Staggered IVF: An Excellent Option When Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate

Many physicians treating infertile women over 40 years old who have patent fallopian tubes still opt to start with the least invasive strategy rather than going straight to IVF. This usually begins with the prescribing of oral and then injectable fertility drugs with or without artificial insemination/IUI. The rationale for this approach is that IVF is significantly more expensive than such alternatives.  While the cost of an IVF procedure is certainly more expensive, what is often ignored is that it is also far more likely to achieve the desired result of a live birth. When one considers that the real price (financial as well as emotional) resides in the cost of having a baby rather than the cost of a procedure, doing IVF often turns out to be less costly.

It is well established that regardless of a woman’s age or the cause of her infertility, the chance of pregnancy following IVF is several-fold greater than with any other method of treatment including  intrauterine insemination (with or without the use of fertility drugs) and that this difference becomes much more pronounced with advancing age. For example, the chance of an ovulating woman of under 35 who has patent Fallopian tubes and a fertile male partner, having a baby after a single attempt at IUI is <15%. For a woman in her mid-40s the chance is <3%. With IVF, the comparable chances of success would be about 40% and 15%, respectively.

This does not mean that all infertile women who have patent Fallopian tubes and fertile male partners should select IVF over less invasive and less expensive treatments. What it does suggest, however, is that women running out of time on the “biological clock” (i.e., women in their 40’s, and women who have diminished ovarian reserve -DOR), should probably go directly to IVF rather than waste precious time on less effective treatment options. It must also be recognized that the older the woman, the greater the risk of miscarriage and of having a chromosomally abnormal baby. For example: At age 30 the risk of miscarriage is about 15% and the chance of a woman giving birth to a chromosomally abnormal baby (e.g. Down syndrome) is <1:1000. Conversely, in the mid-40’s the comparable risk of miscarriage is >40%, and 1:60-80, respectively.

Making strong a case for Embryo banking with Staggered IVF and PGS embryo testing: Against this background, in an attempt to try and put the “biological clock” on hold and provide older infertile women and those with DOR with an alternative to IVF/egg donation, we recently introduced Embryo Banking with Staggered IVF and Preimplantation Genetic Sampling (PGS) of embryos. This approach usually requires  more than one IVF procedure, biopsy of all potentially viable embryos for PGS, holding all biopsied specimens until several (4-8) blastocysts have been cryobanked and then sending the biopsied DNA for PGS (using Comparative Genomic Hybridization [CGH] or Next Generation Gene Sequencing [NGS]testing).

Once the PGS results are known, the woman returns in a subsequent cycle for the selective transfer of up to two PGS-normal embryos to her uterus. Staggered IVF refers to the process whereby embryos are transferred in a different cycle to the one where the eggs were harvested. The use of embryo banking with Staggered IVF and selectively transferring only PGS-normal embryos is an efficiency tool which significantly improves the baby rate per embryo transferred (to as high as 40-50%), reduces the miscarriage rate by a factor of 5-6 and minimizes the risk of the birth of a baby who has chromosomal birth defects (e.g. Down syndrome).

The “competency” (numerical chromosomal integrity) of a woman’s eggs declines rapidly with advancing age (about 1:2 are normal in her early 30’s as compared to 1:6 at 40Y and about 1:20 by 45Y). In addition, the older the woman gets, the more her total egg supply diminishes, ultimately resulting in DOR. For these reasons, advancing age and DOR reduce fertility, increase the risk of miscarriage and result in a rise of chromosomal birth defects (e.g. Down syndrome). IVF can markedly improve outcome by maximizing the number of eggs available for fertilization and making the resulting embryos available for genetic testing. The introduction by SIRM of Staggered IVF, Embryo Banking and PGS with the selective transfer of only “chromosomally competent” embryos represents an excellent “efficiency tool” which markedly improves  pregnancy rate, reduces the chance of miscarriage an minimizes the risk of chromosomal birth defects. As such I strongly recommend this approach for older women and women who (regardless of age) and as such are running out of time on their “biological clocks.”

