Ask Our Doctors – Archive
Our Medical Directors are outstanding physicians that you will find to be very personable and compassionate, who take care to ensure that you have the most cutting-edge fertility treatments at your disposal. This is your outlet to ask your questions to the doctors.
Hi Dr. Sher,
I am a 36 year old woman diagnosed with DOR. I am currently going through my 4th IVF and I think this is the last one.
First IVF we did an antagonist protocol (450 folistim, 150 menopur, ganirelix with BCP before AF). We ended up with 6 follicles, 5 eggs, 2 fertilized and transferred day 3, chemical pregnancy.
Second IVF, BCP, estrogen primimng and lupron protocol (10 lupron twice a day, 450 folistim, 150 menopur). We ended up with 4 follicles,3 eggs and 1 fetilized, BFN.
Third one estrogen priming, no BCP, antagonist (450 folistim, 150 menopur, ganirelix ) and clomid. 9 follicles, 3 eggs (1 immature), none fertilized.
My 4th IVF was testosterone priming, estadriol, testosterone patches for 2 weeks, and progesterone before AF. After AF, clomid, lupron 10 twice a day, 450 folistim, 150 menopur. After 5 days of stims I have 3 follicles, 2 of 17 mm and one 14, and another one that is not measurable. Due to my history, I am pretty sure it won’t be successful.
I am not sure if it’s worth trying anything else. Considering the low number of eggs I produce I was thinking of a mini IVF, but I guess my eggs are almost all bad, so that won’t help. I read a study about testosterone priming, where best results were obtained when testosterone was applied for 4 weeks, while I only did 2. But not sure if that would help. Any advice for me? Or I just should think about donor eggs?
Hi Dr. Sher. We did PGS on all embryos. 6 came back normal. We have 3 girls and 3 boys. We are afraid of autism but still would love a baby boy. Are there any correlations between IVF and autism? Is there any literature on this? What do you think about male embryo grading and autism? We just don’t know. Ideally, we’d love to transfer 1 male and 1 female. Thoughts? So torn. Thank you.
Autism Spectrum Disorder (ASD) encompasses a range of conditions that most commonly affect males and are characterized by lifelong neurodevelopmental derangements manifesting as deficiencies in social interaction, verbal and nonverbal communication, and dysfunctional interests and behavioral pattern that range from social isolation, delayed speech, and repetitious movement, to Asperger’s syndrome, characterized by higher levels of cognition and social behavior.
Over a period of less than 2 decades, the incidence of diagnosed (ASD) has increased from about 1:1000 to more than 1:100. And the incidence continues to increase year by year. In fact, according to the most recent Centers for Disease Control and Prevention estimates, 1 in 68 children in the United States has ASD. This represents a significant increase from the prior estimate of 1:88, in released in 2012. The question arises as to whether this dramatic change is due increased awareness of the condition leading to over-testing and over-diagnosis and/or whether it represents a true epidemiologic phenomenon. Regardless, it is an undeniable fact that we who are actively involved in medically promoting reproduction are commonly confronted by prospective parents who are concerned that their age and reproductive performance could be associated with an increased risk that their offspring could be affected by ASD….
The relationship between infertility treatments and ASD remain a subject of heated debate. Factors such as the effects of fertility medications, fertility procedures performed, a relationship to the cause of the infertility, maternal obesity (BMI), maternal and paternal age, genetics and hormonal factors linked to fetal testosterone have all cited as possible contributing factors to the occurrence of ASD in patients seeking infertility treatment. Of interest is the emergence of evidence to suggest a possible etiologic role of the immune system in ASD. This having been said, it is as yet not possible to establish a clear relationship between infertility, its treatments, and ASD. Infertility diagnoses and treatments.
The question arises as to how/whether IVF itself increases the risk of ASD in the offspring. A relatively recent large study analyzed the birth records of 2.5 million children born in Sweden between 1982 and 2007, and after correcting for confounding variables, found there to be a very small increase in the incidence risk of intellectual impairment in the resulting children (about 4% of IVF children had physical or mental problems at birth compared with 3% of those conceived A naturally) but no link between in vitro fertilization (IVF) and ASD. This having been said, the study was somewhat flawed in the fact that the IVF births reported dated back more than 30 years when IVF technology was still in its infancy. Overall, the main message was a positive and reassuring one for patients undergoing IVF treatment
Here are a few relatively established facts regarding the occurrence of ASD.
1.Gender: ASD is more common in male offspring.
2.Obstetrical History: ASD is more common in first born babies, in multiple births, in premature and small-for-gestational-age babies, following intrauterine bleeding and fetal distress, as well as following birth asphyxia or trauma
3.Age
1.The mother’s age: The incidence of ASD increases with advancing age of the mother In fact, women over age 40Y are 51% more likely than women aged 25-29 to have a child with ASD.
