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.

19,771 Comments

  1. Hello Dr Sher,
    I am struggling here and really need your knowledge and advice.

    I have severe DOR. I am 41, very high fsh but fluctuating, AMH undetectable, AFC 2 last time and i have irregular cycles. Despite my bad stats i manage to get 1-2 eggs here and there and grow blasts.

    I am struggling between two ways of moving forward for my case:
    1) Do one more conventional ivf cycle. This will involve estrogen priming with vivelle patches a few days after ovulation. Then allow the last patch to fall off but meanwhile on cd2 i start injectables.

    2) Or do natural cycles where if FSH is high at baseline i will use estrave+provera or bcp to lower fsh and allow the follicle to grow. I may use a few boosts to help it along.

    a) I have read somewhere that estrogen patches hurt ovarian function. Is this true? Is it a permanent damage?
    b) I am afraid of over suppression. Do severe DOR women ever recover from it or go straight into menopause?
    c) Which is more suppressive? Estrace or bcp or estrogen patches? What do you suggest for severe DOR?
    d) What route would you suggest from the two above? The estrogen priming protocol or do natural cycles with estrace +provera?

    I have already done 5 ivf cycles. My last ivf cycle was an estrogen priming protocol and i did get a blast. However after that cycle i noticed that my ovaries worked less. AFC went down to 1-2 from a stable 3 and my fsh went even higher. Also my ovaries hurt sometimes. That is why i wonder whether patches hurt the ovaries of severe DOR women and suppression in general. I have a feeling that doing one more ivf cycle will push me into menopause. Am i being illogical here or do my fears have some science to back them up??
    I have done tones of research but google is not very helpful on these issues. Hoping to hear from you.
    Regards
    Georgia

    • In my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”.

      Older women as well as those who (regardless of age) have diminished ovarian reserve (DOR) tend to produce fewer and less “competent” eggs, the main reason for reduced IVF success in such cases. The compromised outcome is largely due to the fact that such women tend to have increased LH biological activity which often results in excessive LH-induced ovarian testosterone production which in turn can have a deleterious effect on egg/embryo “competency”.

      Certain ovarian stimulation regimes either promote excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), augment LH/hCG delivered through additional administration (e.g. high dosage menotropins such as Menopur), or fail to protect against body’s own/self-produced LH (e.g. late antagonist protocols where drugs such as Ganirelix/Cetrotide/Orgalutron that are first administered 6-7 days after ovarian stimulation has commenced).

      I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of a modified, long pituitary down-regulation protocol (the agonist/antagonist conversion protocol-A/ACP) augmented by adding supplementary human growth hormone (HGH) and in women like you who have very severely diminished ovarian reserve I would recommend adding estrogen priming to the A/ACP. I further recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing/NGS)-normal blastocysts in such cases. This type of approach will in my opinion, optimize the chance of a viable pregnancy per embryo transfer procedure and provide an opportunity to capitalize on whatever residual ovarian reserve and egg quality still exists, allowing the chance to “make hay while the sun still shines”.
      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.

      •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 Aproach
      •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)
      •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?
      •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
      •Implications of “Empty Follicle Syndrome and “Premature Luteinization”
      •Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.

      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.
      Geoff Sher

  2. Hi Dr. Sher,
    I am 35 and have been diagnosed with DOR. As of a year ago, my AMH was .5 and ive had day 3 fsh levels of 24, 15 and 12. We tried naturally for a year and then this year began fertility treatments. (Note nothing I’ve tried has ever resulted in a pregnancy) I had 3 iuis (1 femara, followed by 2 with 150 of follistim). The 2 cycles with injectables yielded 5 and 7 follicles, so my doctor advised we move to IVF given my good response.

    IVF #1 was starred with bcp, then injectables up to 450 follistim and 150 menopur. I only got one follicle and cycle was converted to iui.

    IVF #2 was antagonist again, but no bcps. I was on 325 follistim and 75 menopur. They retrieved 4 eggs and we had 2, 10-cell, lower grade embryos by day 5.

    IVF #3 was microdose lupron. I did have bcps before this cycle. 375 follistim and 75 menopur. Again they got 4 eggs, but only 1 fertilized and again was 10 cell on day 5, although less fragmented.

    IVF #4 we did estrogen priming. 375 follistim and 75 menopur. They retrieved 6 eggs, but this was a different doctor doing the retrieval than before. Regardless 2 fertilized and they transferred them both (6 cell and 4 cell) on day 3.

