Ask Our Doctors – Archive
Our Medical Directors are outstanding physicians that you will find to be very personable and compassionate, who take care to ensure that you have the most cutting-edge fertility treatments at your disposal. This is your outlet to ask your questions to the doctors.
Hello Dr Sher,
I am a 36 yr old who is currently preparing to do an FET of a PGS tested embryo.
I stopped the bcp on 17th and still on 20 units of lupron. On 19th for suppression check the P4 levels were 1.36. Estrogen was 45. My clinic told me that I was good to go and start the estrogen from today (21st). I wasn’t too sure whether my progesterone levels were low enough, so I checked with my Dr and he said the levels are okay but if I want I can do a repeat test today. So I got the p4 levels tested again today (21st) and it seemed to gone up I.e 1.54. Now, I am being told to not start the estrogen, continue on lupron 20 units and return for blood draw on 25th.
I am wondering if I have been unnecessary paranoid in getting these levels re-checked. ? Does 4 levels at baseline are important to be lower than 1 ?
I have been thro fet cycles in the past and at baseline the levels have been lower than 1. I have not had a successful pregnancy so far due to miscarriages (trisomy), so I have gone thro batching , PGS now to ensure I have viable embryo. That is the reason I am getting super fussy with all these #s.
Is it a cause of concern the p4 levels have gone up without starting meds? Is the P4 level of 1.5 at suppression not the ideal level to start correct?
Thanks for your time. Hoping to hear back from you.
Personally, his would not worry or deter me from starting the cycle, but you need to follow the advice of your own doctor here.
Good luck!
Good luck and G-d bless!
Geoff Sher
Hi Dr. Sher ,
I know you beleive that pgs testing should be done on day 3 vs. day 5 blastocyst .
When doing the biopsy on day 3 embryo is it true this is bad for the embryo because it only has 8 cells ?
A lot of these fertility centers are under the school of thought that it can be detrimental to pgs on day 3 vs day 5 when there is 100 cells or more?
I fully recognize that many RE’s will not agree with my position that it is preferable to perform Preimplantation Genetic Sampling (PGS ) biopsies on blastocysts than on day 3 cleaved embryos. In my opinion this is erroneous and here is why:
For Preimplantation Genetic Sampling (PGS) using array CGH (aCGH) to be reliable and accurate, it requires access to more DNA than is available from a single cell biopsied from a day 3 embryo or from the 1st polar body of an egg. Presently, accurate PGS using single cell (blastomeres) is best performed using Next Generation Gene Sequencing (NGS). Biopsying a multicellular (>100cells) blastocysts by allowing aces to several cells at a time, provides much safe access to much more DNA than when a single cell (blastomere) is extracted from a 5-10 cell day 3 embryo. This serves to explain why those that champion PGS/ aCGH, favor blastocyst biopsies over day 3 biopsies, but does doing this enhance the reliability of PGS. I suggest not…
Consider the fact most numerical chromosomal aberrations (aneuploidy) in day 3 embryos originate during maturational division (meiosis) in the egg and that many such meiotically aneuploid embryos never survive to the blastocyst stage. Embryos affected by meiotic aneuploidy are permanently “incompetent”. They cannot recover. In contrast, much aneuploidy detected in the hypercellular blastocyst, originates during post-fertilization cell replication (mitosis). In the latter situation, some blastocyst cells are aneuploid while others are chromosomally normal (i.e. mosaicism). While mitotic aneuploidy can reverse (autocorrect) with such embryos developing into chromosomally normal concepti. In contrast, as stated, meiotic aneuploidy is irreversible. Since it is presently not possible to reliably differentiate between mitotic and meiotic aneuploidy, it follows that in the process of discarding aneuploid blastocyst we could well (albeit unintentional) be destroying potentially normal concepti.
