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. Hello Dr. Sher. I had a baby naturally with my husband at age 40, easy pregnancy with an unplanned c-section delivery (I was induced at 10 days after due date and he just wasn’t coming after 14 hours of labor). No complications after. We started trying again when he was 10 months old, and since then (now it has been almost 2 years– I am 42) we tried naturally, naturally with hormone supplements, then after 1 year of nothing we moved to Donor Egg IVF. We have had 3 rounds now of failed Donor Egg IVF at a reputable clinic, all 3 with top grade 5- day blastocysts (1 transferred at each try) and good uterine lining. I had the immunological testing done before the 3rd IVF try and it showed very slight increases in some Fields and one very elevated result and so I had an immunoglobulin infusion 5 days prior to my 3rd transfer. I have just learned the 3rd transfer failed to implant, like the other 2. What else can we try? There are no male infertility issues. I am a healthy weight and exercise regularly, eat healthy, don’t have any particularly relevant family history of disease. Thank you for any direction. S.

    • Thank you for your communication. I think I can help you but to do so we would need to talk.

      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).
      My answer to patients who ask me when is the time to stop undergoing IVF is ….Aside from the weight of the financial burden, the time to stop is when in spite of thorough and comprehensive evaluation, there is no remediable and treatable explanation for repeated failure.

      Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and 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.

      •IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
      •Secondary Infertility: Addressing the Root Causes
      •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)
      •Traveling for IVF from Out of State/Country–
      •A personalized, stepwise approach to IVF
      •IVF Egg Donation: A Comprehensive Overview

      I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.

      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.

      Geoff Sher

  2. Hi Dr. Sher!
    None of our embryos made it to the blastocyst stage. My husband had a sperm DNA fragmentation and it came back 29% and 8 million total count. I read that over 30% it is nearly impossible to get pregnant, even with ICSI. What should we do for our next round to prevent this from happening again? Do you recommend TESA to extract the sperm? Thanks!!!

