think there is a high chance of a miscarriage? Also, my husband was wondering if we should be thinking about doing any gene testing or anything to make sure it is okay? I told him I thought I remember you saying if there was a gene mutation (which you all checked for being the day 5 transfer) that the embryo would not have made it anyways to start a pregnancy, but I wasn’t sure, so wanted to ask that too. Sorry for all the questions, but thank you so much for your time and always caring so much about your patients!!!!

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Dr. Geoffrey Sher

Congratulations! I am so happy for you. It goes to show…miracles can and do happen because “man proposes and G-d disposes”.

At this stage the numbers look good but it is too late to intervene with additional therapies for an immunologic issue. So, you need to wait it out and see how things go!

Good luck and G-d bless

Geoff Sher

P>S: Please keep me in the loop!

reply
Tammy

Dr. Sher,

Sorry, if this comment is coming through more than once. On my end it looks like it isn’t going through. :/

An update:

I have PCOS and don’t know when I had my last cycle (they are very irregular and sometimes only spotting). At the ER on Sunday morning my transvaginal ultrasound showed my gestational sac was measuring 5 weeks 4 days. Yesterday (Friday afternoon) my transvaginal ultrasound showed my gestational sac was measuring 6 weeks 3 days, but they did not see any yolk sac or anything so they believe it was probably a blighted ovum, but had my blood drawn to check HCG levels if they went down they know that’s what it was, but if they doubled they said maybe I am earlier than I am measuring. Sunday morning my HCG was 4000, and yesterday (Friday afternoon), it was 13,637. What are the chances I am not as far along as my sac is measuring or does it still sound like a blighted ovum?

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Dr. Geoffrey Sher

If at this stage there is no visible intrauterine gestation, given the high blood hCG, I would be very concerned about an ectopic pregnancy. I suggest you discuss this with your RE.

Approximately 1 out of every 100 embryos will implant and grow outside of the uterine cavity (almost always) in a fallopian tube. This is defined as an ectopic pregnancy. Infrequently, an ectopic pregnancy attaches to an ovary or to one or more other pelvic organs. On very rare occasions (1;1,000), one twin attaches and grows in the uterine cavity with the other growing outside the uterus (i.e. a heterotopic pregnancy).
There is an ever present risk that a tubal (ectopic) pregnancy might rupture causing potentially catastrophic internal hemorrhage. Accordingly any symptoms suggesting that such bleeding has started, requires immediate confirmation of the diagnosis followed by emergency treatment.
While on rare occasions, an extrauterine (ectopic) can proceed well into pregnancy, it almost always happens prior to the 8th week. There is an increase in the incidence of ectopic pregnancy after IVF conceptions where it reportedly occurs in about 3% of cases and a woman who has had one ectopic pregnancy has almost four times as great a risk of an ectopic in a future pregnancy. In fact with every subsequent ectopic this risk of a recurrence increases dramatically.

The fertilization of the human egg normally takes place in the fallopian tube. The embryo then travels into the uterus, where it implants into the endometrial lining 5-6 days after ovulation. Anything that delays the passage of the embryo down the fallopian tube can result in the embryo hatching and sending its “root system” into the wall of the fallopian tube and initiating growth within the tube. One of the most common predisposing factors is pelvic inflammatory disease (PID) in which microorganisms, such as Chlamydia, and Gonococcus damage the inner lining (endosalpinx) and eventually also the muscular walls of the tube(s) by the formation of scar tissue. The endosalpinx has a very complex and delicate internal architecture, with small hairs and secretions that help to propel the embryo toward the uterine cavity. Once damaged, this lining can never regenerate. This is one of the reasons why women who manage to conceive following surgery to unblock fallopian tubes damaged by PID, have about a 1:4 chance of a subsequent pregnancy developing within the fallopian tube (ectopic).

Congenital malformations of the fallopian tube, associated with shortening of, or small pockets and side channels within, the tube are capable of interrupting the smooth passage of the embryo down the fallopian tube, is another cause of an ectopic pregnancy.

Since the lining of the fallopian tube does not represent an optimal site for healthy implantation, a large percentage of pregnancies that gain early attachment to its inner lining will usually be absorbed before the woman even knows that she is pregnant. This is often referred to as a tubal abortion.

The advent of advanced sonographic and hormonal monitoring technology now makes it possible to detect an ectopic pregnancy much earlier than previously, …usually well in advance of it rupturing. A decade or two ago, the diagnosis of an ectopic pregnancy, ruptured or not, was an indication for immediate laparotomy to avoid the risk of catastrophic hemorrhagic shock. This often resulted in the affected fallopian tube having to be completely removed, sometimes along with the adjacent ovary. In the late 1980’s, early conservative surgical intervention by laparoscopy began replacing laparotomy (a wide incision made in the abdominal wall) for the treatment of ectopic pregnancy, often allowing the affected fallopian tube to be preserved and shortening the period of post-surgical convalescence. In the 90’s, early detection combined with the advent of medical management with methotrexate (MTX) has all but eliminated the need for surgical intervention in the majority of patients. If administered early enough, MTX will allow spontaneous resorbtion of the pregnancy and a dramatic reduction in the incidence of catastrophic bleeding. This was especially true in ectopic pregnancies arising from In Vitro Fertilization, where the early progress of pregnancy is usually carefully monitored with hormone levels and ultrasound.

Classically women with an ectopic pregnancy present with the following symptoms:

• Missed menstrual period: Although some patients will have spotting or other abnormal bleeding. The pregnancy test will be positive in such cases.

• Vaginal bleeding. When a pregnancy inadvertently implants in the fallopian tube the lining of the uterus undergoes profound hormonal changes associated with pregnancy (primarily associated with the hormone progesterone). When the embryo dies, the lining of the uterus separates. Initially, vaginal bleeding is dark and usually is quite scanty, even less than with a normal menstrual period. In some cases, of ectopic pregnancy will bleeding is more severe, similar to that experienced in association with a miscarriage. This sometimes leads to an ectopic pregnancy initially being misdiagnosed as a miscarriage and is the reason to examine the material that is passed vaginally, for evidence of products of conception.

