– Geoffrey Sher, MD
Fill in the following information and we’ll get back to you.
Name: Jorja P
Good day
I am looking for info.
I am a 36 year old single female from NY. I would love to adopt a boy embrio, black hair and blue eyes, white. I am not able to have kids of my own due to PCOS and Endometriosis and so on. I will also need a surrogate if possible. I would love to know can this be done and what the costs will be. Thanks so much.
I suggest you call Patti Converse (my assistant) and set up an online consultation with me to review your case and make suggestions.
Geoff Sher
____________________________________________________________________________________
Herewith are online links to 2 E-books recently co-authored with my partner at SFS-NY (Drew Tortoriello MD)……. for your reading pleasure:
I invite you to visit my very recently launched “Podcast”, “HAVE A BABY” on RUMBLE; https://rumble.com/c/c-3304480
If you are interested in having an online consultation with me, please contact my assistant, Patti Converse at 702-533-2691 or email her at concierge@sherivf.com\
Name: Diego O
Valores de espermatozoides
Cantidad de pago
Explícame mejor
Please re-post in English!
Geoff Sher
_______________________________________________________________________________________
Herewith are online links to 2 E-books recently co-authored with my partner at SFS-NY (Drew Tortoriello MD)……. for your reading pleasure:
I invite you to visit my very recently launched “Podcast”, “HAVE A BABY” on RUMBLE; https://rumble.com/c/c-3304480
If you are interested in having an online consultation with me, please contact my assistant, Patti Converse at 702-533-2691 or email her at concierge@sherivf.com\
Name: Monique H
How much is Ivf treatment or is it free I’ve been looking for three 😞
I suggest you call and ask our office manager, Jessica Ortiz (866-747-6692).
Geoff Sher
____________________________________________________________________
Herewith are online links to 2 E-books recently co-authored with my partner at SFS-NY (Drew Tortoriello MD)……. for your reading pleasure:
I invite you to visit my very recently launched “Podcast”, “HAVE A BABY” on RUMBLE; https://rumble.com/c/c-3304480
If you are interested in having an online consultation with me, please contact my assistant, Patti Converse at 702-533-2691 or email her at concierge@sherivf.com\
Name: Julie R
Hi Dr. Sher,
I come from Denmark and here we can’t screen our embryos – so we transfer untested. I have had all initial testing done in August last year before starting my egg retrievals and all my tests were good – nothing out of the ordinary (AMH of 33 and great LH/FSH ratio). I am a healthy, now 40 year old. I have a living child from when I was 22, and had an ectopic pregnancy in 2021. I can get pregnant on my own – but they always result in chemical pregnancies.
I have been through 3 egg retrievals, and of those I got 3 eggs first round, 11 second and 18 third. Of the the first round no blasts, second I got four blasts and third I got four blasts. All 3-5 BB’s.
I have transferred 1 day-3 fresh in the first round. Negative
All four blasts as FETs in the second round – two chemicals and two failure to implant.
With the new round I just transferred a day-6 5BB and used embryo glue. It was a complete failure to implant. I am at my wits end! What would you suggest? Doctors have me on plaquenil and then of course progesterone and estradiol for FET.
I just feel like we are using embryos that are destined to die inside me and it feels awful.
My doctors are not doing any additional testing even though I keep suggesting that something must be wrong.
I appreciate your support!
Implantation dysfunction is often overlooked as a significant reason for IVF failure. This is especially true when IVF failure is unexplained, or when there are recurring pregnancy losses or underlying issues with the uterus, such as endo-uterine surface lesions, thin uterine lining (endometrium), or immunological factors.
IVF success rates have been improving in the past decade. Currently, in the United States, the average live birth rate per embryo transfer for women under 40 years old using their own eggs is about 2:5 per woman undergoing embryo transfer. However, there is a wide range of success rates among different IVF programs, varying from 20% to almost 50%. Based on these statistics, most women in the United States need to undergo two or more IVF-embryo transfer attempts to have a baby. Many IVF practitioners in the United States attribute the differences in success rates to variations in expertise among embryology laboratories, but this is not entirely accurate. Other factors, such as differences in patient selection, the failure to develop personalized protocols for ovarian stimulation, and the neglect of infectious, anatomical, and immunological factors that affect embryo implantation, are equally important.
Approximately 80% of IVF failures occur due to “embryo incompetency,” mainly caused by ( irregularities in chromosome number (aneuploidy), which is often related to the advancing age of the woman, diminished ovarian reserve ( DOR) but can also be influenced by the ovarian stimulation protocol chosen, and sperm dysfunction (male infertility). However, in around 20% of cases with dysfunction, failure is caused by problems with embryo implantation.
