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. Greetings from Ireland,
    I am just looking for your opinion on our case, I just literally found your very up to date forum, which is great. My husband, Gary (36yrs old) and I (35 , turning 36 in a few nonths, we have just undergone our second failed IVF. We are both carriers of the CF mutation, Gary has been found to be a carrier of 2 different mutations. He has CBAVD and had a TESE and successful removal of Sperm (10 vials). I had my first egg collection which resulted in 18 eggs, 11 fertilised and by day 5 this we had only 2 viable embryos, so along with our Fertility clinic we decided to do another egg collection to ”pool” our embryos in order to reduce cost and do 1 PGD rest on our samples. Second egg collection we retrieved 15 eggs, 10 fertilised and by Day 5 we had only 1 more embryo… All my work up bloods were completely normal,only issue being a carrier of the CF gene. Samples taken from our 3, 1 came back as a carrier but it came from Gary’s side, so if we were successful ad it was a male it could be affected in the same way as Gary. Our other 2 came back as ”no signal” so they could not tell if they were or were not affected. So, out only option was to re-biopsy these embryos again.. Which at a cost and high risk, we did, and they came back entirely normal. While these were being re-biopsied we proceeded with FET of out first embryo..My meds were Femotab 3mg BD and Gestone 50mg/ml, along Medrone OD for 4 days and antibiotics before the transfer. Unfortunately this did not work… Did not have bleeding or any unusual symptoms before the test date. Very disappointing, but at least we then had 2 more embryos to work with. We just did another transfer, same meds. I had a slight bleed on day 11 but it was only in the morning and nothing after that. I tested yesterday day 13 and it was negative.. I had my transfer on the 27th of July. I suppose I am wondering what would your next step be, is it worth investigating implantation dysfunction? The last embryo survived a thaw, re-biopsy, re freeze and another thaw and transfer..So I was hopeful as it was a good quality embryo that it would stick!. First embryo was a slight lower grade but had not been through as much. Would it be worth looking at changing my stimulation meds. They were happy with my uterine lining and both transfers went very well.

    Thank you for taking the time to read this and I look forward to your opinion.

    Regards

    Louise

    • The CF mutations and your failure to implant are separate issues. You have been dealing with the first issue and need to deal with the second, independently.

      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.
      •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
      •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.
      •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:
      •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

      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.

  2. I had a Et on 28th July ( 5 Day Embryo) and on 8th August by Beta HCG was counting 110 but today (10 Aug) by beta HCG count dropped to 106?? What is happeneing and what i shall do??

    • This could be reduction from a twin pregnancy down to one or it could be a failing implantation.

      Repeat beta hCG in 2 days (from the last one) will tell. It shoulkd double.

      Good luck!

      Geoff Sher

  3. My wife went through 1 st round ivf today and egg pickup. Same happened to me 5 follicles and no eggs at all came out. She is 29 years old. Kindly help in knowing the reason and please let us know if we have any chances for future.

    • This is what is often erroneously referred to as “Empty Follicle syndrome”.

      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
      •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.
      •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
      •Optimizing Response to Ovarian Stimulation in Women who Have Compromised Ovarian Response to Ovarian Stimulation in Women who Have Compromised Ovarian Reserve: A Personal Approach.
      •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?
      •Traveling for IVF from Out of State/Country–
      •A personalized, stepwise approach to 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. Dear Dr. Sher

    I am now 40 years old. Have a 6 and half year old kid. I had 3 miscarriages in 2014 and 2015. Tested FSH was 8.5 a year ago. this July I went back and it was 10, this month 11.5. My doctor asked me to take DHEA 50mg a day hoping to help with FSH number. but I was reading about DHEA and learned that it could increase estrogen and testosterone at the same time. As you commented, high level of testosterone is bad for the maturation of the egg. so in your opinion, should I take DHEA or not? also is fsh reflecting my egg quality(i know you said mainly is associated with age) or is more reflecting the ovarian reserve?