• Pain. In the early stages this is typically cramp-like in nature, located on one or another side of the lower abdomen. It is caused by spasm of the muscular wall of the fallopian tube(s). When a tubal pregnancy ruptures the woman will usually experience an abrupt onset of severe abdominal followed by light headedness, coldness and clamminess and will often collapse due to shock. Her pulse will become rapid and thready and her blood pressure will drop. Miscarriage. Sometimes the woman will experience pain in the right shoulder. The reason for this is that that blood which tracts along the side of the abdominal cavity finds its way to the area immediately below the diaphragm, above the liver (on the patient’s right side), irritates the endings of the phrenic nerve, which supplies that part of the diaphragm. This results in the referral of the pain to the neck and the right shoulder. The clinical picture is often so typical that making the diagnosis usually presents no difficulty at all. However, with less typical presentations the most important conditions to differentiate from an ectopic pregnancy are: a ruptured ovarian cyst, appendicitis, acute pelvic inflammatory disease (PID), or an inevitable

• Vaginal bleeding. When a pregnancy inadvertently implants in the fallopian tube the lining of the uterus undergoes profound hormonal changes associated with pregnancy (primarily associated with the hormone progesterone). When the embryo dies, the lining of the uterus separates. Initially, vaginal bleeding is dark and usually is quite scanty, even less than with a normal menstrual period. In some cases, of ectopic pregnancy will bleeding is more severe, similar to that experienced in association with a miscarriage. This sometimes leads to ectopic pregnancy initially being misdiagnosis as a miscarriage and is the reason that we often want to examine the material that is passed vaginally, for evidence of products of conception.

The easiest and most common method of diagnosing an ectopic pregnancy is by tracking the rate of rise in the blood levels of hCG. With a normal intrauterine pregnancy, these usually double every two days throughout the first few weeks. While a slow rate of increase in blood hCG usually suggests an impending miscarriage, it might also point to an ectopic pregnancy. Thus the hCG blood levels should be followed serially until a clear pattern emerges.

A vaginal ultrasound examination usually will clinch the diagnosis by showing the ectopic pregnancy within a fallopian tube and if the tube has already ruptured or internal bleeding has occurred, ultrasound examination will inevitably detect the presence of free fluid into the abdominal cavity.

If there has been a significant amount of intra-abdominal bleeding, irritation of the peritoneal membrane will cause the abdominal wall to become hard tense and, depending on the amount of internal bleeding abdominal distention will be evident. Palpation of the abdominal wall will evoke significant pain and when a vaginal examination is done, movement of the cervix will produce excruciating pain, especially on the side of the affected fallopian tube.

Surgical Treatment: In questionable situations laparoscopy is usually performed for diagnostic purposes. If an ectopic pregnancy is in fact detected, a small longitudinal incision over the tubal pregnancy will allow its removal, without necessitating removal of the tube. (linear salpingectomy). Bleeding points on the fallopian tube can usually be accessed directly and appropriately ligated (tied) via the laparoscope. Sometimes the damage to the fallopian tube has been so extensive that the entire tube will require removal.

On occasions where very severe intra-abdominal bleeding heralds a potential catastrophe, a laparotomy (an incision made to open the abdominal cavity) is performed to stop the bleeding post haste. In such cases a blood transfusion is usually required and may be life saving.

Medical Treatment: The introduction of Methotrexate (MTX) therapy for the treatment of ectopic pregnancy has profoundly reduced the need for surgery in most patients. MTX is a chemotherapeutic that kills rapidly dividing cells, such as those present in the “root system” of the conceptus. Extremely low doses of MTX are used to treat ectopic pregnancy. Accordingly the side effects that are often associated with such chemotherapy used for the treatment of other conditions are seldom seen. It is important to confirm that the ectopic pregnancy has not yet ruptured prior to administering MTX.

MTX is given by intramuscular injection. Prior to its administration, blood is drawn to get a baseline blood hCG level. After the injection of MTX the patient is allowed to return home with strict instructions that she should always have someone with her and never be alone in the ensuing week. The concern is that were the patient to be on her own and an intraabdominal bleed were to occur, she might not readily be able to access someone who could get her to the hospital immediately. Instructions are also given to look for early signs that might point towards severe intra-abdominal bleeding such as the sudden onset of severe pain, light-headedness or fainting.

The patient returns to the doctor’s office four days later to check the blood hCG level. Three days later (7 days after MTX), the level is checked again. By this time the hCG level should have dropped at least 15% from the value on day 4. If not, a second MTX injection is given and the blood levels are tested twice weekly until hCG level is undetectable. Once this occurs, vaginal bleeding will usually ensue within a week or two.

It is important to note, especially in cases where more than one embryo or blastocyst has been transferred to the uterine cavity or fallopian tube (as with Tubal embryo transfer –TET/ZIFT), that implantation may occur in two sites simultaneously (i.e. in the fallopian tube as well as inside the uterine cavity). This is referred to as a heterotopic pregnancy. It is therefore important that before administering MTX, which will cause the death and absorption of any early pregnancy, that the physician makes certain that he/she is not dealing with a heterotopic pregnancy. In such cases, surgery is required to treat the tubal ectopic, while every precaution is taken to protect the pregnancy growing within the uterine cavity.

When an ectopic pregnancy occurs following infertility treatment, there is the added advantage that the physician will be on the lookout for the earliest possible signs of trouble. The performance of a vaginal ultrasound within two weeks of a positive blood pregnancy (HCG) test following IVF allows for early detection of the unruptured pregnancy and timely intervention with MTX and/or laparoscopy.

Good luck!

Geoff Sher
PH: 702-533-2691

reply
Ferishteh

Thank you very much Dr Sher for offering hope and for your wishes!

Yes I read about it in your blog too. I cannot find another here that provides Ovarian sclerotherapy but I will look further. I wish we could come over to you for treatment.

Depending on how this turns out – if we decide to proceed with a new cycle – I may arrange a consultation with you to discuss our options and protocol in depth.

All the best and thanks again!

reply
Feri

UPDATE

Dear Dr Sher,

Just wanted to share an update and seek your opinion please.

By way of summary as mentioned above, FET carried out on 3 May 2021. First hcg test on 10dp5dt was 28. Steadily doubled until the last hcg level 5 weeks 6 days later which took over 96 hours to double. Had a scan that same day and couldn’t detect sac.