    • Kelly,

      You arenot correct. I have seen pregnancies whenn the DFI was >70%. In about 40% of infertility cases, male factor is the sole cause. In approximately another 40% it is solely a female factor and in the remainder (20%) both male and female factors are involved. In more than 80% of cases, performance of a semen analysis (sperm concentration, motility, and morphology) will be sufficient to diagnose male factor, while
      There is growing evidence to indicate that DNA damage is prevalent in many cases of male infertility and that this can impact fertility, even in the presence of a normal semen analysis. The latter occurs in 10% of cases when sperm parameters are normal. What remains unclear is at how the DNA damage should be measured, at exactly what level it would impact fertility and precisely, precisely what should be done when there is evidence of such damage and how effective treatment will be.
      While assessing male factor by semen analysis (whether using conventional manual assessment or computer measurement is reliable in about 95% of cases, it tends to be more accurate when it comes to diagnosing normal male fertility, in about 20%-25% of cases where it diagnoses poor sperm parameters it is inaccurate.
      A variety of conditions can cause sperm DNA damage. They include, malignant disease, irradiation, chemotherapy, varicoceles (a collection of surrounding varicose veins in scrotum), white blood cells in the sperm (leucocytospermia) ,cigarette smoking and even cryopreservation (freezing) of sperm.
      Sperm chromatin structure Assay (SCSA).
      Sperm chromatin has a highly specialized and compact structure that is essential for protection and subsequent transmission of the paternal genome.
      The SCSA evaluate for Sperm DNA damage, expressing it as the percentage of sperm DNA fragmentation –(DFI-small breaks in the sperm chromosomes). A DFI of <15% is considered normal while a value of >30% is regarded as abnormal. Fifteen percent (15%)-30% is “intermediate”. Couples where the man has sperm that registers a DFI of >30% reportedly have a four-fold reduction in term pregnancies and a doubling in the miscarriage rate.
      What is true is that the SCSA is measure of sperm DNA damage and does predict male sub/infertility and poor reproductive performance. The SCSA/SDIA measures the degree of abnormalities in the genetic material of the sperm, expressing it numerically as the DNA Fragmentation Index (DFI).
      This having been said, it is important to reemphasize that SCSA data will not always correlate well with standard sperm parameters (count, motility and morphology).
      It is true that varying degrees of DNA damage may be present in sperm from both fertile and infertile men. However a quantitative expression of the DFI often will reveal a hidden abnormality of sperm DNA and as such unveils infertility in cases where prior standard sperm parameters failed to reveal underlying male infertility. Optimal sperm chromatin packaging seems necessary for full expression of male fertility potential. SCSA emerge as predictors of the probability to conceive and carry the pregnancy to viability
      Current information on the clinical role of the SCSA testing in patients undergoing IVF suggests the following:
      •The IVF birth rate could be as much as 1.5-2 times lower in women under 33yrs of age, whose husbands have patently abnormal SCSA assays (with a DFI of >30%). Results seem to become progressively worse with advancing maternal age such that at 35y+, the viable pregnancy rate could be as much as 2-3 times lower.
      •It is possible for abnormal SCSA results to spontaneously revert back to normal, this occurs infrequently. One study reported that even without treatment, 37% of patients with an abnormal result on first SCSA (DFI >30%) were subsequently found to have normal result (DFI < 30%) on a second SCSA test. •Although abnormal SCSA results are detected in men with apparently normal semen analyses, abnormal results are more commonly seen in cases of men who have abnormal sperm parameters (abnormal sperm count, motility and/or morphology) •Abnormal SCSA augers poorly for the outcome of fertility treatments in general and for IVF/ICSI in specific. In the latter cases, fertilization and pregnancy rates are reduced and the chance of early pregnancy loss appears to be increased. However it is important to stress that an abnormal SCSA result does not preclude a successful pregnancy. In fact we have seen many IVF pregnancies occur in spite of abnormal SCSA results….even when the DFI was > 60%
      •The likelihood of a successful outcome with IVF/ICSI in cases where the SCSA is abnormal worsens progressively as the age of the egg provider advances beyond 35yrs.
      •While abnormal SCSA results rarely revert spontaneously to normal this can and does happen on occasion, especially following surgical or interventional radiological treatment of varicoceles (a collection of distended veins surrounding one or both testicles in the scrotum). In addition, there is some suggestion that the use antioxidant/vitamin male fertility blends such as “Proxeed or, Proceptin if taken for 2-3 months can improve the SCSA. In fact, in a relatively recent study, 38 men with an increased percentage of DNA fragmented sperm who received antioxidants, were followed for 2 months after one failed ICSI attempt. A second ICSI cycle was then performed which demonstrated a marked improvement of clinical pregnancy rates (48.2% vs. 6.9%) when compared with pretreatment ICSI outcomes.[

      While the SCSA is not a measure of the sperm’s ability to fertilize an egg, results tend to correlate well with the potential of the fertilized egg, to develop into “competent” embryos (i.e. ones that are capable of propagating live births). As such the introduction of SCSA in the diagnostic armamentarium represents an important advance

      Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and 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
      •Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
      •IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
      •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?
      •Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
      •Male Factor Infertility

      I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.

      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.

      Geoff Sher

  3. Hello Dr Sher

    I would really appreciate some additional information on the following matters.

    DFI Index – Is a man has a high % of DNA fragmentation what impact can this have on embryo implantation. Is PICSI the only way to actually get an idea as to the DNA Integrity of sperm during a cycle?

    Menopur and trigger – In what way does a high dosage of menopur – over 75ml or a half dosage of trigger impact on a cycle? If negative impact – how?

    When PCG /CGH tested embryos are transferred and don’t take what are the reasons besides lining and immunological – is there anything else that you look at?

    Thank you

    • 1. DFI Index – Is a man has a high % of DNA fragmentation what impact can this have on embryo implantation. Is PICSI the only way to actually get an idea as to the DNA Integrity of sperm during a cycle?

