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.
Hi dr.sher,
Is gonapeptyl 0.1 mg the same as Lupron 0.1 mg?
I have to take 7 days of gonapeptyl starting on day 2 of my cycle.
I heard gonapeptyl is stronger than Lupron.
I am worried about headaches. Is there a medicine that is safe to use?
I am using this for supression.
Regards.
Like lupreolide, gonapeptyl is an agonist but it is not the same. It does however work the same way.
Geoff Sher
Hi Dr. Sher,
I have a question regarding Mosaicism and a quick question about my strange egg retrievals and your thoughts:
me: 38 years old, all bloods normal husband 38: high quality/non-fragmenting/no issues
at Columbia (NYC)
protocol: 225 folistim/75 menapur/add ganirelix/HCG trigger
2 Egg retrievals all ICSI
1st: 17 mature/11 fert/ zero on day 5/6
2nd: 18 mature/13 fert/zero on day 5/6
NYU
BCP for a month: protocol: 225 folistim/75 menapur/add ganirelix/HCG trigger
3rd IVF cycle: 29 Retrieved/1/2 ICSI & Natural – 20 Fertilized – 3 made it to blast – PGS
1 Trisomy 13 and 2 Mosaic: 1 monosomy 4 and 1 trisomy 9
QUESTION: any idea why I can produce so many mature eggs w/ high fertilization results and basically no blasts??
Thoughts on transferring a day 5/6 mosaic? Is there a chance of bearing a chromosomal abnormal child?
what would you do with me as your patient?
Thank you so much!
Antonia
In my opinion, when this happens it is usually traceable to the construct of the protocol used for ovarian stimulationand the timing and type of hCG trigger…see the relevant articles below. However, I would require a great deal more information to advise you authoritatively on how I would modify the stimulation….We should talk.
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.
•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
•Why did my IVF Fail
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•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
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.
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 –
We’re currently undergoing fertility treatment and have just received the news that our second round of IVF with ICSI has been unsuccessful. I’d love to hear any advice you have on both protocol and lifestyle changes that will help us get pregnant on our third attempt!
In terms of our background, I’m 35 and my husband is 38. Neither of smoke and we have cut out all alcohol since starting treatment. We were referred for IVF with ICSI due to my husbands low sperm count but tests showed no issues or areas of concern for me. As such, we were told that we stood a good chance with ICSI. However, over the two rounds of treatment so far, we’ve had lots of issues with embryo quality.
Round 1:
Short protocol – Menopur (with the dose being increased a lot towards the end of the stimulation phase), Cetrotide and Ovitrelle.
8 eggs collected, 7 fertilised… but by day 2 all but one embryo had very high fragmentation.
Day 3 transfer of an 8 cell embryo with a small amount of fragmentation.
No pregnancy achieved.
Round 2:
Long protocol – Buserelin, Menopur (dose of 450 throughout stimulation phase) and Pregnyl.
11 eggs collected, 8 fertilised…. We were holding out to get to Day 5 for PGS but by day 5 we only had 3 had made it to blastocyst stage, but none had enough cells to biopsy. We waited until day 6, but two of the three had degenerated, and the third looked too fragile to biopsy (thin trophectoderm).
We transferred the fragile blastocyst on Day 6. By this point it had started to hatch.
But no pregnancy achieved.
It would be great to hear your thoughts on what we should do next? Is there anything we could change in our protocol or lifestyle wise that would help with embryo numbers, and more importantly, quality?
Thanks in advance!
Gemma.
It is probable that in your case the issue might lie with the protocol used for ovarian stimulation. Please refer carefully to the relevant articles below. This having been said, I would require a great deal more information to advise you authoritatively on how I would modify the stimulation….We should talk.
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.
•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
•Why did my IVF Fail
•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.
Dear Dr.Sher
My husband is diagnosed with Non-Obstructive azoospermia with no known reasason.
our doctor has prescribed him Femara for sperm production, so that he could take us towards ICSI.
I want to know Doc that how much chances are there to produce sperms from femara or how long does femara usually takes to make us achieve such results.
my husband have no such things as testicular failure or vericosele.
I’m desperately waiting to hear from you Doctor.
Thank you
Sincerely
Farah Inamullah Shaikh
Hi Farah,
Unless your husband has hypogonadotropic azoospermia ( a low blood FSH/LH/testosterone ) I am afraid the letrozole has little, if any chance of helping. And even then, even if the FSH and LH are low, it still would have a very small chance of success.
Sorry!
Geoff Sher
I should also add to my previous post earlier tonight that I was on 75 mg per day of DHEA for 4 months leading up to my attempted IVF cycles.
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