Had a scan today a week later at 6 weeks 6 days and detected a sac measuring only 7.5mm. Sonographer said I am measuring only 5 weeks 2 days. No yolk sac or fetal pole. He was quite blunt when I asked about my prospects and said that he has never in his career seen an embryo catch up if its lagging that far behind. He said he didn’t want to get my hopes up. Ofcourse, this was devastating. Have been called in for another scan next Tuesday which will be definitive I am told.

My specialist called me up and she said she is not willing to call it a day as there has been a change (sac growth). She thinks there is a slim chance but I really don’t know if it is simply comfort and reliance upon the chance of a miracle.

So here I am in a bit of desperation but also resignation, seeking your opinion – is there still a chance for us? Or is this likely over? I know I have no option but to wait a week but any light you can shed based on your expertise and experience would be greatly appreciated.

Thank you so much for taking the time to respond!

reply
Dr. Geoffrey Sher

Sadly Feri, the absence of a yolk sac and a detectable HB at almost 7 weeks makes the chance of a viable pregnancy very unlikely!

So sorry!

Geoff Sher

reply
Angela

Is there still any benefit to getting a 20% intralipid infusion if you get it only a few days before transfer? Like 5-7 days before? I’m already on a steroid protocol.

reply
Holly

Hello,
Are there any causes/treatments for chronically thick endometrium? No one can give me answers and I am at a loss. 3 FET cycles in 2020 with CD 3 endometrium 10mm+. Had a laparoscopy/hysteroscopy/D&C April 2021 that found significant endometriosis but excised. Just went for baseline CD3 with measurement of 7.7mm went back CD5 and INCREASED to 10.1mm while still bleeding. Of note, I never had this issue before my successful FET and c-section in 2018. Thank you so much. This forum is a blessing!

reply
Dr. Geoffrey Sher

Unless there is underlying uterine pathology, there is no disadvantage to having a thickened endometrium…in my opinion.

Geoff Sher

reply
Jamie

I posted a few days ago about my betas increasing in 62 hours. Today I found out they more than doubled in 48 hours so we booked an ultrasound June 9th when I’ll be close to 7 weeks! Thank you for your help and time.

9dp5dt 118
13dp5dt 344
15dp5dt 730

reply
Samantha

Hi Dr Sher,

I just received my pgs report back. Wondering if any of these are worth transferring?

1. XY +11 abnormal
2. X dup(7)(q33-q) [mos],-X/-Y abnormal
3. XY del(1)(q32.1-qter)[mos],del(6)(q21-q23.2),del(6)(q23.2-qter),del(7)(q21.11-qter ),dup(9)(pter-p13.3)[mos] complex abnormal

4. XX -7[mos], +12,+15,+16,-19,-22 complex abnormal

reply
Lily

Hi Dr!! I am 44, with 4 miscarriages in the past 4 years, no children (did not even try begore this). I was late, did pregnancy test and came out positive (aprox. 5 weeks since last period).
HCG=2825 and progesterone at 25. Began progesterone supplement.
48 hrs later HCG=3838.
Another HCG (4 days after last one)=6559.
No bleeding or real pain.
Dic said keep taking supplements in case…
Ultrasound is scheduled for this week.
Is there hope or will this be loss #5?

reply
Dr. Geoffrey Sher

When it comes to reproduction, humans are the poorest performers of all mammals. In fact we are so inefficient that up to 75% of fertilized eggs do not produce live births, and up to 30% of pregnancies end up being lost within 10 weeks of conception (in the first trimester). RPL is defined as two (2) or more failed pregnancies. Less than 5% of women will experience two (2) consecutive miscarriages, and only 1% experience three or more.
Pregnancy loss can be classified by the stage of pregnancy when the loss occurs:
• Early pregnancy loss (first trimester)
• Late pregnancy loss (after the first trimester)
• Occult “hidden” and not clinically recognized, (chemical) pregnancy loss (occurs prior to ultrasound confirmation of pregnancy)
• Early pregnancy losses usually occur sporadically (are not repetitive).

In more than 70% of cases the loss is due to embryo aneuploidy (where there are more or less than the normal quota of 46 chromosomes). Conversely, repeated losses (RPL), with isolated exceptions where the cause is structural (e.g., unbalanced translocations), are seldom attributable to numerical chromosomal abnormalities (aneuploidy). In fact, the vast majority of cases of RPL are attributable to non-chromosomal causes such as anatomical uterine abnormalities or Immunologic Implantation Dysfunction (IID).
Since most sporadic early pregnancy losses are induced by chromosomal factors and thus are non-repetitive, having had a single miscarriage the likelihood of a second one occurring is no greater than average. However, once having had two losses the chance of a third one occurring is double (35-40%) and after having had three losses the chance of a fourth miscarriage increases to about 60%. The reason for this is that the more miscarriages a woman has, the greater is the likelihood of this being due to a non-chromosomal (repetitive) cause such as IID. It follows that if numerical chromosomal analysis (karyotyping) of embryonic/fetal products derived from a miscarriage tests karyotypically normal, then by a process of elimination, there would be a strong likelihood of a miscarriage repeating in subsequent pregnancies and one would not have to wait for the disaster to recur before taking action. This is precisely why we strongly advocate that all miscarriage specimens be karyotyped.
There is however one caveat to be taken into consideration. That is that the laboratory performing the karyotyping might unwittingly be testing the mother’s cells rather than that of the conceptus. That is why it is not possible to confidently exclude aneuploidy in cases where karyotyping of products suggests a “chromosomally normal” (euploid) female.
Late pregnancy losses (occurring after completion of the 1st trimester/12th week) occur far less frequently (1%) than early pregnancy losses. They are most commonly due to anatomical abnormalities of the uterus and/or cervix. Weakness of the neck of the cervix rendering it able to act as an effective valve that retains the pregnancy (i.e., cervical incompetence) is in fact one of the commonest causes of late pregnancy loss. So also are developmental (congenital) abnormalities of the uterus (e.g., a uterine septum) and uterine fibroid tumors. In some cases intrauterine growth retardation, premature separation of the placenta (placental abruption), premature rupture of the membranes and premature labor can also causes of late pregnancy loss.
Much progress has been made in understanding the mechanisms involved in RPL. There are two broad categories:
1. Problems involving the uterine environment in which a normal embryo is prohibited from properly implanting and developing. Possible causes include:
• Inadequate thickening of the uterine lining
• Irregularity in the contour of the uterine cavity (polyps, fibroid tumors in the uterine wall, intra-uterine scarring and adenomyosis)
• Hormonal imbalances (progesterone deficiency or luteal phase defects). This most commonly results in occult RPL.
• Deficient blood flow to the uterine lining (thin uterine lining).
• Immunologic implantation dysfunction (IID). A major cause of RPL. Plays a role in 75% of cases where chromosomally normal preimplantation embryos fail to implant.
• Interference of blood supply to the developing conceptus can occur due to a hereditary clotting disorder known as Thrombophilia.