This section will focus on embryo implantation dysfunction and IVF failure which in the vast majority of cases is caused by:
When there are problems with the structure of the uterus, it can lead to difficulties in getting pregnant. While uterine fibroids usually don’t cause infertility, they can affect fertility when they distort the uterine cavity or protrude through the lining. Even small fibroids located just beneath the lining and protruding into the cavity can decrease the chances of the embryo attaching. Multiple fibroids within the uterine wall that encroach upon the cavity can disrupt blood flow, impair estrogen delivery, and prevent proper thickening of the lining. These issues can be identified through ultrasound during the menstrual cycle’s proliferative phase. Any lesion on the uterine surface, such as submucous fibroids, adhesions, endometrial polyps, or placental polyps, can interfere with implantation by causing a local inflammatory response similar to the effect of an intrauterine contraceptive device (IUD).
Clearly, even small uterine lesions can have a negative impact on implantation. Considering the high costs and emotional toll associated with in vitro fertilization (IVF) and related procedures, it is reasonable to perform diagnostic tests like hysterosalpingography (HSG), fluid ultrasound examination (hysterosonogram), or hysteroscopy before starting IVF. Uterine lesions that can affect implantation often require surgical intervention. In most cases, procedures like dilatation and curettage (D&C) or hysteroscopic resection are sufficient. Rarely a laparotomy may be needed. Such interventions often lead to an improvement in the response of the uterine lining.
Hysterosonogram( HSN/saline ultrasound) is a procedure where a sterile saline solution is injected into the uterus through the cervix using a catheter. Vaginal ultrasound is then used to examine the fluid-filled cavity for any irregularities that might indicate surface lesions like polyps, fibroid tumors, scarring, or a septum. When performed by an expert, HSN is highly effective in detecting even the smallest lesions and can supplant hysteroscopy in certain cases. HSN is less expensive, less invasive/traumatic, and equally effective as hysteroscopy. The only drawback is that if a lesion is found, hysteroscopy may still be needed for treatment.
Hysteroscopy is a diagnostic procedure performed in an office setting with minimal discomfort to the patient. It involves inserting a thin, lighted instrument called a hysteroscope through the vagina and cervix into the uterus to examine the uterine cavity. Normal saline is used to distend the uterus during the procedure. Like HSN, hysteroscopy allows for direct visualization of the inside of the uterus to identify defects that could interfere with implantation. We have observed that around one in eight IVF candidates have lesions that need attention before undergoing IVF to optimize the chances of success. I strongly recommend that all patients undergo therapeutic surgery, usually hysteroscopy, to correct any identified issues before proceeding with IVF. Depending on the severity and nature of the problem, hysteroscopy may require general anesthesia and should be performed in a surgical facility equipped for laparotomy if necessary.
As far back as In 1989, I and my team made an important discovery about using ultrasound to assess the thickness of the endometrium during the late proliferative phase of both “ natural” and hormone-stimulated cycles. The assessment helped predict the chances of conception. We found that an ideal thickness of over 9mm at the time of ovulation , egg retrieval or with the commencement of progesterone therapy in embryo recipient cycles ( e.g., IVF with egg donation, gestational, surrogacy and embryo adoption) was associated with optimal implantation rates, while an endometrial thickness of less than 8 mm was associated with failure to implant or early pregnancy loss in the vast majority of cases. An endometrium measuring <8mm was almost invariably associated with failure to implant or early pregnancy loss in the while an endometrium measuring 8 to 9 mm was regarded as being intermediate, and while pregnancies did occur in this range, the rates were only slightly lower than with an optimal lining of 9 mm
A “poor” uterine lining typically occurs when the innermost layer of the endometrium (basal or germinal endometrium) is unable to respond to estrogen by developing a thick enough outer “functional” layer to support successful embryo implantation and placental development. The “functional” layer, which accounts for two-thirds of the total endometrial thickness, is shed during menstruation if pregnancy does not occur.
The main causes of a poor uterine lining are:
In 1996 I introduced the Vaginal administration of Sildenafil (Viagra) to improve endometrial thickening. The selective administration of Sildenafil has shown great promise in improving uterine blood flow and increasing endometrial thickening in cases of thin endometrial linings. When administered vaginally, it is quickly absorbed and reaches high concentrations in the uterine blood system, diluting as it enters the systemic circulation. This method has been found to have minimal systemic side effects. However, it is important to note that Viagra may not be effective in all cases, as some cases of thin uterine linings may involve permanent damage to the basal endometrium, rendering it unresponsive to estrogen.