    Thank you so much in advance.
    Lily

    • Hi Lily,

      Dehydroepiandrosterone (DHEA), is steroid hormone produced by the adrenal glands and ovary. It is involved in producing the male hormones, androstenedione testosterone and also estrogen. DHEA blood levels tend to decline naturally with age.
      Under the effect if luteinizing hormone (LH), DHEA is metabolized to testosterone in ovarian connective tissue (theca/stroma). Thereupon the testosterone is transported to the granulosa cells that form the innermost layer of the ovarian follicles where, under the influence of follicle stimulating hormone (FSH)-induced desmolase and aromatase enzymatic activity the testosterone is converted to estradiol. As this happens, granulosa cells multiply, follicle fluid volume increases along with estrogen output and egg development is promoted.
      It is recognition of the essential/indispensable role that male hormones (mainly testosterone) play in follicle and egg development that prompted the belief that by giving DHEA and boosting ovarian testosterone production might benefit follicle/egg development. This belief was given some credence by an Israeli study that in 2010 reported on improved fertility when a group of infertile women were given the administration of 75mg of oral DHEA for 5 months. However, this study was seriously flawed by the fact that it did not separate out women who had diminished ovarian reserve, older women and those with PCOS, all of whom have increased LH-induced production of testosterone. In fact, we recently completed a study (currently being processed for publication) where we conclusively showed that when follicular fluid testosterone levels exceeded a certain threshold, egg quality was seriously prejudiced as evidenced by a marked increase in the incidence of egg chromosomal defects (aneuploidy).
      Consider the following: Ovarian testosterone is needed for follicular development. However, the amount required is small. Too much ovarian testosterone spills over into the follicular fluid and has a deleterious effect on egg/follicle development. Some women (women with diminished ovarian reserve –DOR, older women and those with polycystic ovarian syndrome-PCOS) who tend to have increased LH biological activity, already over-produce testosterone. To such women, the administration of DHEA to such women, by “adding fuel to the fire” can be decidedly prejudicial, in my opinion. Young women with normal ovarian reserve do not over produce LH-induced ovarian testosterone, and are thus probably not at significant risk from DHEA supplementation. It is noteworthy that to date, none of the studies that suggest a benefit from DHEA therapy have differentiated between young healthy normal women with normal ovarian reserve on the one hand and older women, those with DOR and women with PCOS on the other hand.

      In Some countries DHEA treatment requires a medical prescription and medical supervision. Not so in the U.S.A where it can be bought over the counter. Since DHEA is involved in sex hormone production, including testosterone and estrogen, individuals with malignant conditions that may be hormone dependent (certain types of breast cancer or testicular cancer) should not receive DHEA supplementation. Also, if overdosed with DHEA some “sensitive women” might so increase their blood concentrations of testosterone that they develop increased aggressive tendencies or male characteristics such as hirsuites (increased hair growth) and a deepening voice. DHEA can also interact other medications, such as barbiturates, corticosteroids, insulin and with other oral diabetic medications.
      BUT the strongest argument against the use of routine DHEA supplementation is the potential risk of compromising egg quality in certain categories of women and since there is presently no convincing evidence of any benefit, why take the risk in using it on anyone.
      Finally, for those who in spite of the above, still feel compelled to take DHEA, the best advice I can give is to consult their health care providers before starting the process.

      Addendum: One potential advantage of DHEA therapy if used appropriately came from a study conducted by Washington University School of Medicine in St. Louis, MI and reported in the November 2004 issue of the “Journal of the American Medical Association” which showed that judicious (selective) administration of 50mg DHEA daily for 6 months resulted in a significant reduction of abdominal fat and blood insulin in elderly women.

      Geoff Sher

  5. Hi Dr. Sher, My mom and dad (Melinda and Greg Mills) came to you years ago when you were at your clinic in San Francisco. I was conceived on October 3rd, 1991 and born on June 5th, 1992. I was wondering if you had any information on my egg donor that you could give me. I’m not interested in contacting her by any means, just wondering what her heritage was etc — if there is any information you can give me that would be great! Thanks so much! -Danielle Mills

    • Hi Danielle

      I am so glad that things worked out for your mom and dad and thus for you too.

      Unfortunately, I have no access to records in SFO and thus sadly cannot be of help here.

      G-d bless and please come and visit me if you come to LV.

      Geoff Sher