Since events that occur during meiosis in the final maturation of the egg inevitably lead to “irreversible” egg/embryo “incompetence”, it is meiotic aneuploidy that needs to be identified. It follows that the closer to egg retrieval that we perform PGS/biopsies, the greater will be the likelihood that detected aneuploidy detected will be meiotic in origin. It is another e reason why I believe that day 3 PBS embryo biopsy is preferable to blastocyst biopsy.
Finally, we recently observed that a blastocyst which is ultrarapidly frozen ( vitrified) immediately following biopsy for PGS , will have reduced viability as compared to cleaved embryos biopsied on day 3 and are then allowed to recover for a few days before being vitrified.
Geoff Sher
PH: 702-699-7437
Dear Dr Sher
Can an underactivate thyroid impact fertility? If so can this be the actual underlying cause in your experience when dealing with unexplained infertility? Thanks.
Absolutely it can…not because of low thyroid hormones but because in women, one of the commonest causes of an underactive thyroid is autoimmune disease.
Between 2% and 5% of women of the childbearing age have reduced thyroid hormone activity (hypothyroidism). Women with hypothyroidism often manifest with reproductive failure i.e. infertility, unexplained (often repeated) IVF failure, or recurrent pregnancy loss (RPL). The condition is 5-10 times more common in women than in men. In most cases hypothyroidism is caused by damage to the thyroid gland resulting from of thyroid autoimmunity (Hashimoto’s disease) caused by damage done to the thyroid gland by antithyroglobulin and antimicrosomal auto-antibodies.
The increased prevalence of hypothyroidism and thyroid autoimmunity (TAI) in women is likely the result of a combination of genetic factors, estrogen-related effects and chromosome X abnormalities. This having been said, there is significantly increased incidence of thyroid antibodies in non-pregnant women with a history of infertility and recurrent pregnancy loss and thyroid antibodies can be present asymptomatically in women without them manifesting with overt clinical or endocrinologic evidence of thyroid disease. In addition, these antibodies may persist in women who have suffered from hyper- or hypothyroidism even after normalization of their thyroid function by appropriate pharmacological treatment. The manifestations of reproductive dysfunction thus seem to be linked more to the presence of thyroid autoimmunity (TAI) than to clinical existence of hypothyroidism and treatment of the latter does not routinely result in a subsequent improvement in reproductive performance.
It follows, that if antithyroid autoantibodies are associated with reproductive dysfunction they may serve as useful markers for predicting poor outcome in patients undergoing assisted reproductive technologies.
Some years back, I reported on the fact that 47% of women who harbor thyroid autoantibodies, regardless of the absence or presence of clinical hypothyroidism, have activated uterine natural killer cells (NKa) cells and cytotoxic lymphocytes (CTL) and that such women often present with reproductive dysfunction. We demonstrated that appropriate immunotherapy with IVIG or intralipid (IL) and steroids, subsequently often results in a significant improvement in reproductive performance in such cases.
The fact that almost 50% of women who harbor antithyroid antibodies do not have activated CTL/NK cells suggests that it is NOT the antithyroid antibodies themselves that cause reproductive dysfunction. The activation of CTL and NK cells that occurs in half of the cases with TAI is probably an epiphenomenon with the associated reproductive dysfunction being due to CTL/NK cell activation that damages the early “root system” (trophoblast) of the implanting embryo. We have shown that treatment of those women who have thyroid antibodies + NKa/CTL using IL/steroids, improves subsequent reproductive performance while women with thyroid antibodies who do not harbor NKa/CTL do not require or benefit from such treatment.
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
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Unexplained IVF Failure
•Why did my IVF Fail
•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
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•The Role of Nutritional Supplements in Preparing for IVF
I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.
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.
Geoff Sher
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Thank you Doctor, I had no idea of the significance of the under active thyroid. At the moment I am just on Synthroid.
We have shown that treatment of those women who have thyroid antibodies + NKa/CTL using IL/steroids, improves subsequent reproductive performance while women with thyroid antibodies who do not harbor NKa/CTL do not require or benefit from such treatment – I don’t harbour NKA activity as per tests at Reprosource labs.