2. Genetic and/or structural chromosomal abnormality of the embryo.Genetic abnormalities are rare causes of RPL. Structural chromosomal abnormalities are slightly more common but are also occur infrequently (1%). These are referred to as unbalanced translocation and they result from part of one chromosome detaching and then fusing with another chromosome. Additionally, a number of studies suggest the existence of paternal (sperm derived) effect on human embryo quality and pregnancy outcome that are not reflected as a chromosomal abnormality. Damaged sperm DNA can have a negative impact on fetal development and present clinically as occult or early clinical miscarriage. The Sperm Chromatin Structure Assay (SCSA) which measures the same endpoints are newer and possibly improved methods for evaluating.

IMMUNOLOGIC IMPLANTATION DYSFUNCTION
Autoimmune IID: Here an immunologic reaction is produced by the individual to his/her body’s own cellular components. The most common antibodies that form in such situations are APA and antithyroid antibodies (ATA).
But it is only when specialized immune cells in the uterine lining, known as cytotoxic lymphocytes (CTL) and natural killer (NK) cells, become activated and start to release an excessive/disproportionate amount of TH-1 cytokines that attack the root system of the embryo, that implantation potential is jeopardized. Diagnosis of such activation requires highly specialized blood test for cytokine activity that can only be performed by a handful of reproductive immunology reference laboratories in the United States.
Alloimmune IID, i.e., where antibodies are formed against antigens derived from another member of the same species, is believed to be a relatively common immunologic cause of recurrent pregnancy loss.
Autoimmune IID is often genetically transmitted. Thus it should not be surprising to learn that it is more likely to exist in women who have a family (or personal) history of primary autoimmune diseases such as lupus erythematosus (LE), scleroderma or autoimmune hypothyroidism (Hashimoto’s disease), autoimmune hyperthyroidism (Grave’s disease), rheumatoid arthritis, etc. Reactionary (secondary) autoimmunity can occur in conjunction with any medical condition associated with widespread tissue damage. One such gynecologic condition is endometriosis. Since autoimmune IID is usually associated with activated NK and T-cells from the outset, it usually results in such very early destruction of the embryo’s root system that the patient does not even recognize that she is pregnant. Accordingly the condition usually presents as “unexplained infertility” or “unexplained IVF failure” rather than as a miscarriage.
Alloimmune IID, on the other hand, usually starts off presenting as unexplained miscarriages (often manifesting as RPL). Over time as NK/T cell activation builds and eventually becomes permanently established the patient often goes from RPL to “infertility” due to failed implantation. RPL is more commonly the consequence of alloimmune rather than autoimmune implantation dysfunction.
However, regardless, of whether miscarriage is due to autoimmune or alloimmune implantation dysfunction the final blow to the pregnancy is the result of activated NK cells and CTL in the uterine lining that damage the developing embryo’s “root system” (trophoblast) so that it can no longer sustain the growing conceptus. This having been said, it is important to note that autoimmune IID is readily amenable to reversal through timely, appropriately administered, selective immunotherapy, and alloimmune IID is not. It is much more difficult to treat successfully, even with the use of immunotherapy. In fact, in some cases the only solution will be to revert to selective immunotherapy plus using donor sperm (provided there is no “match” between the donor’s DQa profile and that of the female recipient) or alternatively to resort to gestational surrogacy.
DIAGNOSING THE CAUSE OF RPL
In the past, women who miscarried were not evaluated thoroughly until they had lost several pregnancies in a row. This was because sporadic miscarriages are most commonly the result of embryo numerical chromosomal irregularities (aneuploidy) and thus not treatable. However, a consecutive series of miscarriages points to a repetitive cause that is non-chromosomal and is potentially remediable. Since RPL is most commonly due to a uterine pathology or immunologic causes that are potentially treatable, it follows that early chromosomal evaluation of products of conception could point to a potentially treatable situation. Thus I strongly recommend that such testing be done in most cases of miscarriage. Doing so will avoid a great deal of unnecessary heartache for many patients.
Establishing the correct diagnosis is the first step toward determining effective treatment for couples with RPL. It results from a problem within the pregnancy itself or within the uterine environment where the pregnancy implants and grows. Diagnostic tests useful in identifying individuals at greater risk for a problem within the pregnancy itself include:

Karyotyping (chromosome analysis) both prospective parents
• Assessment of the karyotype of products of conception derived from previous miscarriage specimens
• Ultrasound examination of the uterine cavity after sterile water is injected or sonohysterogram, fluid ultrasound, etc.)
• Hysterosalpingogram (dye X-ray test)
• Hysteroscopic evaluation of the uterine cavity
• Full hormonal evaluation (estrogen, progesterone, adrenal steroid hormones, thyroid hormones, FSH/LH, etc.)
• Immunologic testing to include:
a) Antiphospholipid antibody (APA) panel
b) Antinuclear antibody (ANA) panel
c) Antithyroid antibody panel (i.e., antithyroglobulin and antimicrosomal antibodies)
d) Reproductive immunophenotype
e) Natural killer cell activity (NKa) assay (i.e., K562 target cell test)
f) Alloimmune testing of both the male and female partners

TREATMENT OF RPL
Treatment for Anatomic Abnormalities of the Uterus: This involves restoration through removal of local lesions such as fibroids, scar tissue, and endometrial polyps or timely insertion of a cervical cerclage (a stitch placed around the neck of the weakened cervix) or the excision of a uterine septum when indicated.
Treatment of Thin Uterine Lining: A thin uterine lining has been shown to correlate with compromised pregnancy outcome. Often this will be associated with reduced blood flow to the endometrium. Such decreased blood flow to the uterus can be improved through treatment with sildenafil and possibly aspirin.
Sildenafil (Viagra) Therapy. Viagra has been used successfully to increase uterine blood flow. However, to be effective it must be administered starting as soon as the period stops up until the day of ovulation and it must be administered vaginally (not orally). Viagra in the form of vaginal suppositories given in the dosage of 25 mg four times a day has been shown to increase uterine blood flow as well as thickness of the uterine lining. To date, we have seen significant improvement of the thickness of the uterine lining in about 70% of women treated. Successful pregnancy resulted in 42% of women who responded to the Viagra. It should be remembered that most of these women had previously experienced repeated IVF failures.
Use of Aspirin: This is an anti-prostaglandin that improves blood flow to the endometrium. It is administered at a dosage of 81 mg orally, daily from the beginning of the cycle until ovulation.

