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. Hi Dr Sher, Thank you for this great information. I’m just curious if any of my embryos would be worth transferring with these chromosome issues?
    Embryo 1: +17, +20, -6, -7
    Embryo 2: +13, +20, -18, -19
    Embryo 3: -5, -6, -15

    Thank you

    • Sadly, since these are all “complex aneuploid” they are in my opinion, highly unlikely to propagate a viable pregnancy!

      Sorry!

      Geoff Sher

  2. Hi Dr. Sher!
    6 weeks and 3 days here. Fetal heartbeat was 159. That seems quite high compared to what the American Pregnancy Association says is normal. My beta series were quite high from the get-go 580, 4000 and 14k.
    Are any of these indicators of an issue or do I just have a really robust embryo?
    Thank you!

    • This is normal and sounds like a “healthy” pregnancy!

      Good luck!

      Geoff Sher

  3. Hi Dr. Sher, I have been prescribed letrozole for ovulation, but no trigger shot has been discussed. Is conceiving possible without the trigger shot?

    • It is possible…although most would use a “trigger” with it…to be sure!

      Good luck!

      Geoff Sher

  4. Dear Dr Sher
    I would really value your opinion. I am 37, 2 children conceived conceived easily (youngest is 3) and one ectopic pregnancy prior to first child (removed from abdomen by laparoscopy). Since trying to conceive again 12 months ago I’ve had 4 chemical pregnancies- test positive (usually feint) and get a period within a few days of when it was due.

    Amh is 13.5. Recent day 21 bloods show thyroid function, prolactin, testosterone, estroidol (741) and progesterone (83) all normal. Only abnormal result was vitamin d, deficient at 11nmol. Arcuate shaped uterus noted& endometriosis notes during ectopic but assume it’s mild as only symptom I have is very noticeable ovulation pain. Periods were normal up until I had my second child. Had Mirena inserted 3 months post partum, no period of the 2 years it was in& since then periods have been very light (2 days of normal flow) and 1/2 of spotting.

    Hycosy has shown open tubes. Hysteroscopy booked for summer to check for adhesions though gynae thinks it’s unlikely as only surgery has been laparoscopy and c section 3 years ago. Lining has measured thin (6mm) at day 12/13 in 3 cycles.

    What do you think could be the potential cause and would estrogen/ progesterone be likely to help? I’ve tried progesterone but have still miscarried. I know you recommend viagra suppositories but I don’t think they’re available in Europe. I would like to avoid ivf if at all possible. Thank you in advance for considering.

    • We should talk Elaine! I need much more substantive information to provide an authoritative opinion!

      Call Patti (702-533-2691) to set up an online consultation with me to discuss in detail.

      Geoff Sher

  5. Hi there

    I am a 32 year old generally healthy female of slim build, non smoker. I have two children age 14 and 5, both born via csection. First csection due to pre-eclampsia, my second was elective. Since June 2019, I have had three miscarriages at between 5-7 weeks. I attended for a internal ultrasound in June last year prior to TTC, and obstetrician had stated my uterus was satisfactory, lining was around 7.5. After my first miscarriage, another internal scan was carried out and no defects noted. I have had clotting factor bloods obtained which have came back as normal, and unfortunately have no further follow up. I am keen to try again, however also scared incase this may happen again, and I’m unsure what else to do. Any advice would be much appreciated.
    Many thanks , Maria from Scotland

    • Hi Maria,

      What I can tell you is that an estrogen proliferated ling (prior to ovulation) does not reach at least 8mm (preferably >9mm) it will not sustain healthy implantation. There may be other factors as well but from your post, this stands out!

      It was as far back as 1989, when I first published a study that examined the correlation between the thickness of a woman’s uterine lining (the endometrium), and the subsequent successful implantation of embryos in IVF patients. This study revealed that when the uterine lining measured <8mm in thickness by the day of the “hCG trigger” (in fresh IVF cycles), or at the time of initiating progesterone therapy (in embryo recipient cycles, e.g. frozen embryo transfers-FET, egg donation-IVF etc.) , pregnancy and birth rates were substantially improved. Currently, it is my opinion, that an ideal estrogen-promoted endometrial lining should ideally measure at least 9mm in thickness and that an endometrial lining measuring 8-9mm is “intermediate”. An estrogenic lining of <8mm is in most cases unlikely to yield a viable pregnancy.

      A “poor” uterine lining is usually the result of the innermost layer of endometrium (the basal or germinal endometrium from which endometrium grows) ) not being able to respond to estrogen by propagating an outer, “functional” layer thick enough to support optimal embryo implantation and development of a healthy placenta (placentation). The “functional” layer ultimately comprises 2/3 of the full endometrial thickness and is the layer that sheds with menstruation in the event that no pregnancy occurs.

