19,771 Comments

1. Denise on October 9, 2018 at 6:44 pm

   Dr. Sher,
   My FET is tomorrow and my E2 dropped from 455 at mid-cycle to 76 (day before transfer). My Progesterone is 57.
   I used letrozole twice daily for five days then my LH was 1.1 on 10/5/18 so my doctor says I was starting to ovulate on my own and didn’t need a trigger shot. I started Progesterone shots that night of my LH surge.

   Is my E2 level normal and good for a successful FET? I always thought the E2 levels were supposed to increase throughout the cycle and I am worried about the drastic drop. My doctor says this is normal for letrozole cycles?
   Thank you!

   • Dr. Geoffrey Sher on October 9, 2018 at 10:48 pm

     Respectfully, in my opinion it is most likely too low.

     Geoff Sher

2. J on October 9, 2018 at 12:18 pm

   Hello Dr. Sher,
   I have undergone 6 medicated iui’s over the last 10 months. All of them with a hcg trigger and were appropriately timed. We conceived on our 2nd iui but lost the baby to turners syndrome at 9 weeks. Hysteroscopys and tubal perfusion test all look great. Lining always 11mm.
   We have done 1 iui with follistim, others were clomid/letrozole.
   My husband has great sperm counts averaging 60 million but slightly low motility at 20% and morphology 4% .
   My dr suggests moving forward to Ivf at this point and time. I have PCOS and an amh of 13.6
   So my dr thinks to keep doing injectibles cycles for iui is not a great idea and I’m ideal candidate for Ivf
   Do u agree after 6 iui’s it is time to move forward to Ivf?
   Thankyou for your time.

   • Dr. Geoffrey Sher on October 9, 2018 at 1:35 pm

     I absolutely do agree.

     Geoff Sher

3. Anne on October 9, 2018 at 11:52 am

   Dear Sir,

   I do need your help because I am devastated

   I have just received the result of the blood test I had this morning : my second double egg transfer (2 blastocysts, 1 of poor quality) with double gamete donation failed.

   I am French and I am 40 years old. I have been struggling to achieve a pregnancy since December 2016. I experienced 11 failed IUIs with sperm donation, then I moved to IVF with double gamete donation.

   As I failed my first IVF with double egg transfer and double gamete donation, I did an ERA test. The biopsy revealed that I was late receptive (HRT cycles). So we modified the timing of my second attempt, with no result.

   When I look back, there is something I cannot explain : I gave birth to my third child in March 2015 (I conceived my daughter on my first IUI with sperm donation). I started my attempts to conceive another child in December 2016, and since then I only experienced failures. I lost my fertility in such a short period of time !

   There is another point I cannot explain : for my last FET, we had to thaw 4 blastocysts in order to find 1 competent blastocyst for transfer. Is 1/4 a common ratio among egg donors ? For a woman in her 40s, I would understand. But for a woman in her 20s who was purposely selected for the quality of her eggs, I find it a poor result.

   Since December 2016, I have been in consultation at my doctor’s every month (including ultrasound scanning each time). I have gone through two HSGs that detected no abnormalities in my uterus.

   Additionally, I gave birth to three children through IUIs. I suffer from Hashimoto’s disease with anti-TPO antibodies. I receive longlife treatment with Levothyrox (R) 100 µg per day.

   Could you help me pinpoint what is going wrong with me ?

   Thanks in advance for your reply.

   Warm regards,

   Anne Bouyssou

   • Dr. Geoffrey Sher on October 9, 2018 at 1:34 pm

     Since you have had 3 children previously (presumably with the same partner), I doubt that this is an immunologic issue although autoimmune hypothyroidism is associated with activation of natural killer cells (NKa) in about 50% of cases. Nevertheless, I would do a thorough immunologic evaluation.

     I would be very interested to know whether there is an endometrial lining issue. What was the thickness of your endometrial lining at the time of maximal estrogen preparation (just before progesterone administration). It needs to be at least 8mm (preferably >9mm). I say this because it is possible to develop clinical or subclinical endometritis (that damages the uterine lining) due to retained products of conception following any pregnancy.

     I personally do NOT have any belief or place any reliance on ERA.

     Since embryos that fail to make it to blastocyst are almost always aneuploid/incompetent, and so few of your donor’s eggs made it to blastocyst, I suspect (in spite of the youthful age of your egg donor that this might be an egg issue. I suggest PGS with your next attempt at ER.

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

     If you are interested in my advice or medical services, I urge you to contact my patient concierge, ASAP to set up a Skype or an in-person consultation with me. You can also set this up by emailing concierge@sherivf.com or by calling 702-533-2691 and/or 800-780-743. You can also enroll for a consultation with me, online at http://www.SherIVF.com.
     Also, my book, “In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com .

     Geoffrey Sher MD

4. Aud on October 9, 2018 at 9:29 am

   Hi Dr Sher
   I am 15 weeks pregnant (IVF) and found that my sneezing is getting ridiculous. Nowadays I can sneeze 30-40 times a day (violent sneezes) and sneeze 3x in a row. Previously I only sneeze in the morning and when genuinely sick.

   Is there any remedy for this.
   Is sneezing bad for baby?

   Thanks doctor.

   • Dr. Geoffrey Sher on October 9, 2018 at 1:22 pm

     I really do not have a clue. Discuss with your OB.

