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. Does checking prolactin levels have any diagnostic values for IVF or FET failures?

    • Yes!
      Prolactin is a protein hormone (closely related to human growth hormone) that is secreted by specialized cells in the anterior part of the pituitary gland. In addition, the hormone is also produced and secreted by a broad range of other cells in the body, most prominently various immune cells, the brain and the lining of the uterus. Most cells respond to prolactin. In fact it is hard to identify any tissue that does not have prolactin receptors.
      Although prolactin’s major target organ is the breast where it stimulates development and milk production, the hormone has many other functions. Several hundred different actions have been reported for prolactin and
      Immune cells are rich in prolactin receptors and certain types of lymphocytes in fact synthesize and secrete prolactin. These observations suggest that prolactin may to some extent act as a regulator of the body’s immune activity.
      In an area in the brain known as the hypothalamus, a chemical called dopamine is released. Dopamine suppresses prolactin synthesis and release by the pituitary gland. As such it acts as a “hypothalamic brake set” causing prolactin only to be secreted when the “brake” is released. Treatment with dopamine agonists such as bromocriptine (Parlodel) and cabergoline (Dostinex) , by enhancing serotonin production lowers prolactin
      Several other hypothalamic hormones, including thyroid releasing hormone (TRH) and gonadotropin releasing hormone (GnRH) cause an increase in prolactin secretion Stimulation of the nipples (including but not limited to nursing) leads to hypothalamic activation and prolactin release Estrogens also exerts a positive control over prolactin synthesis and secretion
      Even modestly raised prolactin levels (20ng/ml-40ng/ml) can interfere with estrogen-induced endometrial proliferation as well as egg/ ovarian follicle growth and development. Accordingly treatment with dopamine agonists (bromocriptine/ Cabergoline) might be of benefit in such cases.
      Increased PRL secretion reduces the pulsatility of GnRH impairing the pituitary production of FSH and LH and may directly impair the endocrine activity of ovarian follicles as well as endometrial response to estrogen. This can lead to dysfunctional or failed ovulation, a defective luteal phase, and a poorly developed endometrial response to estrogen (a thin endometrial lining). About n 5% of unselected, asymptomatic infertile women have hyperprolactinemia. In such cases long-term use of dopaminergic drugs such as bromocryptine and can normalized prolactin levels leading to reestablishment of functional ovulation and improved endometrial development. About half of the pregnancies occurring during dopaminergic therapy start after the first 6 months of this drug therapy. Treatment should continue for at least 1 year.

      Common manifestations of significantly increased prolactin secretion (hyperprolactinemia):
      •In women:
      oOligo/amenorrhea (reduction or absence of menstrual flow) and galactorrhea (excessive or spontaneous breast secretion of milk).
      oA modest elevation in blood prolactin can also point to an underlying state of hypothyroidism
      oMarkedly elevated prolactin levels (i.e. >60ng/ml) might point to a prolactin producing pituitary macroadenoma or microadenoma as well as other intracranial lesions such as craniopharyngiomas, meningiomas etc.
      •In men: Such men rarely have galactorrhea
      oHypogonadism,
      oBreast enlargement (gynecomastia),
      oErectile dysfunction
      oDecreased Libido,
      oSperm dysfunction resulting in infertility and with impotence..

      Causes of hyperprolactinemia: Main causes of pathologic hyperprolactinemia (40).

      •Idiopathic (commonest variety) ….cause unknown Acromegaly
      •Empty Sella Turcica
      •Renal Failure
      •Polycystic Ovarian Syndrome (PCOS)
      •Certain drugs:
      oAntipsychotic drugs ( phenothiazines, haloperidol, monoamine oxidases (MAO) risperidone, fluoxetine, butyrophenones,
      oAnti-emetics: metoclopramide, domperidone,
      oTricyclic antidepressants
      oOpiates
      oVerapamil
      oAntihypertensives and Ganglion blockers

      Drug-induced hyperprolactinemia can be reversed by modifying or withdrawing the causative medication. In cases where this cannot safely be done, bromocryptine derivatives can be used.

      •Pituitary adenomas (prolactinomas)
      o Some pituitary adenomas are treated by surgical removal but in most case prolonged treatment with bromocryptine or cabergoline will effectively lower blood concentrations and lead to shrinkage/disappearance of the tumor. Such treatment is also safe during pregnancy.
      o Intracranial lesions such as craniopharyngiomas, meningioma causing hyperprolactinemia are usually treated by surgical removal.