      A: In about 40% of infertility cases, male factor is the sole cause. In approximately another 40% it is solely a female factor and in the remainder (20%) both male and female factors are involved. In more than 80% of cases, performance of a semen analysis (sperm concentration, motility, and morphology) will be sufficient to diagnose male factor, while
      There is growing evidence to indicate that DNA damage is prevalent in many cases of male infertility and that this can impact fertility, even in the presence of a normal semen analysis. The latter occurs in 10% of cases when sperm parameters are normal. What remains unclear is at how the DNA damage should be measured, at exactly what level it would impact fertility and precisely, precisely what should be done when there is evidence of such damage and how effective treatment will be.
      While assessing male factor by semen analysis (whether using conventional manual assessment or computer measurement is reliable in about 95% of cases, it tends to be more accurate when it comes to diagnosing normal male fertility, in about 20%-25% of cases where it diagnoses poor sperm parameters it is inaccurate.
      A variety of conditions can cause sperm DNA damage. They include, malignant disease, irradiation, chemotherapy, varicoceles (a collection of surrounding varicose veins in scrotum), white blood cells in the sperm (leucocytospermia) ,cigarette smoking and even cryopreservation (freezing) of sperm.
      Sperm chromatin structure Assay (SCSA).
      Sperm chromatin has a highly specialized and compact structure that is essential for protection and subsequent transmission of the paternal genome.
      The SCSA evaluate for Sperm DNA damage, expressing it as the percentage of sperm DNA fragmentation –(DFI-small breaks in the sperm chromosomes). A DFI of <15% is considered normal while a value of >30% is regarded as abnormal. Fifteen percent (15%)-30% is “intermediate”. Couples where the man has sperm that registers a DFI of >30% reportedly have a four-fold reduction in term pregnancies and a doubling in the miscarriage rate.
      What is true is that the SCSA is measure of sperm DNA damage and does predict male sub/infertility and poor reproductive performance. The SCSA/SDIA measures the degree of abnormalities in the genetic material of the sperm, expressing it numerically as the DNA Fragmentation Index (DFI).
      This having been said, it is important to reemphasize that SCSA data will not always correlate well with standard sperm parameters (count, motility and morphology).
      It is true that varying degrees of DNA damage may be present in sperm from both fertile and infertile men. However a quantitative expression of the DFI often will reveal a hidden abnormality of sperm DNA and as such unveils infertility in cases where prior standard sperm parameters failed to reveal underlying male infertility. Optimal sperm chromatin packaging seems necessary for full expression of male fertility potential. SCSA emerge as predictors of the probability to conceive and carry the pregnancy to viability
      Current information on the clinical role of the SCSA testing in patients undergoing IVF suggests the following:
      •The IVF birth rate could be as much as 1.5-2 times lower in women under 33yrs of age, whose husbands have patently abnormal SCSA assays (with a DFI of >30%). Results seem to become progressively worse with advancing maternal age such that at 35y+, the viable pregnancy rate could be as much as 2-3 times lower.
      •It is possible for abnormal SCSA results to spontaneously revert back to normal, this occurs infrequently. One study reported that even without treatment, 37% of patients with an abnormal result on first SCSA (DFI >30%) were subsequently found to have normal result (DFI < 30%) on a second SCSA test. •Although abnormal SCSA results are detected in men with apparently normal semen analyses, abnormal results are more commonly seen in cases of men who have abnormal sperm parameters (abnormal sperm count, motility and/or morphology) •Abnormal SCSA augers poorly for the outcome of fertility treatments in general and for IVF/ICSI in specific. In the latter cases, fertilization and pregnancy rates are reduced and the chance of early pregnancy loss appears to be increased. However it is important to stress that an abnormal SCSA result does not preclude a successful pregnancy. In fact we have seen many IVF pregnancies occur in spite of abnormal SCSA results….even when the DFI was > 60%
      •The likelihood of a successful outcome with IVF/ICSI in cases where the SCSA is abnormal worsens progressively as the age of the egg provider advances beyond 35yrs.
      •While abnormal SCSA results rarely revert spontaneously to normal this can and does happen on occasion, especially following surgical or interventional radiological treatment of varicoceles (a collection of distended veins surrounding one or both testicles in the scrotum). In addition, there is some suggestion that the use antioxidant/vitamin male fertility blends such as “Proxeed or, Proceptin if taken for 2-3 months can improve the SCSA. In fact, in a relatively recent study, 38 men with an increased percentage of DNA fragmented sperm who received antioxidants, were followed for 2 months after one failed ICSI attempt. A second ICSI cycle was then performed which demonstrated a marked improvement of clinical pregnancy rates (48.2% vs. 6.9%) when compared with pretreatment ICSI outcomes.