     Geoff Sher

5. Sam on October 9, 2018 at 1:50 am

   Dear Dr. Sher,
   As an embryologist, I never thought I would not have a chance of not having a blast at the end of my IVF cycle. In general I don’t have a good reserve, but the main reason I started my IVF cycle after 5 failed IUI was male factor. My husband total motile count varies between 2 to 7 millions per ejaculation. I started my IVF cycle with 8 follicles and Long lupron protocol. First 3 days 300 Gonal F then 225 Gonal F and 75 menopur for another 3 day and 150 goal F and 150 menopur since day 7 until day 11. My Trigger was with Ovidrel 250.
   We got 14 eggs, 8 mature, ICSI with PICSI dish (I barely had 8 sperms attached to Hyaluronan drops. 7 got fertilized but on D3 just one of them were 8 cells and the rest maily 6 cells with uneven cells. We ended up with all arrested embryos. My eggs were good quality with a smooth cytoplasm. Since not that many sperms attached to hayluronan, I am thinking it can be a sperm issue. Please advise.

   • Dr. Geoffrey Sher on October 9, 2018 at 3:07 am

     I can understand and appreciate why/how you might feel that your embryo arrested cleavage was due to a male factor, but I ask you to consider the possibility that nit might have been due to imperfect meiosis possibly attributable to the fact that 250mcg Ovidrel might be insufficient to promote optimal reproductive division. It is my firm opinion that at least 500mcg of hCGr (Ovidrel) or 10,000U hCGu (Pregnyl/Profasi/Novarel) is required to optimize reduction division and minimize the risk of egg meiotic aneuploidy.

     Ideal egg development sets the scene for optimal egg maturation that occurs 36-42h prior to ovulation or egg retrieval. Without prior optimal egg development (ovogenesis), egg maturation will be dysfunctional and most eggs will be rendered “incompetent” and unable upon fertilization to propagate viable embryos. In IVF, optimal ovogenesis requires the selection and implementation of an individualized approach to controlled ovaria stimulation (COS). Thereupon, at the ideal time, maturational division of the egg’s chromosomes (i.e. meiosis) is “triggered” through the administration of hCG or an agonist such as Lupron, which induces an LH surge. The, dosage and timing of the “trigger shot” profoundly affects the efficiency of meiosis, the potential to yield “competent (euploid) mature (M2) eggs, and as such represents a rate limiting step in the IVF process .

     “Triggering meiosis with Urine-derived hCG (Pregnyl/Profasi/Novarel) versus recombinant hCG (Ovidrel): Until quite recently, the standard method used to “trigger” egg maturation was through the administration of 10,000 units of hCGu. Subsequently,, a DNA recombinant form of hCGr (Ovidrel)was introduced and marketed in 250 mcg doses. But clinical experience strongly suggests that 250 mcg of Ovidrel is most likely not equivalent in biological potency to 10,000 units of hCG. It probably only has 50%-70%of the potency of a 10,000U dose of hCGu and as such might not be sufficient to fully promote meiosis, especially in cases where the woman has numerous follicles. For this reason, I firmly believe that when hCGr is selected as the “trigger shot” the dosage should best be doubled to 500 mcg at which dosage it will probably have an equivalent effect on promoting meiosis as would 10,000 units of hCGu. Failure to “trigger” with 10,000U hCGu or 500mcg hCGr, will in my opinion increase the likelihood of disorderly meiosis, “incompetent (aneuploid) eggs” and the risk of follicles not yielding eggs at egg retrieval (“empty follicles”). Having said this, it is my personal opinion that it is unnecessary to supplant hCGu with hCGr since the latter is considerably more expensive and is probably no more biopotent than the latter.

     Some clinicians, when faced with a risk of OHSS developing will deliberately elect to reduce the dosage of hCG administered as a trigger in the hope that by doing so the risk of critical OHSS developing will be lowered. It is my opinion, that such an approach is not optimal because a low dose of hCG (e.g., 5000 units, hCGu or 250mcg hCGr) is likely inadequate to optimize the efficiency of meiosis particularly when it comes to cases such as this where there are numerous follicles. It has been suggested that the preferential use of an “agonist (Lupron) trigger” in women at risk of developing severe ovarian hyperstimulation syndrome could potentially reduce the risk of the condition becoming critical and thereby placing the woman at risk of developing life-endangering complications. It is with this in mind that many RE’s prefer to trigger meiosis by way of an “agonist (Lupron) trigger rather than through the use of hCG. The agonist promptly causes the woman’s pituitary gland to expunge a large amount of LH over a short period of time and it is this LH “surge” that triggers meiosis. The problem with using this approach, in my opinion, is that it is hard to predict how much LH will be released in by the pituitary gland. For this reason, I personally prefer to use hCGu for the trigger, even in cases of ovarian hyperstimulation hyperstimulated, with one important proviso…that being that is she underwent “prolonged coasting” in order to reduce the risk of critical OHSS, prior to the 10,000 unit hCGu “ trigger”.

     The timing of the “trigger shot “to initiate meiosis: This should coincide with the majority of ovarian follicles being >15 mm in mean diameter with several follicles having reached 18-22 mm. Follicles of larger than 22 mm will usually harbor overdeveloped eggs which in turn will usually fail to produce good quality eggs. Conversely, follicles less than 15 mm will usually harbor underdeveloped eggs that are more likely to be aneuploid and incompetent following the “trigger”.

     If you are interested in my advice or medical services, I urge you to contact my patient concierge, ASAP to set up a Skype or an in-person consultation with me. You can also set this up by emailing concierge@sherivf.com or by calling 702-533-2691 and/or 800-780-743. You can also enroll for a consultation with me, online at http://www.SherIVF.com.
     Also, my book, “In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com .

     Geoffrey Sher MD