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.
I think the most common issue women have is trying to figure out when they are ovulating..They do the OPK’s and basal readings and they still struggle….Any ideas to help? what do you recommend?
It is important to know that the onset of the LH surge precedes ovulation by about 38-42 hours. It only becomes detectable in the urine about 10-12 hours after the rise in LH starts.However, since the earliest that such a rise will be detectable in the urine (by the OPK) is about 10-12 yours later. Morerover LH will remain detectable for up 24 hours after it reaches its peak and thus ovulatrion might already have occurred by then. This could be problematic because because the cervical mucous (at the entrance to the uterus) becomes impermeable to sperm immediately after ovulation has occurred. This means that for pregnancy to occur intercourse or vaginal insemination should take place immediately prior to ovulation, which makes it imperative to detect the rise in LH as early as possible so as to time intercourse or vaginal insemination optimally.
Here is how I advise my patients to use and intedrprett the OPK results so as to optimally time intercourse or insemination: Commencing at least 17 days before the expected menstrual period (i.e.; usually about 10 days following the initiation of menstruation), urine should be collected twice daily and tested for the onset of the spontaneous luteinizing hormone (LH) surge. The initiation of the LH surge usually precedes ovulation by 8 to 36 hours. In order to detect the onset of the LH surge accurately, an early morning urine specimen is needed. Ideally, the bladder should be emptied first thing in the morning, upon awakening. About one half-hour later urine is collected (only a very small amount is required) and tested using an over-the-counter LH – kit (obtainable over the counter, at a drug store). AS soon as the earliest color change is indicative of the onset of the surge, intercourse/vaginal insemination should take place.
Geoff Sher
Hi Dr Sher, I ‘m going to post some questions from my private facebook group once in a while and put your response with the group.
1- Why after a loss ( miscarriage) – Does it take so long to get your cycle back and why is it so different than before. AF longer and O is much later?
THthe reason relates to the disruption of the hormone balance. It can often take 6 weeks or longer for normal pituitary ovarian cyclicity to be re-established.
Geoff Sher
Hello Dr Sher,
1) if someone has a mild protein c deficiency do you believe Fragmin should be used during the IVF cycle and pregnancy?
2) do the steroids used in IVF for IID cause weight gain despite calorie consumption or exclusively because of an increase calories due to increased appetite? Basically is this something I can control with exercise/will power/calorie restriction? I’m worried because I’m already overweight. Do you recommend anything that can be used while using steroids too, to decrease appetite?
Thank you
Hi Dr Sher,
I believe you accidentally didn’t see my question, as you answered the one above and below it but not mine.
1) if someone has a mild protein c deficiency do you believe Fragmin should be used during the IVF cycle and pregnancy?
A: No! But please check with your RE and follow his/her recommendations.
2) do the steroids used in IVF for IID cause weight gain despite calorie consumption or exclusively because of an increase calories due to increased appetite? Basically is this something I can control with exercise/will power/calorie restriction? I’m worried because I’m already overweight. Do you recommend anything that can be used while using steroids too, to decrease appetite?
A: Mainly due to water retention.
Geoff Sher
Hi Dr. Sher,
I usually get my period like clockwork and I was expecting to get it next on July 15th. Since i am on vacation until the 17th, my reproductive endocrinologist said that she would be willing to see me after I return, as late as cycle day 5 to do a baseline ultrasound and labs and start ovarian stimulation. The earliest possible date that I could see her is July 18th, which means that the earliest date that would have been ok to get my period would have been July 14th. It turns out that the estrogen patch and cetrotide that i started taking earlier this week may have entirely changed my internal clock, and my period came on July 13th. It has never come this early and what bad luck! What are the implications of this physiologically that could make stimming less ideal than if i had started by cycle day 5? Is it because after cycle day 5, a dominant follicle has already been chosen and it will be tougher to recruit the remaining folicles? Is all hope lost for me on this round or have you seen people sometimes start stimming on cycle day 6 or 7? Also, will they be able to tell by ultrasound and labs if it’s worth pushing forward, or is it difficult to get an idea until stimming has started and the trends are monitored? Thanks!
Frankly, I do not think it will have an adverse effect at all. Unless the US shows an ovarian cyst, I would not be concerned.
Good luck!
Geoff Sher
Good afternoon Dr. Sher, I am 37 years old and have been diagnosed with unexplained infertility. We have been trying to conceive for a year now and have gone through 3 IUI with oral medications- letrazole and ovidrel injection , 1 hybrid IUI cycle with gonadotropins, 1 IVf cycle and 1 FET cycle. With the IVF cycle they were only able to get 4 eggs from me, my body did not seem to produce a lot of eggs even with the a higher dose of the medicines i took, it has always been a lower number of eggs for me from the time the 4 IUIs were done. During the IVF and the FET the embryos in the blastocyst stage were good according to our doctor. But both procedures were not successful. the doctor said it may been a weak embryo that is why the IVF failed but now that the FET also failed I have not consulted with our fertility doctor as i was not yet ready to do so. What tests should I undergo to find out why both IVF and FET were not succesful. I am not young and my age alone is a big factor in the success of conceiving children. What steps should I take in order to shed light to my situation. Are there tests for me to find out why I cannot conceive a child.
Thank you Doctor for taking the time to read and answer my question.
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
•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?
•Blastocyst Embryo Transfers Should be the Standard of Care 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
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