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
I have been diagnosed with sperm antibodies due to I assuse an operation for an u descended testicle when I was younger. We have gone through one round of ivf inside which was successful but we list our baby at 12 weeks. I found the whole experience very invading so if there anything I can take short term to reduce the antibodies as I only need to take this until my wife is pregnant.
Many thanks Ray
Sadly Ray, if you have significant ASA you need IVF with ICSI. Nothing else will help adequately.
Geoff Sher
Hi Dr. Sher,
I recently questioned you regarding fluid in my uterus prior to egg retrieval and your answer was based on our assumptions that it was mucus. I’ve since had the ER and there is still fluid in the upper part of my uterus and it’s definitely not mucus. They retrieved 7 eggs, 6 have fertilised and we are set to transfer in 2 days (this Monday morning). My prior cycles I struggled with getting a lining over 7mm, however have had a singleton and twin successful pregnancies. My last scan showed a fantastic lining of 10.6mm before starting progesterone suppositories, so I am thrilled. My question is whether or not my RE should try removing the fluid just prior to ET or leave it alone? Everything I read says it will hinder implantation, is there anything to do prevent this impacting implantation or is it a lost cause? I don’t have any tubal blockage that would cause this fluid, and they don’t seem to have any idea what has caused it. Thanks again for all your wonderful assistance…you are a true blessing to many women struggling with infertility
I would NOT try to remove it. Usually (but not invariably)the progesterone will over a few days result in it being absorbed. Introducing a foreign body (catheter) into the uterus can in my opinion only do more harm than good.
Geoff Sher
Dr Sher,
Is there any detriment to do estrogen priming if one doesn’t have DOR?
Not usually… but usually no advantage either.
Geoff Sher
Hello Doctor, I am 32, never got pregnant because of male infertility factor. My AMH jumped from 1.5 (Oct 2016), 1.2 (Dec 2016) to 4.1 (May 2017) and AFC from 9 to 18 in 3 months after taking supplements, healthy diet, exercise, and fertility massage. Does this sudden change in AMH guarantees good quality of eggs too? My stimulation will start soon.
I had 2 failed IVF cycles in Oct 2016 and Jan 2017.
The ovarian reserve won’t change with supplements. I question the reliability of one or more of the tests.
Geoff Sher
Hi Dr. Sher,
Your online answering service is much appreciated!
I am a 33 year old woman and have attempted two IVF/ICSI cycles due to first diagnosed Male Factor Issues, with no success. Below are some questions I have regarding egg quality and quantity:
1. If AMH, FSH, LH and Prolactin levels are normal, and the antral follicle count is well between 12-15, is poor embryo quality and fragmentation due to poor egg quality?
2. Two different protocols agonist and antagonist, both yielded different numbers, but similar fragmentation levels. A second opinion we sought elsewhere suggested that the trigger timing may not have been optimal. What are your thoughts on trigger time and embryo quality in young(ish) women?
3. Can very high doses of gonadotropins cause poor embryo quality in women with otherwise normal ovarian reserve and hormone numbers? Gonal 375IU and Menopur 75IU.
4. What are your thoughts on Human Growth Hormones in such cases, in addition to supplementing with DHEA, CoQ10, Pycnogynol, Reservatrol, Myo Inositol, VitaminD in addition to regular prenatal vitamins?
5. Is there such a thing as cytoplasmic immaturity even though MII has occurred in an egg, causing poor embryo quality by day3?
We are considering a new cycle with a different specialist and would like to know if egg quality is the cause for poor embryo quality or if lowering doses can bring about improvement.
Best regards,
Rita
1. If AMH, FSH, LH and Prolactin levels are normal, and the antral follicle count is well between 12-15, is poor embryo quality and fragmentation due to poor egg quality?
A: More than likely so….but given your young age, this is more than likely a function of the protocol used for ovarian stimulation and/or its implementation. This needs to be carefully reviewed and probably revised.
2. Two different protocols agonist and antagonist, both yielded different numbers, but similar fragmentation levels. A second opinion we sought elsewhere suggested that the trigger timing may not have been optimal. What are your thoughts on trigger time and embryo quality in young(ish) women?
A: See below.
3. Can very high doses of gonadotropins cause poor embryo quality in women with otherwise normal ovarian reserve and hormone numbers? Gonal 375IU and Menopur 75IU.
A: In my opinion…only if the timing of the hCG trigger was brought forward because of a fear of OHSS, a lower than appropriate dosage of hCG was used and/or you were triggered with an agonist (e.g. Lupron)
4. What are your thoughts on Human Growth Hormones in such cases, in addition to supplementing with DHEA, CoQ10, Pycnogynol, Reservatrol, Myo Inositol, VitaminD in addition to regular prenatal vitamins?