      Hyperprolactinemia and Reproductive Dysfunction:
      •Hypothyroidism in women is often caused by an autoimmune process where antithyroid antibodies progressively replace thyroid glandular tissue with functionless connective tissue. In roughly 50% of such cases there will be increased uterine natural killer cell activity (NKa) which may profoundly impair implantation leading to “perceived infertility” or recurrent pregnancy loss. Thus, ATA with NKa can be present prior to the development of clinically overt autoimmune hypothyroidism (Hashimoto’s disease). Since women with NKa are often infertile, or experience recurrent pregnancy loss, it is important that any unexplained hyperprolactinemia associated with reproductive failure or infertility be evaluated for an immunologic implantation dysfunction (IID) through testing for the presence of antithyroid antibodies and if the ATA level is elevated, that an NKa test (K-562 target cell test) be done. What is not often commonly recognized is that even in cases where autoimmune hypothyroidism is clinically overt, treatment with thyroid hormone replacement will usually not solve the reproductive dysfunction which will usually require selective immunotherapy with Intralipid (IL) infusions plus steroid therapy. IL is administered intravenously about 4-7 days prior to ovulation or egg retrieval and then repeated one more time upon biochemical confirmation of early pregnancy. The steroids are continued to the 8th week of pregnancy and then tailed off over 2 weeks.

      •Ovarian Hyperstimulation Syndrome (OHS): Prolactin facilitates production by ovarian follicle cells of VEGF (a vasoactive substance that increases vascular permeability of blood vessels) In cases of severe ovarian With severe ovarian hyperstimulation syndrome (OHSS) where there are a large number of follicles present (>25) and the blood estradiol level is markedly elevated (4,000pg/ml), even modestly elevated prolactin release can markedly worsen the situation. There is strong evidence to suggest that women with ovarian Hyperstimulation (>20 follicles and blood estradiol levels that peak above 3,000pg/ml) who receive O.5mg of oral administration Cabergoline daily for 7 days, starting on the day of the hCG trigger, experience a significant reduction in the risk and severity of severe ovarian stimulation syndrome (OHSS). This is thought to be due to Cabergoline suppressing the production of vascular vasoactive substances such as VEGF that are produced by luteinized follicular granulosa cells, that increase the vascular permeability of local pelvic blood vessels.

      I hope that helps!

      Geoff Sher

      :

  2. Hi Dr Sher, im 43, had two ivf cycles with transfers to my partner but they didnt wk in 2016, so i decided to do acupuncture and Chinese herbs for last 8 months , and in april 2017 after my period .. starting april 2nd i took aspirin 25mg clomid and 50 mg letrozole, then stopped letrozole and started on menopur and clomid on april 7, had one follicle and they triggered my with ovidrel april10, and took one dose of menopur but made a mistake and took ovidrel first and then the menopur…had my retrieval today and no egg.. my dr is david cohen in chicago.. he said i dont have any eggs in my ovaries? anymore? is that true? im hoping he will let me do another cycle.. since i was hopingthat the acupuncture and herbs would have made better quality eggs… what do you think?

    • Hi Mini,

      I would need a great deal molre information to comment and advise authoritatively. What I can say here is that in my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”.
      Older women as well as those who (regardless of age) have diminished ovarian reserve (DOR) tend to produce fewer and less “competent” eggs, the main reason for reduced IVF success in such cases. The compromised outcome is largely due to the fact that such women tend to have increased LH biological activity which often results in excessive LH-induced ovarian testosterone production which in turn can have a deleterious effect on egg/embryo “competency”.
      Certain ovarian stimulation regimes either promote excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), augment LH/hCG delivered through additional administration (e.g. high dosage menotropins such as Menopur), or fail to protect against body’s own/self-produced LH (e.g. late antagonist protocols where drugs such as Ganirelix/Cetrotide/Orgalutron that are first administered 6-7 days after ovarian stimulation has commenced).
      I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of a modified, long pituitary down-regulation protocol (the agonist/antagonist conversion protocol-A/ACP) augmented by adding supplementary human growth hormone (HGH). I further recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing/NGS)-normal blastocysts in such cases. This type of approach will in my opinion, optimize the chance of a viable pregnancy per embryo transfer procedure and provide an opportunity to capitalize on whatever residual ovarian reserve and egg quality still exists, allowing the chance to “make hay while the sun still shines”.
      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.
      •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
      •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?
      •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
      •Implications of “Empty Follicle Syndrome and “Premature Luteinization”
      •Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.