Severe endometrial damage leading to poor responsiveness to estrogen can occur in various situations. These include post-pregnancy endometritis (inflammation after childbirth), chronic granulomatous inflammation caused by uterine tuberculosis (rare in the United States), and significant surgical injury to the basal endometrium (which can happen after aggressive D&C procedures).
There is a growing recognition that problems with the immune function in the uterus can lead to embryo implantation dysfunction. The failure of proper immunologic interaction during implantation has been implicated as a cause of recurrent miscarriage, late pregnancy fetal loss, IVF failure, and infertility. Some immunologic factors that may contribute to these issues include antiphospholipid antibodies (APA), antithyroid antibodies (ATA) , and activated natural killer cells (NKa).
During ovulation and early pregnancy, the uterine lining is frequented by NK cells and T-cells, which together make up more than 80% of the immune cells in the uterine lining. These cells travel from the bone marrow to the endometrium where they proliferate under hormonal regulation. When exposed to progesterone, they produce TH-1 and TH-2 cytokines. TH-2 cytokines help the trophoblast (embryo’s “root system”) to penetrate the uterine lining, while TH-1 cytokines induce apoptosis (cell suicide), limiting placental development to the inner part of the uterus. The balance between TH1 and TH-2 cytokines is crucial for optimal placental development. NK cells and T-cells contribute to cytokine production. Excessive TH-1 cytokine production is harmful to the trophoblast and endometrial cells, leading to programmed cell death and ultimately to implantation failure. Functional NK cells reach their highest concentration in the endometrium around 6-7days after ovulation or exposure to progesterone, which coincides with the time of embryo implantation. It’s important to note that measuring the concentration of blood NK cells doesn’t reflect NK cell activation (NKa). The activation of NK cells is what matters. In certain conditions like endometriosis, the blood concentration of NK cells may be below normal, but NK cell activation is significantly increased.
There are several laboratory methods to assess NK cell activation (cytotoxicity), including immunohistochemical assessment of uterine NK cells and measuring TH-1 cytokines in the uterus or blood. However, the K-562 target cell blood test remains the gold standard. In this test, NK cells isolated from a woman’s blood are incubated with specific “target cells,” and the percentage of killed target cells is quantified. More than 12% killing indicates a level of NK cell activation that usually requires treatment. Currently, there are only a few Reproductive Immunology Reference Laboratories in the USA capable of reliably performing the K-562 target cell test.
There is a common misconception that adding IL (intralipid) or Intravenous gammaglobulin (IVIg) to NK cells can immediately downregulate NK cell activity. However, neither IL and IVIg cannot significantly suppress already activated NK cells. They are believed to work by regulating NK cell progenitors, which then produce downregulated NK cells. To assess the therapeutic effect, IL/IVIg infusion should be done about 14 days before embryos are transferred to the uterus to ensure a sufficient number of normal functional NK cells are present at the implantation site during embryo transfer. Failure to recognize this reality has led to the erroneous demand from IVF doctors for Reproductive Immunology Reference Laboratories to report on NK cell activity before and immediately after exposure to IVIg or IL at different concentrations. However, since already activated NK cells cannot be deactivated in the laboratory, assessing NKa suppression in this way has little clinical benefit. Even if blood is drawn 10-14 days after IL/IVIg treatment, it would take another 10-14 days to receive the results, which would be too late to be practically advantageous.
Many women who struggle with IVF failure or recurrent pregnancy loss, as well as those with a personal or family history of autoimmune diseases like lupus erythematosus, rheumatoid arthritis, scleroderma, and dermatomyositis, often test positive for antiphospholipid antibodies (APAs). Over 30 years ago, I proposed a treatment for women with positive APA tests. This involved using a low dose of heparin to improve the success of IVF implantation and increase birth rates. Research indicated that heparin could prevent APAs from affecting the embryo’s “root system” ( the trophoblast), thus enhancing implantation. We later discovered that this therapy only benefits women whose APAs target specific phospholipids (phosphatidylethanolamine and phosphatidylserine). Nowadays, longer-acting low molecular weight heparinoids like Lovenox and Clexane have replaced heparin.
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 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.
Almost 50% of women with antithyroid antibodies do not have activated cytotoxic T lymphocytes (CTL) or natural killer cells (NK cells). This suggests that the antibodies themselves may not be the direct cause of reproductive dysfunction. Instead, the activation of CTL and NK cells, which occurs in about half of the cases with thyroid autoimmunity (TAI), is likely an accompanying phenomenon that damages the early “root system” (trophoblast) of the embryo during implantation.
Treating women who have both antithyroid antibodies and activated NK cells/CTL with intralipid (IL) and steroids improves their chances of successful reproduction. However, women with antithyroid antibodies who do not have activated NK cells/CTL do not require this treatment.