2.The father’s age: Traditionally, the negative effects of the advancing “biological clock” on reproduction have been linked to women, while the question of the effect of the man’s advancing age has been largely ignored. But now, a recent study published in the magazine Nature suggests that the risk of ASD (and perhaps schizophrenia too) increases as the age of the father progresses. When the man siring the child is under 35 years of age, the risk of ASD is about 1:100, while when the man is over 50, the incidence doubles to 1:50. Consider the fact that about 1:88 children born develop ASD.
Several recent studies have shown that certain genetic mutations implicated in ASD are four times more likely to originate in the sperm than in the egg. This is probably explained by the fact that unlike women, who are born with a lifelong component of eggs, a man’s sperm are in a constant state of being generated. During the process of sperm generation, dividing precursor cells are easily susceptible to acquiring new mutations with each successive division. The finding that conditions such as ASD (and schizophrenia) can be influenced by a man’s age is likely to change the reproductive conversation, pushing it more into the mainstream. It is about time that men start to realize that it is not only women that should be worried about unduly putting off parenting. Hopefully, it will also prompt physicians to recommend to their married male patients that they begin considering their “reproductive options” sooner rather than later and that the topic be taught in medical school.
1.Genetics/Epigenetics: With identical twins, when one has ASD, the other is about 90% likely to also be so affected. In non-identical twins, the concordance rate is twenty times lower. This points strongly to a genetic link. There is new evidence that defects in epigenetic regulatory genes and in certain gene regions on chromosomes likely play a role in the development of autism. About 10% of ASD cases have definite links to genetic disorders such as Fragile X, neurofibromatosis and tuberous sclerosis which can often (although not easily) be detected through meticulous parental clinical history taking and can be diagnosed pre- and postnatal using genetic testing, ultrasound examination and by sophisticated chromosomal and DNA testing.
2.Predicting/Diagnosing ASD: It is as yet not possible to diagnose ASD through preimplantation genetic diagnosis (PGD) or through prenatal testing. Unfortunately, only a few specific gene mutations known to be linked to autism have, as yet, been identified. But this could all change in the next few years with the rapid advancement in genetic research. Recent reports have emerged of a newly found ability to isolate fetal cells from the mother’s blood, even early in pregnancy. Once sophisticated genetic testing for specific mutations evolves, it is likely that it will become possible to draw blood from the pregnant woman, isolate fetal cells, and thereby gain access to the entire fetal genome for genetic testing.
3.Preventing ASD: The risk of ASD in the offspring can sometimes be reduced by the taking of folic acid supplements (4-6mg daily) for several months prior to conception. This is especially true in cases where the mother has a form of thrombophilia (a hereditary clotting disorder) associated with MTHFR pleomorphic (most particularly those associated with the C677T variant) where such pre-conceptual folic acid supplementation could be especially beneficial.
Good luck!
Geoff Sher
Dr. Sher, I have done ivf and it did not work. I had 5 good quality eggs. 3 died will defrosting and the other 2 that were put in did not result in a pregnancy. I am now doing iui again with Letrozole. I had 1- 2.0 2- 1.5 and 1- 1.3 follicles on FRiday at 9:00am. My blood work was progesteron .45 and TSH 1.6 and Estrogen 71.5. They said I can afford to wait and do the trigger the next day which is Saturday night. Then they scheduled my iui on Sunday which is barely 12 hours later. I didn’t go because I do not think waiting 12 hours to do the iui would be successful. I would think waiting 36 hours would be better. My question is did we wait too late to do the trigger? Shouldn’t we have waited until 36-42 hours to do the trigger. Instead I am doing timed intercourse and waiting 42 hours after trigger where the egg is released. Do you recommend this? My husband has morphology and motility issues and I am 38 years old with a good amh at 7.39. I have completed IVF, I have tried so many iuis and I have tried clomid and letrozole. I have mild stage 2 endometriosis and I did a laproscopy. I have had 4 polyp removed from my uterus (month of ivf treatment). I do not have any children or have ever got pregnant, except once which my beta was an 8. Can you please help me and let me know if maybe an ivf at your clinic would work for me and please let me know if iui timing and trigger was incorrect.
It could have been a day late for the trigger, but hopefully not. More importantly, it needs to be determined why all prior attempts (including IVF) have failed. You could have an undiagnosed implantation dysfunction since 1/3 of women who have endometriosis, regardless of its severity will have an immunologic implantation dysfunction linked to uterine natural killer cell activation (NKa) and/or antiphospholipid antibodies.