Treating Immunologic Implantation Dysfunction with Selective Immunotherapy: Modalities such as IL/IVIg, heparinoids (Lovenox/Clexane), and corticosteroids (dexamethasone, prednisone, prednisolone) can be used in select cases depending on autoimmune or alloimmune dysfunction.
The Use of IVF in the Treatment of RPL
In the following circumstances, IVF is the preferred option:
1. When in addition to a history of RPL, another standard indication for IVF (e.g., tubal factor, endometriosis, and male factor infertility) is superimposed.
2. In cases where selective immunotherapy is needed to treat an immunologic implantation dysfunction.
The reason for IVF being a preferred approach in such cases is that in order to be effective, the immunotherapy needs to be initiated well before spontaneous or induced ovulation. Given the fact that the anticipated birthrate per cycle of COS with or without IUI is at best about 15%, it follows that short of IVF, to have even a reasonable chance of a live birth, most women with immunologic causes of RPL would need to undergo immunotherapy repeatedly, over consecutive cycles. Conversely, with IVF, the chance of a successful outcome in a single cycle of treatment is several times greater and, because of the attenuated and concentrated time period required for treatment, IVF is far safer and thus represents a more practicable alternative
Since embryo aneuploidy is a common cause of miscarriage, the use of preimplantation genetic diagnosis (PGD), with tests such as CGH, can provide a valuable diagnostic and therapeutic advantage in cases of RPL. PGD requires IVF to provide access to embryos for testing.
There are a few cases of intractable alloimmune dysfunction due to absolute DQ alpha matching where Gestational Surrogacy or use of donor sperm could represent the only viable recourse, other than abandoning treatment altogether and/or resorting to adoption. Other non-immunologic factors such as an intractably thin uterine lining or severe uterine pathology might also warrant that last resort consideration be given to gestational surrogacy.
The good news is that if a couple with RPL is open to all of the diagnostic and treatment options referred to above, a live birthrate of 70%–80% is ultimately achievable.
I strongly recommend that you visit http://www.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
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
• Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• IVF: How Many Attempts should be considered before Stopping?
• “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
• IVF Failure and Implantation Dysfunction:
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF

______________________________________________________
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.

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

reply
Brittany Slater

Hi Dr. Sher! Well, I find myself here after not finding any answers with a few OBGYNs. Thankyou in advance for your time if you’re reading this-
I am 34 with a 22 month old Son. My pregnancy with him went very well. He was an S.U.A. baby so we dis get scans throughout the pregnancy to check on his growth. He was measuring well. However, unrelated, I got a terrible bronchitis at 30 weeks (which left me with persistent asthma even now) and he largely stopped growing so, i was induced at 38 weeks. Then, had emergency c-section bec his h/r was dropping when i was contracting. He came out a very healthy baby but small at 5.1 ounces.
For the last year i had been wanting to fall pregnant but because i am still breastfeeding my son all day and night, i wasnt having any positive ovulation predictor tests and while my periods were consistent every month, there was NO cramping. I was also having night sweats. (Did blood work and all was good).
So, i got my progesterone levels tested and they were 2.2 on 4/20 and 3.0 on 4/22. I was told i most likely didnt ovulate and was probably experiencing menopause like symptoms from breastfeeding. Funny enough, as i found out the following week- i was actually pregnant (or at least had definitely conceived) when i got the progesterone tests done.
Well, so here’s why I’m seeking your opinion- On 5/3 i got my hcg and progesterone levels taken. They were 2,960 & 20. 48 hours later on 5/5 they were 5,841 & 18. Because i had some nerves, I requested a 3rd test 48 hours later on 5/7. They were 6,163 and 17. I waited thru the weekend and i got another hcg and progesterone test done. It was 5567 and 16. The next day i did a scan that showed me at 5w4days with a gestational sac and yolk sac but no fetal pole. My doctors prepared me for a miscarriage but to be conservative we did a scan the following week. The next week, they found a heartbeat of 115 and baby measuring 6.2 days. My doctor was stumped and said, screw the hcg and progesterone numbers, lets just go by the scans. She put me on progesterone too. The NEXT week we found a healthy strong baby again measuring 7w1day with heartbeat of 142. My doctors couldnt answer my questions about if a baby could properly survive and thrive off of such little hcg, so I requested another hcg and progesterone draw to better mentally prepare me. I felt pregnant but minimally and i didnt feel good the hcg and progesterone. My hcg and progesterone came back at only 5,584 & 11.1. This upset me greatly but i knew what was most likely going to happen and it did. The next week’s scan showed that the baby grew until 8weeks1 day but there was no heartbeat any longer. So, it grew wonderfully but it died.
I dont understand what happened. Why did my hcg stop rising but my baby seemed healthy and was able to grow for almost a month after the hcg stopped rising? Any thoughts on this? Im lost and confused. Thanks a lot. Be well i feel like my body deprived it of nutrition. I take asthma steroid inhalers. Wondering if that caused it.

reply
Brittany Slater

I forgot to mention- im also wondering if my breastfeeding killed my baby. Was that why the hcg and progesterone dropped? Seems odd but possibly?

reply
Dr. Geoffrey Sher

What you experienced was likely due chromosomal abnormality of the conceptus or due to an implantation dysfunction. Without a karyotype (chromosomal analysis) analysis of the products it is not possible to discern. Hopefully this is an isolated occurrence and will not recur in a subsequent pregnancy.

Good luck and G-d bless!

Geoff Sher

reply
Brittany Slater

Thankyou SO much for your time and expertise. Im going in for a d&c and asking them to test the baby. Be well. I appreciate your blessings too!

Brittany Slater

So, the testing came back as no chromosomal issues. Any reasons, why you think my baby passed at 8w1 day in my case?