Is there anything further I could be doing to combat the underactive thyroid besides synthroid?
Thank you for this important information.
Hi
I am 40 and have just done IVF flair cycle using gonalF pen but was unsuccessful. 6mths ago we done a previous conventional IVF treatment using Menpur which was unsuccessful. I have had AMH bloods done in Feb 2015 whereby the result was (8) I was prescribed DHEA in which I took for 8mths and then asked for a re-test and my bloods showed my AMH count of (16). I do have a 4 year old son, conceived using 75mg Clomipnene. Before my viable pregnancy of my son I did a conventional IVF in Dec 2010 whereby my embryos went to blastocyst and were grade 1 but unsuccessful. Since having my son and before having the recent IVF treatment I fell pregnant when my son was 1yrs old using 75mg Clomipnene but had an early bleed. Then 9mths later again I fell pregnant using 100mg Clomipnene unfortunatelt this pregnancy turned out to be ectopic. My right Fallopian tube was removed. Since then I have not fallen pregnant. Each IVF cycle (apart from Dec 2010) my eggs haven’t been good quality, arresting by day 3 or not fertilised. My last I F flair cycle using a different medication of GonalF pen I had 10 eggs collected, 6 fertilised and only 2 were on Early blastocyst and transferred back in. The rest of the embryos arrested/died. As you can imagine myself and my husband do not know which path to go down now, we have decided to try another attempt at IVF but have agreed this will be the last, due to our emotional journey and financially. Any ideas, suggestion would be greatly received. Thank you kindly for taking the time to rea our journey. Fiona
Hi again Dr Sher
Sorry, I should have mentioned in my earlier post that I was diagnosed with a mild form of PCOS hence why my Obstetrician prescribed me clomiphene. My husbands sperm has been tested again and is excellent, 68billion apparently!! I am going through your blogs and papers which are very useful to read and is giving me hope that there maybe something else that my consultant is missing in my case. I have had dye through my left Fallopian tube and it doesn’t show any blockages or damage, I have also had an Endometrial Scratch to assist with the implantation process which was recent. My medication on my recent IVF flair cycle was 225 gonalF using 0.2 buserelin. My previous short cycle of conventional ivf my medication was 325 menpur, using prendisolone / progynova. I believe to lower my immune system so my body doesn’t push our the embryo asa foreign body, that’s what we were told. However, I had to stop the prendisolone as it was giving me severe heart palpitations. 3 clinics see have been to also don’t seem to feel that killer cells testing is not relevant towards implantation, when I have asked for this they don’t seem to be concerned. I am not so sure especially reading your document on Immunologic Implantation Dysfunction? I look forward to hearing back from you, thanks kindly again for your time
Hi Fiona,
The most common reason for this type of response is in my opinion, o the protocol used for ovarian stimulation. I believe that this needs to ve carefully reviewed and perhaps revised in your case (see below). I also advise against taking DHEA. It converts to testosterone in the ovary and too much testosterone can adversely affect egg quality.
Please visit my new Blog on this very site, https://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
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• 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.
• Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• The Role of Nutritional Supplements in Preparing for IVF
I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.
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.
Geoff Sher
Hi, I had my first egg retrieval yesterday. When I left they told me they retrieved 10 eggs. I got a call this morning that only 3 were mature, of those 3, 2 fertilized with ICSI. This seems like such a low number and I’m so discouraged. This is my first IVF attempt. I have done 3 iui with clomid and another 3 with bravelle. All unsuccessful, we have been told that it is unexplained infertility but with the low number of mature eggs is that the problem? If that’s the case can anything be done ?
Hi Michelle!
In my opinion, the commonest cause for this happening relates to the protocol used for ovarian stimulation. I believe that this needs to ve carefully reviewed and perhaps revised in your case (see below).
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
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•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.
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•The Role of Nutritional Supplements in Preparing for IVF
I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.
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.
Geoff Sher