Types of Immunologic Implantation Dysfunction (IID) and NK Cell Activation:
Like the genes for eye color, DQ alpha/HLA gene combinations differ between people. Thus, the male (whose sperm created an embryo is likely to have different DQ alpha/HLA gene combinations than the potential mother . However, there are rare situations in which the male and the female partners have DQ-alpha/HLA gene combinations are the same.
The endometrial immune system is programmed to accept embryos with different DQ alpha/HLA gene combinations than its own. This is known as “alloimmune recognition.” So, if the man shares a similar DQ alpha/HLA gene combination with the woman, and his sperm creates an embryo that tries to implant , her endometrial immune system will see the embryo’s DQ alpha/HLA gene as “too similar” to its own and assume it is a foreign body.
Usually, this will lead to NK/T cell activation, the overproduction of TH-1 cytokines, and reproductive failure (i.e., infertility, and pregnancy loss). The severity with which this occurs is an important determinant of whether total implantation failure will occur or whether there would remain enough residual trophoblastic activity that would allow the pregnancy to limp along until the nutritional supply can no longer meet the demands of the pregnancy, at which point pregnancy loss occurs.
In cases of paternal-maternal DQ alpha/HLA matching, it will often take several pregnancies for NK cell activation to build to the point that women with alloimmune implantation dysfunction will present with clinical evidence of implantation dysfunction. Sometimes it starts off with one or two live births, whereupon NK/T cell activity starts to build, leading to one or more early miscarriages. Eventually the NK/T cell activation is so high that subsequent pregnancies can be lost before the woman is even aware that she was pregnant at all. At this point, she is often diagnosed with secondary, “unexplained” infertility and/or “unexplained” IVF failure.
Alloimmune Implantation Dysfunction is diagnosed by testing the blood of both the male and female partners for matching DQ alpha genes and NK/T cell activation.
There are two types of DQ alpha/HLA genetic matching:
It should be emphasized that poor embryo quality is not always the main cause of reproductive dysfunction and that the complex interaction between embryonic cells and the lining of the uterus plays a critical role in successful implantation. Women with personal or family histories of autoimmune disease or endometriosis and those with unexplained (often repeated) IVF failure or recurrent pregnancy loss, often have immunologic implantation dysfunction (IID as the underlying cause . For such women, it is important to understand how IID leads to reproductive failure and how selective treatment options such as intralipid (IL), corticosteroid and heparinoid therapy, can dramatically improve reproductive outcomes. Finally, there is real hope that proper identification and management of IID can significantly improve the chance of successful reproduction and ultimately contribute to better quality of life after birth.
_____________________________________________________________________________________________
PLEASE SHARE THIS WITH OTHERS AND HELP SPREAD THE WORD!!
Herewith are online links to 2 E-books recently co-authored with my partner at SFS-NY (Drew Tortoriello MD)……. for your reading pleasure:
I invite you to visit my very recently launched “Podcast”, “HAVE A BABY” on RUMBLE; https://rumble.com/c/c-3304480
If you are interested in having an online consultation with me, please contact my assistant, Patti Converse at 702-533-2691 or email her at concierge@sherivf.com\
Name: Nathan K
Do you help a women get pregnant with twin babies if she’s 29 years old?
There is no guarantee that if you transfer >1 embryo you will get a multiple pregnancy. I suggest you call Patti Converse (my assistant) and set up an online consultation with me to discuss.
Geoff Sher
___________________________________________________________________________________________________________
PLEASE SHARE THIS WITH OTHERS AND HELP SPREAD THE WORD!!
Herewith are online links to 2 E-books recently co-authored with my partner at SFS-NY (Drew Tortoriello MD)……. for your reading pleasure:
I invite you to visit my very recently launched “Podcast”, “HAVE A BABY” on RUMBLE; https://rumble.com/c/c-3304480
If you are interested in having an online consultation with me, please contact my assistant, Patti Converse at 702-533-2691 or email her at concierge@sherivf.com\
Name: Alex B
Dear Dr. Sher,
We have only one embrio with following NGS data:
seq[GRCh37] (20p13p11.21)x1[0.27],(X,Y)x1
Would you please tell, how much are the risks in the case of transfer?
Thank you
In my opinion, it is worth transferring BUT …if/once pregnant, you should do a CVS or amniocentesis to assess the pregnancy.
