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.
So, karyotype testing for both my partner and myself came back normal.. the only things that have been found wrong is my thyroid is 3.1 and my glucose level was high so they switched me to extended release metformin and upped the dose.. Could these two factors honestly be the reasons our Frozen embryo transfers have ended in chemical pregnancies both times?
It is possible that your TSHn of 3.1 might be suggesting an underlying sub-clinical and developing hypothyroid state which if this is the case is most often autoimmune and is often associated with an immunologic implantation dysfunction.
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.
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 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.
•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
•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!
•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
•Endometriosis and Infertily
•Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
•Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
•Treating Ovarian Endometriomas with Sclerotherapy.
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.
my thyroid level was tested in August and was fine and then again in October and that is when they found it at 3.1 can they just fix the issue with upping my synthyroid? (they upped it from 50 to 75)
Hi Dr. Sher.
My husband and I recently watched your seminar about the IVF protocols. We have a question about. I am 31 years old. We have severe male factor infertility (azoospermia). I was diagnosed with stage IV endometriosis on 2015 and they removed my right ovary and tube due to a chocolate endometrioma cyst on it. We finally decided to start IVF this year. The clinic I am at is making many semen collections for my husband (total amount very low, so far about 60 frozen sperm and not all motile but we will give it a shot and do surgery on him in another clinic if this round doesn’t work). My AMH is 2.17, day 3 FSH = 7.4 mIU/mL , LH= 6.3 mIU/mL , estradiol=25.3 pg/mL, estrogen= 44.3 pg/mL . I have extra hair around my neck and chin region for a long time now but my periods were always regular (28-29 days). Our concern is that our doctor is overstimulating me. So I would like to get your feedback on this matter since this is our first IVF. I haven’t done the baseline ultrasound yet since I will start injections next sat. So the doctor said the dosage might change based on the ultrasound. But for now he is putting me on 225 units/day of follistim and 150 units of menopur from day 1 of estimulation, and around day 4/5 he is adding ganirelix, and later HCG 10k units. I am on birth control for almost 40 days now and not in lupron. When I asked him why he is giving me such a large dosage, he said he is not basing it on my AMH but in the fact I have only one ovary. However, I’ve seen one study they compared women with one ovary against women with 2 ovaries and the outcome was similar in IVF since the ovary left tries to compensate. So my question is: should I be concerned that this protocol is too much dosage for me, and would it be better to introduce menopur later in the estimulation and also move ganirelix to day 1 of my estimulation? Your feedback would help us a lot. I appreciate you taking the time to answer. Have a good day. Caroline
Hi Caroline,
It is difficult to comment authoritatively on your protocol without much more information. A few general comments are in order however: 1) Your AMH is normal and that (rather than having one versus two ovaries) should in my opinion set the basis for selecting a protocol, 2) 225U of Menopur is a rather high dosage. this only concerns nme because of the high LH/hCG activity in Menopur. I try to confine my simulations to no more than 75U Menopur daily.3) In my opinion, any cycle started with BCP should be overlapped with an agonist such as Lupron (see below on use of BCP in IVF). I presume you will be receiving an antagonist (e.g. Ganirelix or Cetrotide) starting on day 6 or 7 of stimulation. Since you have normal ovarian reserve , that should be OK (although I do not use late antagonist suppression protocols at all). 4) Endometriosis is associated with an immunologic implantatioin dysfunction in about 1/3 of cases and this should ideally be assessed and addressed…see below.
More than half of women who have endometriosis harbor antiphospholipid antibodies (APA) that can compromise development of the embryo’s root system (trophoblast). In addition and far more serious, is the fact that in about one third of cases endometriosis, regardless of its severity is associated with NKa and cytotoxic uterine lymphocytes (CTL) which can seriously jeopardize implantation. This immunologic implantation dysfunction (IID) is diagnosed by testing the woman’s blood for APA, for NKa (using the K-562 target cell test or by endometrial biopsy for cytokine activity) and, for CTL (by a blood immunophenotype). Activated NK cells attack the invading trophoblast cells (developing “root system” of the embryo/early conceptus) as soon as it tries to gain attachment to the uterine wall. In most cases, this results in rejection of the embryo even before the pregnancy is diagnosed and sometimes, in a chemical pregnancy or an early miscarriage. As such, many women with endometriosis, rather than being infertile, in the strict sense of the word, often actually experience repeated undetected “mini-miscarriages”.