More than half of women who have endometriosis harbor antiphospholipid antibodies (APA) that can compromise development of the embryo’s root system (trophoblast). In addition and far more serious, is the fact that in about one third of cases endometriosis, regardless of its severity is associated with NKa and cytotoxic uterine lymphocytes (CTL) which can seriously jeopardize implantation. This immunologic implantation dysfunction (IID) is diagnosed by testing the woman’s blood for APA, for NKa (using the K-562 target cell test or by endometrial biopsy for cytokine activity) and, for CTL (by a blood immunophenotype). Activated NK cells attack the invading trophoblast cells (developing “root system” of the embryo/early conceptus) as soon as it tries to gain attachment to the uterine wall. In most cases, this results in rejection of the embryo even before the pregnancy is diagnosed and sometimes, in a chemical pregnancy or an early miscarriage. As such, many women with endometriosis, rather than being infertile, in the strict sense of the word, often actually experience repeated undetected “mini-miscarriages”.
Women who harbor APA’s often experience improved IVF birth rates when heparinoids (Clexane/Lovenox) are administered from the onset of ovarian stimulation with gonadotropins until the 10th week of pregnancy. NKa is treated with a combination of Intralipid (IL) and steroid therapy: Intralipid (IL) is a solution of small lipid droplets suspended in water. When administered intravenously, IL provides essential fatty acids, linoleic acid (LA), an omega-6 fatty acid, alpha-linolenic acid (ALA), an omega-3 fatty acid.IL is made up of 20% soybean oil/fatty acids (comprising linoleic acid, oleic acid, palmitic acid, linolenic acid and stearic acid) , 1.2% egg yolk phospholipids (1.2%), glycerin (2.25%) and water (76.5%).IL exerts a modulating effect on certain immune cellular mechanisms largely by down-regulating NKa.
The therapeutic effect of IL/steroid therapy is likely due to an ability to suppress pro-inflammatory cellular (Type-1) cytokines such as interferon gamma and TNF-alpha. IL/steroids down-regulates NKa within 2-3 weeks of treatment the vast majority of women experiencing immunologic implantation dysfunction. In this regard IL is just as effective as Intravenous Gamma globulin (IVIg) but at a fraction of the cost and with a far lower incidence of side-effects. Its effect lasts for 4-9 weeks when administered in early pregnancy.
The toxic pelvic environment caused by endometriosis, profoundly reduces natural fertilization potential. As a result normally ovulating infertile women with endometriosis and patent Fallopian tubes are much less likely to conceive naturally, or by using fertility agents alone (with or without intrauterine (IUI) insemination. The only effective way to bypass this adverse pelvic environment is through IVF. I am not suggesting here that all women who have endometriosis require IVF! Rather, I am saying that in cases where the condition is further compromised by an IID associated with NKa and/or for older women(over 35y) who have diminished ovarian reserve (DOR) where time is of the essence, it is my opinion that IVF is the treatment of choice.
Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
1.Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
2.Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3.The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
4.Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
a.A“ thin uterine lining”
b.A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c.Immunologic implantation dysfunction (IID)
d.Endocrine/molecular endometrial receptivity issues
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•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
. Endometriosis and Infertility
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Dr Sher,
Do you recommend steroids/dexamethasone on all FET? What about baby aspirin? Trying to figure out a different course of action for this next cycle. Many thanks.
I prescribe dexamethasone…but not aspirin.
Geoff Sher
Hello Dr.
Im 40 and my youngest is 2. I conceived her with no difficulties. Since trying this last Sept I’ve had 2 chemical pregnancies. I just had CD3 testing and my results were…
AMH 1.05ng
FSH 7.3 ng
LH 5.0 ng
Estrogen 106 ng
TSH 1.450
My Dr. is doing a saline scan on CD9 and check my natural follies and look for any lining issues then give progesterone for 3dpo. Next cycle he mentioned giving Clomid or Femera a try. Now that my CD3 results are back do you feel the protocol will be the same? Are my results good enough to conceive narurally?
Thank you!
Your AMH suggests a degree of DOR . This + your age (your advanced biological clock) is in my opinion a relative contraindication to the use of clomiphene for two reasons: 1) the success rate at 40Y with clomiphene (with or without IUI) is very low (about 1:30 per cycle of treatment) and, 2) your diminished AMH indicates that you could be running low on eggs and thus do not have time to waste, if you are very serious about having a baby. You need IVF with embryo banking and PGS.
The older a woman becomes, the more likely it is that her eggs will be chromosomally/genetically “incompetent” (not have the potential upon being fertilized and transferred, to result in a viable pregnancy). That is why, the likelihood of failure to conceive, miscarrying and of giving birth to a chromosomally defective child (e.g. with Down Syndrome) increases with the woman’s advancing age. In addition, as women age beyond 35Y there is commonly a progressive diminution in the number of eggs left in the ovaries, i.e. diminished ovarian reserve (DOR). So it is that older women as well as those who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.
While it is presently not possible by any means, to reverse the age-related effect on the woman’s “biological clock, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can 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 older women and those 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 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, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist 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
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:
Email: Julied@sherivf.com
OR
Phone: 702-533-2691
800-780-7437
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.