    IVF #5 we switched to a clinic who recommended mini ivf. I took estrogen and progesterone prior to the cycle. Then took cloud 50mg for several days, then 25mg, in addition to 150 follistim. They retrieved 4 eggs, and 2 fertilized but never progressed past 2 cells each.

    In your opinion, what is my next option? Am I crazy to keep trying? Thank you for any advice or suggestions you may have.

    • That should read Clomid (not “cloud”) above for the meds I took for the last cycle. 🙂

  3. Hello Doctor,
    My mother has had a IVF procedure done twice and both times her doctor gave her very high hopes, sadly neither of the process worked. Her HCG level wouldn’t rise, on the first time she did her cycle they only rised to 13 and dropped from there. The second time she did her treatment her doctor said everything looked great, but when her levels were tested they were in the negative range. Do you know this could be happening or do you have any advise on what to do. My mother is 47 years old and she has used a egg donor with her spouses sperm to create the embryos. She has only had one child and that was 20 years ago. Would there be a true reason why she hasn’t been able to get pregnant?

    • 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 (What follows applies whether own eggs or donor eggs are used):
      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

      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.

  4. Hi Dr Sher, at age 37 I was diagnosed with low amh. It was 5.8 on the Australian used scale, I think less than 1 on the US scale. I therefore did 3 rounds of IVF and froze eggs. The 1st end 9 eggs, then 11 and then 13. I am now 42 and decided to use the eggs. I started with the first 9 ( they were frozen, not vitrified). Unfortunately only 1 fertilised and produced a low grade embryo at day 2 which the FE decided to freeze for banking. Do you have any idea why the fertilisation rate was so low? Can I expect the same ferilisation rate for the next 2 batches (they were vitrified, not frozen)? My protocol for egg retrieval was 450m gonal-f, ovidrel and orgalutran. Thank you. Tiff

    • What you experienced is not unusual. That is why even for young women most centers suggest that at least 15 mature eggs be frozen and even then, upon thawing and fertilizing them, very few will produce blastocysts and of those the baby rate per transferred blastocyst is relatively small. As women get older, the protocol used for ovarian stimulation will have an effect on egg competency. The likelihood is great that the same obstacles could present for your remaining frozen eggs.

      I suggest that you now consider changing strategy and moving to embryo banking of PGS-selected blastocysts.

      In my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”.
      Older women as well as those who (regardless of age) have diminished ovarian reserve (DOR) tend to produce fewer and less “competent” eggs, the main reason for reduced IVF success in such cases. The compromised outcome is largely due to the fact that such women tend to have increased LH biological activity which often results in excessive LH-induced ovarian testosterone production which in turn can have a deleterious effect on egg/embryo “competency”.
      Certain ovarian stimulation regimes either promote excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), augment LH/hCG delivered through additional administration (e.g. high dosage menotropins such as Menopur), or fail to protect against body’s own/self-produced LH (e.g. late antagonist protocols where drugs such as Ganirelix/Cetrotide/Orgalutron that are first administered 6-7 days after ovarian stimulation has commenced).
      I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of a modified, long pituitary down-regulation protocol (the agonist/antagonist conversion protocol-A/ACP) augmented by adding supplementary human growth hormone (HGH). I further recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing/NGS)-normal blastocysts in such cases. This type of approach will in my opinion, optimize the chance of a viable pregnancy per embryo transfer procedure and provide an opportunity to capitalize on whatever residual ovarian reserve and egg quality still exists, allowing the chance to “make hay while the sun still shines”.
      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.

      •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 Aproach
      •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)
      •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?
      •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
      •Implications of “Empty Follicle Syndrome and “Premature Luteinization”
      •Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.

      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.

      Geoff Sher

  5. Dr. Sher,
    Based on my ultrasound, I was carrying twins and weeks later, both twins had a heartbeat. Twin A has 102 and Twin B has 110. The following week the heartbeat of twin A was 108 while twinB was 121. On my 7th week, Twin A’s heartbeat stopped while twinB’s heartbeat was 157. My doctor said that there might be chromosomal abnormality. He also said that they don’t have to do anything on the twin whose heartbeat has stopped since my body will just reabsorb it. What is your take on this? And in your opinion, is there a chance for the remaining twin to survive into full term? Your opinion is greatly appreciated. Many thanks.

    • Hi Beatrix,

      I agree fully with your doctor!

      Geoff Sher