Dr. Geoffrey Sher

It now sounds as if it could be due to implantation dysfunction.

Implantation dysfunction is unfortunately often overlooked as an important cause of IVF failure. In the pursuit of optimizing outcome with IVF, the clinician has a profound responsibility to meticulously assess and address this important issue if IVF success is to be optimized. This is especially relevant in cases of “unexplained IVF failure, Recurrent Pregnancy Loss (RPL) and in women suspected of having underlying anatomical and immunologic factors. Doing so will not only maximize the chance of a viable pregnancy but enhancing placentation, will at the same time promote the noble objective of optimizing the quality of life after birth.”
IVF success rates have been improving over the last decade. The average live birth rate per embryo transfer in the U.S.A for women under 40y using their own eggs , is currently better than 1:3 women. However, there is still a wide variation from program to program for IVF live birth rates, ranging from 20% to near 50%. Based upon these statistics, the majority of women undergoing IVF in the United States require two or more attempts to have a baby. IVF practitioners in the United States commonly attribute the wide dichotomy in IVF success rates to variability in expertise of the various embryology laboratories. This is far from accurate. In fact, other factors such as wide variations in patient selection and the failure to develop individualized protocols for ovarian stimulation or to address those infective, anatomical and immunologic factors that influence embryo implantation are at least equally important.
About 80% of IVF failures are due to “embryo incompetency” that is largely due to an irregular quota of chromosomes (aneuploidy) which is usually related to advancing age of the woman and is further influenced by other factors such as the protocol selected for ovarian stimulation, diminished ovarian reserve (DOR)m and severe male factor infertility. However in about 20% of dysfunctional cases embryo implantation is the cause of failure.
Anatomical Endo-uterine Lesions: This blog article will focus on implantation dysfunction and IVF failure due to:
• Anatomical abnormalities in the uterine cavity (e.g. scarring, polyps and encroaching fibroid tumors)
• A thin endometrial lining
• Immunologic rejection of the embryos
Several studies performed both in the United States and abroad have confirmed that a dye X-Ray or hysterosalpingogram (HSG) will fail to identify small endouterine surface lesions in >20% of cases. This is significant because even small uterine lesions have the potential to adversely affect implantation. Hysteroscopy is the traditional method for evaluating the integrity of the uterine cavity in preparation for IVF. It also permits resection of most uterine surface lesions, such as submucous uterine fibroids (myomas), intrauterine adhesions and endometrial or placental polyps. All of these can interfere with implantation by producing a local “inflammatory- type” response similar in nature to that which is caused by an intrauterine contraceptive device. Hysterosonography (syn; HSN/ saline ultrasound examination) and hysteroscopy have all but supplanted HSG to assess the uterine cavity in preparation for IVF. HSN which is less invasive and far less expensive than is than hysteroscopy involves a small amount of a sterile saline solution is injected into the uterine cavity, whereupon a vaginal ultrasound examination is performed to assess the contour of the uterine cavity.
Endometrial Thickness: As far back as in 1989 I first reported on the finding that ultrasound assessment of the late proliferative phase endometrium following ovarian stimulation in preparation for IVF, permits better identification of those candidates who are least likely to conceive. We noted that the ideal thickness of the endometrium at the time of ovulation or egg retrieval is >9 mm and that a thickness of less than 8 mm bodes poorly for a successful outcome following IVF.
Then in 1993, I demonstrated that sildenafil (Viagra) introduced into the vagina prior to hCG administration can improve endometrial growth in many women with poor endometrial development. Viagra’s mechanism of action is improvement in uterine blood flow with improved estrogen delivery…thereby enhancing endometrial development.
Immunologic factors: These also play a role in IVF failure. Some women develop antibodies to components of their own cells. This “autoimmune” process involves the production of antiphospholipid, antithyroid, and/or anti-ovarian antibodies – all of which may be associated with activation of Natural Killer (NK) cells in the uterine lining. Activated NK cells (NKa) release certain cytokines (TH-I) that if present in excess, often damage the trophoblast (the embryo’s root system) resulting in immunologic implantation dysfunction (IID). This can manifest as “infertility” or as early miscarriages). In other cases (though less common), the problem is due to “alloimmune” dysfunction. Here the genetic contribution by the male partner renders the embryo “too similar” to the mother. This in turn activates NK cells leading to implantation dysfunction. These IID’s are treated using combinations of medications such as heparin, Clexane, Lovenox, corticosteroids and intralipid (IL).

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

• A Fresh Look at the Indications for IVF
• The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• IVF and the use of Supplementary Human Growth Hormone (HGH) : Is it Worth Trying and who needs it?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• IVF: Approach to Selecting the Best Embryos for Transfer to the Uterus.
• Fresh versus Frozen Embryo Transfers (FET) Enhance IVF Outcome
• Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
• Genetically Testing Embryos for IVF
• Staggered IVF
• Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
• Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
• IVF: Selecting the Best Quality Embryos to Transfer
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
• PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
• PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
• Endometrial Receptivity Array (ERA): Is There an actual “There, There”?
• IVF Failure and Implantation Dysfunction:
• Diagnosing and Treating Immunologic Implantation Dysfunction (IID)
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• A Thin Uterine Lining: Vaginal Viagra is Often the Answer (update)
• Cervical Ureaplasma Urealyticum Infection: How can it Affect IUI/IVF Outcome?
• The Role of Nutritional Supplements in Preparing for IVF
• The Basic Infertility Work-Up
• Defining and Addressing an Abnormal Luteal Phase
• Male Factor Infertility
• Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in Favor
• Hormonal Treatment of Male Infertility
• Hormonal Treatment of Male Infertility
• Antisperm Antibodies, Infertility and the Role of IVF with Intracytoplasmic Sperm Injection (ICSI)
• Endometriosis and Infertily
• Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF
• Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
• Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
• Early -Endometriosis-related Infertility: Ovulation Induction (with or without Intrauterine Insemination) and Reproductive Surgery Versus IVF
• Deciding Between Intrauterine Insemination (IUI) and In Vitro Fertilization (IVF).
• Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & Con’s!IUI-Reflecting upon its Use and Misuse: Time for a Serious “Reality Check
• Mode of Action, Indications, Benefits, Limitations and Contraindications for its ue
• Clomiphene Induction of Ovulation: Its Use and Misuse!
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.