Two decades ago, a groundbreaking technique emerged: full embryo karyotyping through preimplantation genetic sampling (PGS)/preimplantation genetic testing for aneuploidy (PGT-A). This method revolutionized the field by allowing us to identify and characterize an embryo’s karyotype, enabling the selective transfer of euploid embryos (those with a complete set of 46 chromosome! into the uterus. This innovation led to a remarkable increase in implantation and birth rates, coupled with a significant reduction in early pregnancy losses following in vitro fertilization (IVF). Today, PGS/PGT-A is a standard practice worldwide.
However, this advancement presents a moral and ethical dilemma. Many IVF programs require patients to consent to the disposal of all aneuploid embryos—those with irregular chromosome quotas. Recent evidence has raised questions about whether some aneuploid embryos, when transferred, can “autocorrect” during development, potentially resulting in healthy babies. This dilemma forces us to reconsider our approach to discarding embryos.
The crux of this embryo “autocorrection” lies in the fact that many embryos labeled as aneuploid through PGS/PGT-A also contain chromosomally normal (euploid) cells. This coexistence of aneuploid and euploid cells within the same embryo is known as “mosaicism.”
In response to this complexity, more IVF practitioners are opting to cryobank certain PGS/PGT-A-identified aneuploid embryos, preserving the option for future transfer. To make informed decisions in such cases, it’s crucial to understand the two types of embryo aneuploidy:
Meiotic aneuploidy: This results from chromosomal numerical abnormalities originating in the egg or sperm during preconceptual maturational division (meiosis). Meiotic aneuploidy is permanent, affecting all subsequent embryo cells and often leading to implantation failure, early pregnancy loss, or chromosomal birth defects.
2. Mitotic aneuploidy (Mosaicism): This occurs when some cells of a meiotically normal early embryo, in the process of cell replication (mitosis), mutate and become aneuploid after fertilization. The outcome depends on whether aneuploid or euploid cells predominate. Mosaic embryos with more euploid cells are likely to undergo autocorrection once arriving in the uterus, leading to the propagation of chromosomally normal and healthy pregnancies.
Differentiating between these two types of aneuploidy is crucial, and next-generation gene sequencing (NGS) has significantly improved the accuracy of full embryo karyotyping, aiding in the diagnosis of mosaicism.
Several factors influence the autocorrection potential of mosaic embryos, including the stage of embryo development at diagnosis, affected chromosomes, the complexity of aneuploidy, and the percentage of aneuploid cells. Embryos diagnosed as “mosaic” at earlier stages may autocorrect as they develop into blastocysts. Segmental mosaic aneuploidies and lower percentages of mitotically aneuploid cells in the blastocyst increase the chances of autocorrection.
Transferring embryos with autosomal meiotic trisomy often results in implantation failure, miscarriage, or the birth of a defective child. In contrast, autosomal mitotic trisomies, which can autocorrect, require careful consideration. Patients are advised to undergo prenatal genetic testing and be prepared to make difficult decisions if necessary.
When dealing with meiotic autosomal monosomy, the chances of a viable pregnancy are minimal, with those that do implant often ending in early spontaneous miscarriage. However, mosaic autosomal monosomic embryos can often autocorrect, making them a viable option for transfer. Nevertheless, full disclosure to patients and a commitment to prenatal genetic testing are essential in such cases.
When we biopsy an embryo for PGS/PGT-A, we test only a few cells, typically around six. If at least one of these cells is healthy (euploid) while the others are not (aneuploid), it’s called a “mosaic” embryo, and is potentially capable of self-correcting in the womb and leading to a healthy baby. On the other hand, if all the tested cells are aneuploid, it’s highly likely that the rest of the untested cells in the embryo are also abnormal, making it an unsalvageable, meiotically aneuploid embryo. However, we can’t be certain because we haven’t tested all the cells. So, even if we diagnose an embryo as aneuploid, in a few cases, it might still be mosaic and have a chance to develop normally in the uterus.
In summary, while we can confidently diagnose euploid embryos, diagnosing mosaic embryos is currently not perfect, and there’s a possibility that some may have the potential to develop into healthy babies. Embryo mosaicism adds complexity to the world of IVF, forcing us to navigate a delicate balance between minimizing risks and providing opportunities for patients to have healthy babies. The evolution of diagnostic techniques like NGS has brought us closer to understanding and harnessing the potential of mosaic embryos, but the journey remains intricate and ethically charged.
_______________________________________________________
Herewith are online links to 2 E-books recently co-authored with my partner at SFS-NY (Drew Tortoriello MD)……. for your reading pleasure:
I invite you to visit my very recently launched “Podcast”, “HAVE A BABY” on RUMBLE; https://rumble.com/c/c-3304480
If you are interested in having an online consultation with me, please contact my assistant, Patti Converse at 702-533-2691 or email her at concierge@sherivf.com\