10 Comments

Chien Nguyen Ngoc

Hi Dr Sher, i am a specialist in IVF working in Hanoi, Vietnam. I usually reading your articles and post, they are very interesting and helpful for me. I would like to ask you about Viagra vaginal treatment for thin endometrium. The problem is that here in Vietnam we do not have vaginal Viagra. So my question is that if orally Viagra can use for vaginal way and if this approach is as effective as vaginal Viagra? If the answer is not, how can i get vaginal Viagra for my patients? Thank you very much.

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Dr. Geoffrey Sher

Yes! only Viagra works, but it must ne vaginal and compounded correctly. I suggest you contact MDR Pharmacy in S. California and talk to their pharmacist (David Mhakane) for details on how to compound it correctly. You can obtain contact information via Google!

About seventeen years ago, after reporting on the benefit of vaginal Sildenafil (Viagra) for to women who had implantation dysfunction due to thin endometrial linings I was proud to announce the birth of the world’s first “Viagra baby.” For those of you who aren’t familiar with the use of Viagra in IVF, allow me to provide some context.

It was as far back as 1989, when I first published a study that examined the correlation between the thickness of a woman’s uterine lining (the endometrium), and the subsequent successful implantation of embryos in IVF patients. This study revealed that when the uterine lining measured <8mm in thickness by the day of the “hCG trigger” (in fresh IVF cycles), or at the time of initiating progesterone therapy (in embryo recipient cycles, e.g. frozen embryo transfers, egg donation-IVF etc.) , pregnancy and birth rates were substantially improved. Currently, it is my opinion, that an ideal estrogen-promoted endometrial lining should ideally measure at least 9mm in thickness and that an endometrial lining measuring 8-9mm is “intermediate”. An estrogenic lining of <8mm is in most cases unlikely to yield a viable pregnancy.

A “poor” uterine lining is usually the result of the innermost layer of endometrium (the basal or germinal endometrium from which endometrium grows) ) not being able to respond to estrogen by propagating an outer, “functional” layer thick enough to support optimal embryo implantation and development of a healthy placenta (placentation). The “functional” layer ultimately comprises 2/3 of the full endometrial thickness and is the layer that sheds with menstruation in the event that no pregnancy occurs.

The main causes of a “poor” uterine lining are:

1. Damage to the basal endometrium as a result of:
a. Inflammation of the endometrium (endometritis) most commonly resulting from infected products left over following abortion, miscarriage or birth
b. Surgical trauma due to traumatic uterine scraping, (i.e. due to an over-aggressive D & C)
2. Insensitivity of the basal endometrium to estrogen due to:
a. Prolonged , over-use/misuse of clomiphene citrate
b. Prenatal exposure to diethylstilbestrol (DES). This is a drug that was given to pregnant women in the 1960’s to help prevent miscarriage
3. Over-exposure of the uterine lining to ovarian male hormones (mainly testosterone): Older women, women with diminished ovarian reserve (poor responders) and women with polycystic ovarian syndrome -PCOS tend to have raised LH biological activity.. This causes the connective tissue in the ovary (stroma/theca) to overproduce testosterone. The effect can be further exaggerated when certain methods for ovarian stimulation such as agonist (Lupron/Buserelin) “flare” protocols and high dosages of menotropins such as Menopur are used in such cases.
4. Reduced blood flow to the basal endometrium:
Examples include;
a. Multiple uterine fibroids - especially when these are present under the endometrium (submucosal)
b. Uterine adenomyosis (excessive, abnormal invasion of the uterine muscle by endometrial glands).

“The Viagra Connection”

Treatments such supplementary estrogen therapy, aspirin administration and/or administration of high dosage gonadotropin fertility drugs, aimed at improving endometrial development have all yielded disappointing results.