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

Dr. Geoffrey Sher

It sounds like an implantation dysfunction.

Implantation dysfunction is unfortunately often overlooked as an important cause of IVF failure. In the pursuit of optimizing outcome with IVF, the clinician has a profound responsibility to meticulously assess and address this important issue if IVF success is to be optimized. This is especially relevant in cases of “unexplained IVF failure, Recurrent Pregnancy Loss (RPL) and in women suspected of having underlying anatomical and immunologic factors. Doing so will not only maximize the chance of a viable pregnancy but enhancing placentation, will at the same time promote the noble objective of optimizing the quality of life after birth.”
IVF success rates have been improving over the last decade. The average live birth rate per embryo transfer in the U.S.A for women under 40y using their own eggs , is currently better than 1:3 women. However, there is still a wide variation from program to program for IVF live birth rates, ranging from 20% to near 50%. Based upon these statistics, the majority of women undergoing IVF in the United States require two or more attempts to have a baby. IVF practitioners in the United States commonly attribute the wide dichotomy in IVF success rates to variability in expertise of the various embryology laboratories. This is far from accurate. In fact, other factors such as wide variations in patient selection and the failure to develop individualized protocols for ovarian stimulation or to address those infective, anatomical and immunologic factors that influence embryo implantation are at least equally important.
About 80% of IVF failures are due to “embryo incompetency” that is largely due to an irregular quota of chromosomes (aneuploidy) which is usually related to advancing age of the woman and is further influenced by other factors such as the protocol selected for ovarian stimulation, diminished ovarian reserve (DOR)m and severe male factor infertility. However in about 20% of dysfunctional cases embryo implantation is the cause of failure.
Anatomical Endo-uterine Lesions: This blog article will focus on implantation dysfunction and IVF failure due to:
• Anatomical abnormalities in the uterine cavity (e.g. scarring, polyps and encroaching fibroid tumors)
• A thin endometrial lining
• Immunologic rejection of the embryos
Several studies performed both in the United States and abroad have confirmed that a dye X-Ray or hysterosalpingogram (HSG) will fail to identify small endouterine surface lesions in >20% of cases. This is significant because even small uterine lesions have the potential to adversely affect implantation. Hysteroscopy is the traditional method for evaluating the integrity of the uterine cavity in preparation for IVF. It also permits resection of most uterine surface lesions, such as submucous uterine fibroids (myomas), intrauterine adhesions and endometrial or placental polyps. All of these can interfere with implantation by producing a local “inflammatory- type” response similar in nature to that which is caused by an intrauterine contraceptive device. Hysterosonography (syn; HSN/ saline ultrasound examination) and hysteroscopy have all but supplanted HSG to assess the uterine cavity in preparation for IVF. HSN which is less invasive and far less expensive than is than hysteroscopy involves a small amount of a sterile saline solution is injected into the uterine cavity, whereupon a vaginal ultrasound examination is performed to assess the contour of the uterine cavity.
Endometrial Thickness: As far back as in 1989 I first reported on the finding that ultrasound assessment of the late proliferative phase endometrium following ovarian stimulation in preparation for IVF, permits better identification of those candidates who are least likely to conceive. We noted that the ideal thickness of the endometrium at the time of ovulation or egg retrieval is >9 mm and that a thickness of less than 8 mm bodes poorly for a successful outcome following IVF.
Then in 1993, I demonstrated that sildenafil (Viagra) introduced into the vagina prior to hCG administration can improve endometrial growth in many women with poor endometrial development. Viagra’s mechanism of action is improvement in uterine blood flow with improved estrogen delivery…thereby enhancing endometrial development.
Immunologic factors: These also play a role in IVF failure. Some women develop antibodies to components of their own cells. This “autoimmune” process involves the production of antiphospholipid, antithyroid, and/or anti-ovarian antibodies – all of which may be associated with activation of Natural Killer (NK) cells in the uterine lining. Activated NK cells (NKa) release certain cytokines (TH-I) that if present in excess, often damage the trophoblast (the embryo’s root system) resulting in immunologic implantation dysfunction (IID). This can manifest as “infertility” or as early miscarriages). In other cases (though less common), the problem is due to “alloimmune” dysfunction. Here the genetic contribution by the male partner renders the embryo “too similar” to the mother. This in turn activates NK cells leading to implantation dysfunction. These IID’s are treated using combinations of medications such as heparin, Clexane, Lovenox, corticosteroids and intralipid (IL).

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

• A Fresh Look at the Indications for IVF
• The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• IVF and the use of Supplementary Human Growth Hormone (HGH) : Is it Worth Trying and who needs it?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• IVF: Approach to Selecting the Best Embryos for Transfer to the Uterus.
• Fresh versus Frozen Embryo Transfers (FET) Enhance IVF Outcome
• Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
• Genetically Testing Embryos for IVF
• Staggered IVF
• Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
• Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
• IVF: Selecting the Best Quality Embryos to Transfer
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
• PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
• PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
• Endometrial Receptivity Array (ERA): Is There an actual “There, There”?
• IVF Failure and Implantation Dysfunction:
• Diagnosing and Treating Immunologic Implantation Dysfunction (IID)
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• A Thin Uterine Lining: Vaginal Viagra is Often the Answer (update)
• Cervical Ureaplasma Urealyticum Infection: How can it Affect IUI/IVF Outcome?
• The Role of Nutritional Supplements in Preparing for IVF
• The Basic Infertility Work-Up
• Defining and Addressing an Abnormal Luteal Phase
• Male Factor Infertility
• Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in Favor
• Hormonal Treatment of Male Infertility
• Hormonal Treatment of Male Infertility
• Antisperm Antibodies, Infertility and the Role of IVF with Intracytoplasmic Sperm Injection (ICSI)
• Endometriosis and Infertily
• Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF
• Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
• Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
• Early -Endometriosis-related Infertility: Ovulation Induction (with or without Intrauterine Insemination) and Reproductive Surgery Versus IVF
• Deciding Between Intrauterine Insemination (IUI) and In Vitro Fertilization (IVF).
• Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & Con’s!IUI-Reflecting upon its Use and Misuse: Time for a Serious “Reality Check
• Mode of Action, Indications, Benefits, Limitations and Contraindications for its ue
• Clomiphene Induction of Ovulation: Its Use and Misuse!
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.