A: HCG supplementation and some of the other supplements are OK, but I would not use DHEA.It is important to nurture and take care of yourself mentally and physically when preparing and going through your IVF journey. This starts with trying to have a positive attitude about what you are about to go through, creating a stress support system for yourself by using tools such as visualization, acupuncture and meditation, eating the right foods taking a few supplements (see below) and balancing exercise with sufficient rest. . Not only will it help your experience but it may also help to increase your chances for IVF success
This article will focus on the role of nutritional supplements in preparing for IVF. You’ve probably wondered whether commercially available fertility supplements could help you achieve your goal. The answer is complex.
Here is my take: Nutrition is indeed a vital prerequisite for optimal reproductive function. However, a well-balanced diet that meets food preferences, coupled with modest vitamin, mineral and antioxidant supplementation (as can be found in many prenatal vitamin preparations) should suffice.
This having been said, conceiving is a delicate process, and eating the right foods is essential to optimize reproductive potential. Indeed, a balanced diet (i.e. a lot of organic and brightly colored foods) will provide most of the nutrients you need. But the truth is that most people do not have a balanced diet and are unwittingly often deficient in important nutrients.
A balanced diet is one that is rich in good quality protein, low in sugar, salt, caffeine and industrially created trans-fats (trans-fatty acids or partially hydrogenated oils) and soy, uncontaminated by heavy metals, free of nicotine, alcohol and recreational drugs. This is why routine supplementation with the following nutrients could enhance preconception readiness:
•Folic acid (400 micrograms daily)
•Vitamins D-3 1,000U daily; Viamin A (2565 IU daily); B6 (6mg -10 mg daily); B12 (12-20 mcg per day); C- (2,000 mg a day for both men and women); E (both sexes should get 150-200U daily)
•Co-enzyme Q10 (400-600mg daily )
•Amino acids such as L-Carnitine (3 grams daily) and L-arginine (1 gram per day )
•Omega 3 fatty acids (2,000mg per day)
•Minerals, mainly zinc (15mg per day); selenium (70-100mcg per day); iron (up to 20mg per day ); magnesium (400mg per day )
There are likely to be significant reproductive health benefits (including enhanced fertility and intrauterine development) associated with the use of nutritional supplements. However there are also certain potential pitfalls associated with their use. Some supplements are not as safe as they would seem. For example, excessive intake of fat-soluble vitamins (A, D, E and K) can even be dangerous to your health and may be associated with fetal malformations.
Additionally, numerous supplements have been found to contain contaminants such as toxic plant materials, heavy metals and even prescription medications that can compromise fetal development. Prior to the passage of the Dietary Supplement Health and Education Act of 1994, supplements (vitamins, minerals, amino acids, and botanicals) were required to demonstrate safety. However, since passage of “the Act”, they are now presumed to be safe until shown otherwise, thus establishing a rather hazardous situation where a typical prenatal vitamin that will provide sufficient vitamins and minerals for a healthy early pregnancy and potentially dangerous supplements can and are being sold in the same store without product liability.
What about the use of dehydroepiandrosterone (DHEA)? DHEA is a male hormone supplement that is metabolized to androstenedione and testosterone in the ovaries. While a small amount of ovarian testosterone is needed for optimal follicle and egg development, too much testosterone could be decidedly harmful. DHEA supplements probably won’t do harm if taken by healthy young women who have normal ovarian reserve, but they probably would not derive any benefit either. However, in my opinion, DHEA supplementation could be potentially harmful when taken by women with diminished ovarian reserve (DOR), women who have polycystic ovarian syndrome (PCOS) and older women in their 40’s as such women often already tend to have increased LH-activity, leading to increased ovarian testosterone. Additional ovarian testosterone in such women, could thus potentially compromise follicle development and egg quality/competency.
In summary: Maximizing reproductive performance and optimizing outcome following fertility treatment requires a combined strategy involving a balanced diet (rich in protein, low in sugars, soy and trans-fats), modest nutritional supplementation, limiting/avoiding foods and contaminants that can compromise reproductive potential, and adopting disciplined lifestyle modification such as not smoking, reducing stress, minimizing alcohol intake, avoiding nicotine and recreational drug consumption, and getting down to a healthy weight through diet and exercise.
5. Is there such a thing as cytoplasmic immaturity even though MII has occurred in an egg, causing poor embryo quality by day3?
A: Not in my opinion! There is a great deal of confusion when it comes to defining egg “quality.” Most people interpret terms such as “mature/immature/post-mature” eggs as implying that the timing of egg retrieval was off. This is, at best, a gross over-simplification and at worst, dangerously misleading.