It was in the 90’s that Sildenafil (brand named Viagra) was gaining popularity as a treatment for erectile dysfunction. The mechanism by which it acted was through increasing penile blood flow through increasing nitric oxide activity. This prompted me to investigate whether Viagra administered vaginally, might similarly improve uterine blood flow and in the process cause more estrogen to be delivered to the basal endometrium and thereby increase endometrial thickening. We found that when Viagra was administered vaginally it did just that! However oral administration was without any significant benefit in this regard. We enlisted the services of a compound pharmacy to produce vaginal Viagra suppositories. Initially, four (4) women with chronic histories of poor endometrial development and failure to conceive following several advanced fertility treatments were evaluated for a period of 4-6 weeks and then underwent IVF with concomitant Viagra therapy. Viagra suppositories were administered four times daily for 8-11 days and were discontinued 5-7 days prior to embryo transfer in all cases.

Our findings clearly demonstrated that vaginal Viagra produced a rapid and profound improvement in uterine blood flow and that was followed by enhanced endometrial development in all four cases. Three (3) of the four women subsequently conceived. . I expanded the trial in 2002 and became the first to report on the administration of vaginal Viagra to 105 women with repeated IVF failure due to persistently thin endometrial linings. All of the women had experienced at least two (2) prior IVF failures attributed to intractably thin uterine linings. About 70% of these women responded to treatment with Viagra suppositories with a marked improvement in endometrial thickness. Forty five percent (45%) achieved live births following a single cycle of IVF treatment with Viagra The miscarriage rate was 9%. None of the women who had failed to show an improvement in endometrial thickness following Viagra treatment achieved viable pregnancies.
Following vaginal administration, Viagra is rapidly absorbed and quickly reaches the uterine blood system in high concentrations. Thereupon it dilutes out as it is absorbed into the systemic circulation. This probably explains why treatment is virtually devoid of systemic side effects

Since the introduction of this form of treatment, thousands of women with thin uterine linings have been reported treated and many have gone on to have babies after repeated prior IVF failure.

It is important to recognize that Viagra will NOT be effective in improving endometrial thickness in all cases. In fact, about one third of women treated fail to show any improvement. This is because in certain cases of thin uterine linings, the basal endometrium will have been permanently damaged and left unresponsive to estrogen. This happens in cases of severe endometrial damage due mainly to post-pregnancy endometritis (inflammation), chronic granulomatous inflammation due to uterine tuberculosis (hardly ever seen in the United States) and following extensive surgical injury to the basal endometrium (as sometimes occurs following over-zealous D&C’s).

To be effective, Viagra must be administered vaginally. It is NOT effective when taken orally. We prescribe 20mg vaginal suppositories to be inserted four times per day. Treatment is commenced soon after menstruation ceases and is continued until the day of the “hCG trigger.” While ideally the treatment should be sustained throughout the first half of the cycle, most women will respond within 48-72 hours. For this reason, Viagra can be used to “rescue” a poor lining after the cycle has already started, provided that there is enough time remaining prior to ovulation, egg retrieval or progesterone administration.

Geoff Sher

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Sinthea

I know this is an old log entry, but do you think it should be updated before reposting and shared on your Facebook page? Currently PGDIS has new standards that say NGS is the only real credible method for chromosomal analysis in PGS.

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Dr. Geoffrey Sher

My position is reflected in this article I wrote on my blog in 2016.
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Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): The Method of Choice.
Geoffrey Sher MD