Women who harbor APA’s often experience improved IVF birth rates when heparinoids (Clexane/Lovenox) are administered from the onset of ovarian stimulation with gonadotropins until the 10th week of pregnancy. NKa is treated with a combination of Intralipid (IL) and steroid therapy: Intralipid (IL) is a solution of small lipid droplets suspended in water. When administered intravenously, IL provides essential fatty acids, linoleic acid (LA), an omega-6 fatty acid, alpha-linolenic acid (ALA), an omega-3 fatty acid.IL is made up of 20% soybean oil/fatty acids (comprising linoleic acid, oleic acid, palmitic acid, linolenic acid and stearic acid) , 1.2% egg yolk phospholipids (1.2%), glycerin (2.25%) and water (76.5%).IL exerts a modulating effect on certain immune cellular mechanisms largely by down-regulating NKa.
The therapeutic effect of IL/steroid therapy is likely due to an ability to suppress pro-inflammatory cellular (Type-1) cytokines such as interferon gamma and TNF-alpha. IL/steroids down-regulates NKa within 2-3 weeks of treatment the vast majority of women experiencing immunologic implantation dysfunction. In this regard IL is just as effective as Intravenous Gamma globulin (IVIg) but at a fraction of the cost and with a far lower incidence of side-effects. Its effect lasts for 4-9 weeks when administered in early pregnancy.
The toxic pelvic environment caused by endometriosis, profoundly reduces natural fertilization potential. As a result normally ovulating infertile women with endometriosis and patent Fallopian tubes are much less likely to conceive naturally, or by using fertility agents alone (with or without intrauterine (IUI) insemination. The only effective way to bypass this adverse pelvic environment is through IVF. I am not suggesting here that all women who have endometriosis require IVF! Rather, I am saying that in cases where the condition is further compromised by an IID associated with NKa and/or for older women(over 35y) who have diminished ovarian reserve (DOR) where time is of the essence, it is my opinion that IVF is the treatment of choice.
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 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.
. Use of the BCP 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:
•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
•Endometriosis and Infertily
•Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
•Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
•Treating Ovarian Endometriomas with Sclerotherapy.
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.
Hi Dr Sher,
I went through a ivf cycle and am currently 12 wks pregnant. I was diagnosed with vanishing twin at my 10 wk scan and did not have any symptoms until this Friday when i noticed bright red blood when i wiped and went to er. They did all test along with us and said that the baby was fine with a hb of 161 and the other twin was being absorbed however never gave me a reason for the bleed. The bleeding has now changed to brown spotting. Would you please be able to advise as to what might be the reason for this spotting.
Many thanks in advance!
It is likely to be due to absorbtion opf thed second twin. T^he brown spotting suggests the uterine bleeding has stopped and what you are seeing is altered old blood in the vagina. I suspect all will likely be fine.
Good luck!
Geoff sher
Hi Dr Sher, on a natural IVF cycle with the one follicle, at what size would you trigger as a minimum so the follicle is likely to contain a mature egg?
At 18-21mm size.
Good luck!
Geoff Sher
My embrayo transfer done on 11th November. It was a day 3 transfer of two great quality embrayos consisting of 8 cells and 6 cells. My last hcg shot was given on 20th november that was 5000 iu. Today my first b hcg came 3316.90 U/ml.
I have few questions :
1. Is this level indicate a viable pregnancy? Is there any chance of twin pregnancy?
2. This is my 2nd attempt of ivf. Last time i had an chemical pregnancy. Now Is there any risk of the same?
3. When should i go for my 2nd beta test and ultrasound?
4. At which hcg level I could hear a fetal heart beat?
5. How can I protect my pregnancy from misscarrying? I m 39 years old.
It would be a great help if u could manage some time to reply my questions.
Thanks doctor.
1. Is this level indicate a viable pregnancy? Is there any chance of twin pregnancy?
A: Hard to say how much hCG is residual from the shot and how much is being produced by a pregnancy on the make
2. This is my 2nd attempt of ivf. Last time i had an chemical pregnancy. Now Is there any risk of the same?
A: Not possible to tell from this.
3. When should i go for my 2nd beta test and ultrasound?
A: In 2 days after the last one was measured.
4. At which hcg level I could hear a fetal heart beat?
A: If you were successful it would be 4-5 weeks after the ET was done.
5. How can I protect my pregnancy from misscarrying? I m 39 years old.
A: There is nothing to be done other than to take progesterone and estrogen and then wait and see.
Good luck!
Geoff Sher