      While the SCSA is not a measure of the sperm’s ability to fertilize an egg, results tend to correlate well with the potential of the fertilized egg, to develop into “competent” embryos (i.e. ones that are capable of propagating live births). As such the introduction of SCSA in the diagnostic armamentarium represents an important advance

      2. Menopur and trigger – In what way does a high dosage of menopur – over 75ml or a half dosage of trigger impact on a cycle? If negative impact – how?

      A: Menopur contains hCG/LH , and too much of this can adversely affect egg quality in women who have DOR and in older women. The LH/HCG activity causes ovarian testosterone production, too much of which is deleterious.

      As for a half dosage of hCG. You need at least 10,000U to consistently drive appropraite egg maturation.

      3. When PCG /CGH tested embryos are transferred and don’t take what are the reasons besides lining and immunological – is there anything else that you look at?

      A: Yes! The thickness of the uterine linig, the regularity of the uterine cavity, the technique used for ET etc, all play a role too.

      Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and 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
      •Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
      •IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS).
      •Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
      •IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
      •Why did my IVF Fail
      •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)
      •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
      •The Issue of Left-over Frozen Embryos: A moral/ethical Dilemma!

      Geoff Sher

    • 1. DFI Index – Is a man has a high % of DNA fragmentation what impact can this have on embryo implantation. Is PICSI the only way to actually get an idea as to the DNA Integrity of sperm during a cycle?

      A: In about 40% of infertility cases, male factor is the sole cause. In approximately another 40% it is solely a female factor and in the remainder (20%) both male and female factors are involved. In more than 80% of cases, performance of a semen analysis (sperm concentration, motility, and morphology) will be sufficient to diagnose male factor, while
      There is growing evidence to indicate that DNA damage is prevalent in many cases of male infertility and that this can impact fertility, even in the presence of a normal semen analysis. The latter occurs in 10% of cases when sperm parameters are normal. What remains unclear is at how the DNA damage should be measured, at exactly what level it would impact fertility and precisely, precisely what should be done when there is evidence of such damage and how effective treatment will be.
      While assessing male factor by semen analysis (whether using conventional manual assessment or computer measurement is reliable in about 95% of cases, it tends to be more accurate when it comes to diagnosing normal male fertility, in about 20%-25% of cases where it diagnoses poor sperm parameters it is inaccurate.
      A variety of conditions can cause sperm DNA damage. They include, malignant disease, irradiation, chemotherapy, varicoceles (a collection of surrounding varicose veins in scrotum), white blood cells in the sperm (leucocytospermia) ,cigarette smoking and even cryopreservation (freezing) of sperm.
      Sperm chromatin structure Assay (SCSA).
      Sperm chromatin has a highly specialized and compact structure that is essential for protection and subsequent transmission of the paternal genome.
      The SCSA evaluate for Sperm DNA damage, expressing it as the percentage of sperm DNA fragmentation –(DFI-small breaks in the sperm chromosomes). A DFI of 30% is regarded as abnormal. Fifteen percent (15%)-30% is “intermediate”. Couples where the man has sperm that registers a DFI of >30% reportedly have a four-fold reduction in term pregnancies and a doubling in the miscarriage rate.
      What is true is that the SCSA is measure of sperm DNA damage and does predict male sub/infertility and poor reproductive performance. The SCSA/SDIA measures the degree of abnormalities in the genetic material of the sperm, expressing it numerically as the DNA Fragmentation Index (DFI).
      This having been said, it is important to reemphasize that SCSA data will not always correlate well with standard sperm parameters (count, motility and morphology).
      It is true that varying degrees of DNA damage may be present in sperm from both fertile and infertile men. However a quantitative expression of the DFI often will reveal a hidden abnormality of sperm DNA and as such unveils infertility in cases where prior standard sperm parameters failed to reveal underlying male infertility. Optimal sperm chromatin packaging seems necessary for full expression of male fertility potential. SCSA emerge as predictors of the probability to conceive and carry the pregnancy to viability
      Current information on the clinical role of the SCSA testing in patients undergoing IVF suggests the following:
      •The IVF birth rate could be as much as 1.5-2 times lower in women under 33yrs of age, whose husbands have patently abnormal SCSA assays (with a DFI of >30%). Results seem to become progressively worse with advancing maternal age such that at 35y+, the viable pregnancy rate could be as much as 2-3 times lower.
      •It is possible for abnormal SCSA results to spontaneously revert back to normal, this occurs infrequently. One study reported that even without treatment, 37% of patients with an abnormal result on first SCSA (DFI >30%) were subsequently found to have normal result (DFI 60%
      •The likelihood of a successful outcome with IVF/ICSI in cases where the SCSA is abnormal worsens progressively as the age of the egg provider advances beyond 35yrs.
      •While abnormal SCSA results rarely revert spontaneously to normal this can and does happen on occasion, especially following surgical or interventional radiological treatment of varicoceles (a collection of distended veins surrounding one or both testicles in the scrotum). In addition, there is some suggestion that the use antioxidant/vitamin male fertility blends such as “Proxeed or, Proceptin if taken for 2-3 months can improve the SCSA. In fact, in a relatively recent study, 38 men with an increased percentage of DNA fragmented sperm who received antioxidants, were followed for 2 months after one failed ICSI attempt. A second ICSI cycle was then performed which demonstrated a marked improvement of clinical pregnancy rates (48.2% vs. 6.9%) when compared with pretreatment ICSI outcomes.[