About 12 years ago, Levent Keskintepe PhD and I introduced Comparative Genomic Hybridization (CGH) into the clinical IVF arena, as a preimplantation genetic sampling (PGS) method that enables full karyotyping (numerically chromosomal analysis) of all 23 pairs of an embryo’s chromosomes so mas to determine its subsequent ability to propagate a viable pregnancy (i.e. its “competence”). Since then we have, over a period of a 12 years, authored many articles on the clinical utility and advantages associated with the selective performance of embryo PGS and with it have witnessed embryo karyotyping emerge as a valuable efficiency tool in the IVF arena. Several alternatives to CGH have since emerged and while none are perfect, they have all enhanced our ability to better select the most “competent embryos for transfer to the uterus, thereby improving the efficiency of IVF, and reducing the risk of chromosomal miscarriages and birth defects.
One recently introduced method known as “Next Generation Gene Sequencing (NGS)” bears special mention since its improved accuracy and reliability over previously used methodologies, has established it as a method of choice when it comes to embryo karyotyping..
Gene Sequencing is a method that determines the precise order of nucleotides within a DNA molecule. The method/ technology determines the order of the four bases—adenine, guanine, cytosine, and thymine—in a strand of DNA. A new generation of sequencing technologies known as NGS now provides unprecedented opportunities for high-throughput functional genomic research. NGS is currently being applied to identify the karyotype of the human embryo and in my opinion is more reliable than other available PGS methodologies.
NGS can be conducted reliably on blastomeres (derived from day 5-6, cleaved embryos) d from a blastocyst. .
Based upon available data, it is my opinion that the time has arrived to recommend that blastocyst NGS be used as the preferred method for PGS in IVF.

Geoff Sher

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Nadiahailu

I am 45 years old, i have 5 miscarriage. I want have a baby. What is my option

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Dr. Geoffrey Sher

At 45y, you need to c onsider IVF with egg donation. However, please read below as well!

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

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

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

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

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

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
• Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• IVF: How Many Attempts should be considered before Stopping?
• “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
• IVF Failure and Implantation Dysfunction:
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF

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

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

Geoffrey Sher MD

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Dr. Geoffrey Sher

You are very welcome!

Please help spread the word about this website and the blog!

GS

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M

Hi, we used a “staggered” process, testing 18 blastocysts from 4 ivf cycles at ages 41 – 42. We realise were extremely lucky to have this number of embryos suitable for testing. The pgs results were 6 normal embryos and 1 ‘no result’. We have so far transferred 2 embryos and our second FET was successful. Our questions are – what effects does age have on transfer? (I’m now 44). And is continuing to breastfeed a negative for FET success rates. Our long awaited (and possibly only?) baby is not wanting to wean, but we would like for our baby to have sibling/s. It remains a delicate balancing act making ivf related family decisions!
Thank you

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Dr. Geoffrey Sher

I aplaud you and your RE for doing Staggered IVF with banking of PGS-normal balatocysts. That was the right thing to do and it seems to have paid off.

Provided the uterus is healthy and there are no anatomical and immunologic impediments to implantation, age should not significantly compromise implantation.

As for breast feeding, I would wean sooner rather than later, wait 2 full regular cycles thereafter and then resume the FET journey.

I am proud to announce the establishment of my new website, http://www.DrGeoffreySherIVF.com which also hosts my new blog which I will be servicing with articles on an ongoing basis and where I will be addressing your questions and comments.

From the home page of this website you can access the blog and the “search bar” where you can type in a topics (below) , click and you will be taken to the article of your choice. I will also continue to answer all questions you post on the “IVFauthority” blog but will no longer be contributing new articles on that site.

• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF at SIRM”; Parts 1 & 2 (posted March, 2012)
• The Role of Nutritional Supplements in Preparing for IVF
• Frozen Embryo Transfer (FET): What Does it Involve?
• Hereditary Clotting Defects (Thrombophilia)
• Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
• PGS-Biopsy for the Assessment of Embryo Numerical Chromosomal integrity (Ploidy): Should it be done on Day 3 or on Day 5-6 post fertilization?
• Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
• Launching Ovarian Stimulation with a BCP: How Does it Affect Response?
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.

If you are interested in having a Skype consultation with me and discussing your case in detail, please call 1-702-699-7437 or 1-800-780-7437.
Finally, perhaps you would be interested in accessing the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores.

Geoff Sher

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