      The main causes of a “poor” uterine lining are:

      1.Damage to the basal endometrium as a result of:
      a.Inflammation of the endometrium (endometritis) most commonly resulting from infected products left over following abortion, miscarriage or birth
      b.Surgical trauma due to traumatic uterine scraping, (i.e. due to an over-aggressive D & C)
      2.Insensitivity of the basal endometrium to estrogen due to:
      a.Prolonged , over-use/misuse of clomiphene citrate
      b.Prenatal exposure to diethylstilbestrol (DES). This is a drug that was given to pregnant women in the 1960’s to help prevent miscarriage
      3.Over-exposure of the uterine lining to ovarian male hormones (mainly testosterone): Older women, women with diminished ovarian reserve (poor responders) and women with polycystic ovarian syndrome -PCOS tend to have raised LH biological activity.. This causes the connective tissue in the ovary (stroma/theca) to overproduce testosterone. The effect can be further exaggerated when certain methods for ovarian stimulation such as agonist (Lupron/Buserelin) “flare” protocols and high dosages of menotropins such as Menopur are used in such cases.
      4.Reduced blood flow to the basal endometrium:
      Examples include;
      a.Multiple uterine fibroids - especially when these are present under the endometrium (submucosal)
      b.Uterine adenomyosis (excessive, abnormal invasion of the uterine muscle by endometrial glands).

      “The Viagra Connection”

      Eighteen years ago years ago, after reporting on the benefit of vaginal Sildenafil (Viagra) for to women who had implantation dysfunction due to thin endometrial linings I was proud to announce the birth of the world’s first “Viagra baby.” Since the introduction of this form of treatment, thousands of women with thin uterine linings have been reported treated and many have gone on to have babies after repeated prior IVF failure.

      For those of you who aren’t familiar with the use of Viagra in IVF, allow me to provide some context. It was in the 90’s that Sildenafil (brand named Viagra) started gaining popularity as a treatment for erectile dysfunction. The mechanism by which it acted was through increasing penile blood flow through increasing nitric oxide activity. This prompted me to investigate whether Viagra administered vaginally, might similarly improve uterine blood flow and in the process cause more estrogen to be delivered to the basal endometrium and thereby increase endometrial thickening. We found that when Viagra was administered vaginally it did just that! However oral administration was without any significant benefit in this regard. We enlisted the services of a compound pharmacy to produce vaginal Viagra suppositories. Initially, four (4) women with chronic histories of poor endometrial development and failure to conceive following several advanced fertility treatments were evaluated for a period of 4-6 weeks and then underwent IVF with concomitant Viagra therapy. Viagra suppositories were administered four times daily for 8-11 days and were discontinued 5-7 days prior to embryo transfer in all cases.

      Our findings clearly demonstrated that vaginal Viagra produced a rapid and profound improvement in uterine blood flow and that was followed by enhanced endometrial development in all four cases. Three (3) of the four women subsequently conceived. I expanded the trial in 2002 and became the first to report on the administration of vaginal Viagra to 105 women with repeated IVF failure due to persistently thin endometrial linings. All of the women had experienced at least two (2) prior IVF failures attributed to intractably thin uterine linings. About 70% of these women responded to treatment with Viagra suppositories with a marked improvement in endometrial thickness. Forty five percent (45%) achieved live births following a single cycle of IVF treatment with Viagra The miscarriage rate was 9%. None of the women who had failed to show an improvement in endometrial thickness following Viagra treatment achieved viable pregnancies.

      Following vaginal administration, Viagra is rapidly absorbed and quickly reaches the uterine blood system in high concentrations. Thereupon it dilutes out as it is absorbed into the systemic circulation. This probably explains why treatment is virtually devoid of systemic side effects

      It is important to recognize that Viagra will NOT be effective in improving endometrial thickness in all cases. In fact, about 30%-40% of women treated fail to show any improvement. This is because in certain cases of thin uterine linings, the basal endometrium will have been permanently damaged and left unresponsive to estrogen. This happens in cases of severe endometrial damage due mainly to post-pregnancy endometritis (inflammation), chronic granulomatous inflammation due to uterine tuberculosis (hardly ever seen in the United States) and following extensive surgical injury to the basal endometrium (as sometimes occurs following over-zealous D&C’s).

      Combining vaginal Viagra Therapy with oral Terbutaline;
      In my practice I sometimes recommend combining Viagra administration with 5mg of oral terbutaline. The Viagra relaxes the muscle walls of uterine spiral arteries that feed the basal (germinal) layer of the endometrium while Terbutaline, relaxes the uterine muscle through which these spiral arteries pass. The combination of these two medications interacts synergistically to maximally enhance blood flow through the uterus, thereby improving estrogen delivery to the endometrial lining. The only drawback in using Terbutaline is that some women experience agitation, tremors and palpitations. In such cases the terbutaline should be discontinued. Terbutaline should also not be used women who have cardiac disease or in those who have an irregular heartbeat.

      About 75% of women with thin uterine linings see a positive response to treatment within 2-3 days. The ones that do not respond well to this treatment are those who have severely damaged inner (basal/germinal) endometrial linings, such that no improvement in uterine blood flow can coax an improved response. Such cases are most commonly the result of prior pregnancy-related endometrial inflammation (endometritis) that sometimes occurs post abortally or following infected vaginal and/or cesarean delivery.

      Viagra therapy has proven to be a god send to thousands of woman who because of a thin uterine lining would otherwise never have been able to successfully complete the journey “from infertility to family”.

      ___________________________________________________
      ADDENDUM: PLEASE READ!!
      INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
      Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.

      Patients are encouraged to share the information I provide, with their treating Physicians and/or to avail themselves of my personal hands-on services, provided through batched IVF cycles that I conduct every 3 months at Los Angeles IVF (LAIVF) Clinic, Century City, Los Angeles, CA.

      If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).

      PLEASE SPREAD THE WORD ABOUT SFS!

      Geoff Sher