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

Dr. Geoffrey Sher

It sounds like an implantation dysfunction.

Implantation dysfunction is unfortunately often overlooked as an important cause of IVF failure. In the pursuit of optimizing outcome with IVF, the clinician has a profound responsibility to meticulously assess and address this important issue if IVF success is to be optimized. This is especially relevant in cases of “unexplained IVF failure, Recurrent Pregnancy Loss (RPL) and in women suspected of having underlying anatomical and immunologic factors. Doing so will not only maximize the chance of a viable pregnancy but enhancing placentation, will at the same time promote the noble objective of optimizing the quality of life after birth.”
IVF success rates have been improving over the last decade. The average live birth rate per embryo transfer in the U.S.A for women under 40y using their own eggs , is currently better than 1:3 women. However, there is still a wide variation from program to program for IVF live birth rates, ranging from 20% to near 50%. Based upon these statistics, the majority of women undergoing IVF in the United States require two or more attempts to have a baby. IVF practitioners in the United States commonly attribute the wide dichotomy in IVF success rates to variability in expertise of the various embryology laboratories. This is far from accurate. In fact, other factors such as wide variations in patient selection and the failure to develop individualized protocols for ovarian stimulation or to address those infective, anatomical and immunologic factors that influence embryo implantation are at least equally important.
About 80% of IVF failures are due to “embryo incompetency” that is largely due to an irregular quota of chromosomes (aneuploidy) which is usually related to advancing age of the woman and is further influenced by other factors such as the protocol selected for ovarian stimulation, diminished ovarian reserve (DOR)m and severe male factor infertility. However in about 20% of dysfunctional cases embryo implantation is the cause of failure.
Anatomical Endo-uterine Lesions: This blog article will focus on implantation dysfunction and IVF failure due to:
• Anatomical abnormalities in the uterine cavity (e.g. scarring, polyps and encroaching fibroid tumors)
• A thin endometrial lining
• Immunologic rejection of the embryos
Several studies performed both in the United States and abroad have confirmed that a dye X-Ray or hysterosalpingogram (HSG) will fail to identify small endouterine surface lesions in >20% of cases. This is significant because even small uterine lesions have the potential to adversely affect implantation. Hysteroscopy is the traditional method for evaluating the integrity of the uterine cavity in preparation for IVF. It also permits resection of most uterine surface lesions, such as submucous uterine fibroids (myomas), intrauterine adhesions and endometrial or placental polyps. All of these can interfere with implantation by producing a local “inflammatory- type” response similar in nature to that which is caused by an intrauterine contraceptive device. Hysterosonography (syn; HSN/ saline ultrasound examination) and hysteroscopy have all but supplanted HSG to assess the uterine cavity in preparation for IVF. HSN which is less invasive and far less expensive than is than hysteroscopy involves a small amount of a sterile saline solution is injected into the uterine cavity, whereupon a vaginal ultrasound examination is performed to assess the contour of the uterine cavity.
Endometrial Thickness: As far back as in 1989 I first reported on the finding that ultrasound assessment of the late proliferative phase endometrium following ovarian stimulation in preparation for IVF, permits better identification of those candidates who are least likely to conceive. We noted that the ideal thickness of the endometrium at the time of ovulation or egg retrieval is >9 mm and that a thickness of less than 8 mm bodes poorly for a successful outcome following IVF.
Then in 1993, I demonstrated that sildenafil (Viagra) introduced into the vagina prior to hCG administration can improve endometrial growth in many women with poor endometrial development. Viagra’s mechanism of action is improvement in uterine blood flow with improved estrogen delivery…thereby enhancing endometrial development.
Immunologic factors: These also play a role in IVF failure. Some women develop antibodies to components of their own cells. This “autoimmune” process involves the production of antiphospholipid, antithyroid, and/or anti-ovarian antibodies – all of which may be associated with activation of Natural Killer (NK) cells in the uterine lining. Activated NK cells (NKa) release certain cytokines (TH-I) that if present in excess, often damage the trophoblast (the embryo’s root system) resulting in immunologic implantation dysfunction (IID). This can manifest as “infertility” or as early miscarriages). In other cases (though less common), the problem is due to “alloimmune” dysfunction. Here the genetic contribution by the male partner renders the embryo “too similar” to the mother. This in turn activates NK cells leading to implantation dysfunction. These IID’s are treated using combinations of medications such as heparin, Clexane, Lovenox, corticosteroids and intralipid (IL).

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

• A Fresh Look at the Indications for IVF
• The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• IVF and the use of Supplementary Human Growth Hormone (HGH) : Is it Worth Trying and who needs it?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• IVF: Approach to Selecting the Best Embryos for Transfer to the Uterus.
• Fresh versus Frozen Embryo Transfers (FET) Enhance IVF Outcome
• Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
• Genetically Testing Embryos for IVF
• Staggered IVF
• Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
• Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
• IVF: Selecting the Best Quality Embryos to Transfer
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
• PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
• PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
• Endometrial Receptivity Array (ERA): Is There an actual “There, There”?
• IVF Failure and Implantation Dysfunction:
• Diagnosing and Treating Immunologic Implantation Dysfunction (IID)
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• A Thin Uterine Lining: Vaginal Viagra is Often the Answer (update)
• Cervical Ureaplasma Urealyticum Infection: How can it Affect IUI/IVF Outcome?
• The Role of Nutritional Supplements in Preparing for IVF
• The Basic Infertility Work-Up
• Defining and Addressing an Abnormal Luteal Phase
• Male Factor Infertility
• Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in Favor
• Hormonal Treatment of Male Infertility
• Hormonal Treatment of Male Infertility
• Antisperm Antibodies, Infertility and the Role of IVF with Intracytoplasmic Sperm Injection (ICSI)
• Endometriosis and Infertily
• Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF
• Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
• Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
• Early -Endometriosis-related Infertility: Ovulation Induction (with or without Intrauterine Insemination) and Reproductive Surgery Versus IVF
• Deciding Between Intrauterine Insemination (IUI) and In Vitro Fertilization (IVF).
• Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & Con’s!IUI-Reflecting upon its Use and Misuse: Time for a Serious “Reality Check
• Mode of Action, Indications, Benefits, Limitations and Contraindications for its ue
• Clomiphene Induction of Ovulation: Its Use and Misuse!
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.

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

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