Egg Maturation involves reduction of the number of chromosomes from 46 (the diploid number) to 23 (haploid) through reproductive division (meiosis) that begins 36-42 hours prior to ovulation or egg extraction. The fact that meiosis has occurred can be confirmed through the detection of a small membranous body under the outer envelopment (zona pellucida) of the egg, known as the 1st polar body (PB-1) which contains chromosomes that are discarded with meiosis.
In the natural ovulation cycle meiosis is triggered by a spontaneous LH surge (measurable by home ovulation testing) which precedes ovulation by 38-42 hours, or so. In ART cycles, meiosis can be triggered through inducing the same LH surge by way of administering a GnRH agonist (GnRHa) such as Lupron or Buserelin or through the administration of hCG (e.g. Pregnyl/ Profasi/ Novarel/ Ovidrel) that acts similar to LH.
Clearly, in order for an egg to fertilize, it must first mature (M2). Ordinarily, an M1 egg cannot fertilize normally. However in some cases, extended culture for several hours prior to fertilization will allow M1 eggs to undergo meiosis in the petri dish and become M2s.
So, a mature egg (M2) is one that has gone through meiosis while an “immature” egg (M1), has not. However, the fact that all M2 eggs have indeed undergone meiosis, does not imply that the meiotic process was orderly. In fact, the vast majority of M2 eggs are aneuploid (i.e. they do not have the exact required haploid number of 23 chromosomes.) Upon fertilization, such aneuploid embryos that have more or less than 46 chromosomes will be “incompetent” and unable to propagate a healthy pregnancy. They will either arrest during development, fail to attach to the uterine lining, be lost as early miscarriages or develop into chromosomally compromised babies (e.g. Down syndrome). One of the largest “misconceptions” is that all M2 (mature) eggs are equally competent to fertilize and propagate viable embryos. Nothing could be further from the truth.
Since all M1, and most M2 eggs are aneuploid and “incompetent”, use of the term “immature” to differentiate between “competent” and “incompetent” eggs can be highly misleading. In addition, some M2 eggs are incompetent because they are “post-mature” Thus the term “dysmature” would better characterizes the status of such eggs.
While advanced maternal age is by far the commonest cause of egg dysmaturity, implementation of suboptimal protocols for ovarian stimulation can have the same effect. And here, independent of age, women who have diminished ovarian reserve (DOR) are the most vulnerable and here, the combination of advanced age + DOR is the most lethal combination of all.
I have in the past repeatedly pointed out that in my opinion, over-exposure of developing eggs/follicles to excess LH-induced testosterone can and often does compromise development and maturation. This is most prevalent in older women with DOR on drugs and/or stimulation protocols that increase LH-induced ovarian testosterone production. Examples include the use of clomiphene or Letrozole, “flare” agonist (e.g. Lupron, Buserelin) protocols, supplementation with hCG or testosterone during ovarian stimulation or over-dosage with LH/hCG containing gonadotropins (e.g. Menopur.) In my opinion, for women with DOR, a long pituitary down regulation protocol, coming off a birth control pill or off a natural cycle, with subsequent conversion to an antagonist (Ganirelix/Orgalutron/Cetrotide) at the onset of menstruation, followed by an FSH-recombinant stimulation and 10,000U hCG (Pregnyl/Profasi/Novarel) or 500mcg Ovidrel “trigger”, is preferred.
And, for women at high risk of developing severe ovarian hyperstimulation syndrome-OHSS (e.g. those with PCOS and women with hypogonadotropic ovulation dysfunction), I argue against cutting the period of ovarian stimulation short in order to arrest the hyperstimulation process, use of a lower “trigger “dosage of hCG or the using of an agonist (Lupron/Buserelin) “trigger”. Instead, I recommend use of a low-gonadotropin, long pituitary agonist down-regulation protocol combined selectively with “prolonged coasting.” In my opinion, use of the former, while capable of reducing OHSS-related maternal complications, does so at the expense of egg maturation, while the latter protects against OHSS while (provided it is implemented correctly) does so without prejudicing egg development.
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.
•Why did my IVF Fail
•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
•How Many Embryos should be transferred: A Critical Decision in IVF.
ANNOUNCEMENTS:
1.About my Retirement by mid-2018:
After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to plan on retiring from full-time clinical medicine within a year. If you are interested in my medical services prior to my retirement, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com. You can also apply online at http://www.SherIVF.com.
2.The 4th edition of my newest book ,
“In Vitro Fertilization, the ART of Making Babies” is now available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoffrey Sher MD