      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.
      Geoff Sher

  3. Hi Dr. Sher.

    I’m 30 years old, PCOS, with no prior pregnancies.

    I just got the Beta results from my first round of IVF with our only embryo and we were unsuccessful. During the egg retrieval, I had 41 eggs, 16 fertilized with ICSI, 4 made it to day 5 blast, but only one was genetically normal. The one normal one had an “average” rating.

    I am gearing up to start another cycle in about 3 months and wonder what your take is on supplements to increase eqq quality? I’ve read a lot about Royal Jelly, Vitex, Macca, and CoQ10. Do you recommend any of these or specifically discourage any of these for a PCOS diagnosis? (I’ve read that DHEA can make the case worse with PCOS). If I do take any of these, am I safe to take these all the way through my egg retrieval? This is our last IVF attempt and any advice you can give regarding increasing egg quality would be greatly appreciated.

    Thank you!

    • Let me start by saying that there is no doubt that PCOS exacts a toll on egg quality. This having been said, the egg quality can in large part protected through the judicious implementation of an individualized protocol for ovarian stimulation.
      Women with PCOS are hypersensitive to gonadotropin stimulation and are often at risk of developing serious complications associated with severe ovarian hyperstimulation syndrome (OHSS). Concern for this occurring often leads the treating physician to take precautionary measures aimed at slowing down or stopping hyperstimulation. Such measures include:
      1.Cutting the stimulation short to prevent the E2 from rising too high. Unfortunately this often results in the eggs being underdeveloped at the time of the “trigger” and thus, far more likely to end up being “immature”., “dysmature” and “incompetent”.
      2.Administering a lower “trigger dosage” of hCG , supplanting it (partially or completely) with an Agonist trigger (e.g. Lupron/Buserelin/aminopeptidyl/Superfact). While such measures can certainly reduce the risk/severity of OHSS, it often comes at the expense of egg competency (see below).
      In my opinion, another error of commission during ovarian stimulation of women with PCOS is the indiscriminate use of drugs that either elicit an exaggerated ovarian LH-induced testosterone response (e.g. clomiphene or Letrozole), or provide too much LH (e.g. Menopur/Menogon). Too much ovarian testosterone is harmful to egg development and thus prejudicial to embryo quality/competency.
      In my opinion the best way to approach ovarian stimulation for IVF in women with PCOS, is through the use of a low dosage, FSH-dominant Long ovarian down-regulation protocol, done in readiness for “prolonged coasting” (see below) and “triggering” egg maturation with a full 10,00U dosage of hCG or (no less than) 500mcg of recombinant hCG (Ovidrel)….see belowis If this is implemented appropriately, with proper timing, egg/embryo quality can be optimized.
      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.
      •The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
      •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
      •Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
      •Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
      •Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas
      •Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
      •A personalized, stepwise approach to IVF
      •Taking A Fresh Look at Ovarian Hyperstimulation Syndrome (OHSS), its Presentation, Prevention and Management
      •Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting”
      •Understanding Polycystic Ovarian Syndrome (PCOS) and the Need to Customize Ovarian Stimulation Protocols.
      •“Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
      •The “Lupron Trigger” to Prevent Severe OHSS: What are the Pro’s and Con’s?

      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.

  4. Hi Dr Sher, is it ok to keep doing IVF cycles with a month’s break in between? Is there a maximum that can be done in a certain amount of time? We don’t have a lot of time to take breaks due to our age.
    Thanks in advance!

    • In my opinion, there needs to be at least 1 resting cycle between attempts.

      Geoff Sher

  5. Dr Sher, I’m 40 and starting a stim cycle after a month being on BCP with no Lupron. On cycle day 4, my FSH was 10.46 and my LH was 6.73. Last month before starting BCP on cycle day 5 my FSH was 8.54 and LH was 8.44. My stim plan is 150 of Gonal and 75 Menopur. I’m concerned that my FSH went up so much, I’m not sure if that’s due to age or the BCP. I’ve been labeled a high responded on last cycles, but my FSH has gone up significantly since my first cycle. Should I discuss increasing the Gonal dosage with my dr? I’m concerned I want respond well with the lower dosage and increased FSH.

    • Please see below.

      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.
      •The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
      •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
      •Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
      •Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
      •Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas
      •Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
      •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

      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.