      While the SCSA is not a measure of the sperm’s ability to fertilize an egg, results tend to correlate well with the potential of the fertilized egg, to develop into “competent” embryos (i.e. ones that are capable of propagating live births). As such the introduction of SCSA in the diagnostic armamentarium represents an important advance
      .
      2. Menopur and trigger – In what way does a high dosage of menopur – over 75ml or a half dosage of trigger impact on a cycle? If negative impact – how?

      A: Dosage will vary from one person to the other. It is very much influenced by the woman’s ovarian reserve (see below)

      3. When PCG /CGH tested embryos are transferred and don’t take what are the reasons besides lining and immunological – is there anything else that you look at?

      A: While chromosomal integrity of the embryo is certainly the most important factor in determining outcome it is only part of the story. There are other genetic egg/embryo factors that play a role as do local metabolic factors. Also the absence of surface lesions in the uterine cavity as well as the thickness of the uterine lining plays a role. In addition, the technique and skill in performing embryo transfer is important.

      Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and 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
      •Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
      •IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
      •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.
      •Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
      •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?

      I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.

      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.

      Geoff Sher

  4. I am 29! Did my first round of IVF transferred two AA 5 day blastocyst on the 28th of Feburary.
    Tested 9 days post transfer and got an hcg value of 18.6!
    Tested again two days later and the value was even lower, down to 11!
    Still haven’t gotten my period ( the nurse asked me to stay on progesterone pressaries until 18th March)
    I would really want to know what could have gone wrong, as the doctor was very very hopeful on my case, as my embryos were of good quality.

    • Hi Sonia,

      Sadly, this is a chemical pregnancy.

      Geoff Sher
      702-699-7437

  5. Dear Dr. Sher,

    I am 9w3d pregnant with twins after donor ivf. Last night I had very heavy bleeding but, fortunately, the babies are ok. I live in Iran at the moment where I don’t have anyone apart from my husband who is all day at work. I would like to go and stay with my family which would mean taking two flights, one 3 hour flight and one 1 and a half hour flight. Is it dangerous according to you to take a flight after heavy bleeding. Thank you for your help. Lili

    • No Lili. It should be fine in the pressurized cabin of a commercial airliner.

      Geoff Sher