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.
Dear Dr. Sher,
I’m just coming off another extremely disappointing IVF cycle (#2) and was hoping you might weigh in. A quick background: Both me and husband are 38. Pregnant 6 years ago that resulted in miscarriage at 8 weeks. Nothing since then. I test negative for all genetic mutations/risks – husband is positive for Tay Sachs and has a varicocele and ASA and some morphology issues = but good numbers when washed.
Protocol the same for both cycles:
First cycle & 2nd cycle : 225iu Follistim, 1 unit Menpur for 5 days – add Ganirelix for the next 8 days – triggered day 8 and retrieve day 10
First cycle: 18 Mature/11 Fertilized (ICSI) on day 1 and none made it (they only open incubator on day 5/6)
2nd cycle: 17 Mature/13 Fertilized (ICSI) – day 3 – all were alive – day 5 – none were alive
My doctor refused to hear my plea to do a Fragmentation test on husband – we’ve thought his varicocele could be an issue for years, she didn’t think it would make a difference. She was didn’t’ think diet/vitamins (though we were on vitamins/CoQ10/Folic/vitamin D etc. etc) would make a difference. Her only suggestion was to say that if it was the same result the 2nd time, then we should consider donor eggs. I think this is BS.
Any thoughts??? Suggestions??? Feeling so heart broken… this has been over an 8 year struggle for us.
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.
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.
•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
•Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•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
•How Many Embryos should be transferred: A Critical Decision in IVF.
•The Role of Nutritional Supplements in Preparing for IVF
•IVF Egg Donation: A Comprehensive Overview
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.
Both of my fallopian tubes are gone as they were riddled with endometriosis. Everything else is in place and I have been on birth control to control endometriosis.
In the next few years, I might actually want a baby. Could I still become pregnant, through IVF or some other medical intervention?
Yes you could!
When women with infertility due to endometriosis seek treatment, they are all too often advised to first try ovarian stimulation (ovulation Induction) with intrauterine insemination (IUI) ………as if to say that this would be just as likely to result in a baby as would in vitro fertilization (IVF). Nothing could be further from reality It is time to set the record straight. And hence this blog!
Bear in mind that the cost of treatment comprises both financial and emotional components and that it is the cost of having a baby rather than cost of a procedure. Then consider the fact that regardless of her age or the severity of the condition, women with infertility due to endometriosis are several fold more likely to have a baby per treatment cycle of IVF than with IUI. It follows that there is a distinct advantage in doing IVF first, rather than as a last resort.
So then, why is it that ovulation induction with or without IUI is routinely offered proposed preferentially to women with mild to moderately severe endometriosis? Could it in part be due to the fact that most practicing doctors do not provide IVF services but are indeed remunerated for ovarian stimulation and IUI services and are thus economically incentivized to offer IUI as a first line approach? Or is because of the often erroneous belief that the use of fertility drugs will in all cases induce the release (ovulation) of multiple eggs at a time and thereby increase the chance of a pregnancy. The truth however is that while normally ovulating women (the majority of women who have mild to moderately severe endometriosis) respond to ovarian stimulation with fertility drugs by forming multiple follicles, they rarely ovulate > 1 (or at most 2) egg at a time. This is because such women usually only develop a single dominant follicle which upon ovulating leaves the others intact. This is the reason why normally ovulating women who undergo ovulation induction usually will not experience improved pregnancy potential, nor will they have a marked increase in multiple pregnancies. Conversely, non-ovulating women (as well as those with dysfunctional ovulation) who undergo ovulation induction, almost always develop multiple large follicles that tend to ovulate in unison. This increases the potential to conceive along with an increased risk multiple pregnancies.
So let me take a stab at explaining why IVF is more successful than IUI or surgical correction in the treatment of endometriosis-related infertility:
1.The toxic pelvic factor: Endometriosis is a condition where the lining of the uterus (the endometrium) grows outside the uterus. While this process begins early in the reproductive life of a woman, with notable exceptions, it only becomes manifest in the 2ndhalf of her reproductive life. After some time, these deposits bleed and when the blood absorbs it leaves a visible pigment that can be identified upon surgical exposure of the pelvis. Such endometriotic deposits invariably produce and release toxins” into the pelvic secretions that coat the surface of the membrane (the peritoneum) that envelops all abdominal and pelvic organs, including the uterus, tubes and ovaries. These toxins are referred to as “the peritoneal factor”. Following ovulation, the egg(s) must pass from the ovary (ies), through these toxic secretions to reach the sperm lying in wait in the outer part the fallopian tube (s) tube(s) where, the sperm lie in waiting. In the process of going from the ovary(ies) to the Fallopian tube(s) these eggs become exposed to the “peritoneal toxins” which alter s the envelopment of the egg (i.e. zona pellucida) making it much less receptive to being fertilized by sperm. As a consequence, if they are chromosomally normal such eggs are rendered much less likely to be successfully fertilized. Since almost all women with endometriosis have this problem, it is not difficult to understand why they are far less likely to conceive following ovulation (whether natural or induced through ovulation induction). This “toxic peritoneal factor impacts on eggs that are ovulated whether spontaneously (as in natural cycles) or following the use of fertility drugs and serves to explain why the chance of pregnancy is so significantly reduced in normally ovulating women with endometriosis.
2.The Immunologic Factor: About one third of women who have endometriosis will also have an immunologic implantation dysfunction (IID) linked to activation of uterine natural killer cells (NKa). This will require selective immunotherapy with Intralipid infusions, and/or heparinoids (e.g. Clexane/Lovenox) that is much more effectively implemented in combination with IVF.
3.Surgical treatment of mild to moderate endometriosis does not usually improve pregnancy potential:. The reason is that endometriosis can be considered to be a “work in progress”. New lesions are constantly developing. So it is that for every endometriotic seen there are usually many non-pigmented deposits that are in the process of evolving but are not yet visible to the naked eye and such evolving (non-visible) lesions can also release the same “toxins that compromise fertilization. Accordingly, even after surgical removal of all visible lesions the invisible ones continue to release “toxins” and retain the ability to compromise natural fertilization. It also explains why surgery to remove endometriotic deposits in women with mild to moderate endometriosis usually will fail to significantly improve pregnancy generating potential. In contrast, IVF, by removing eggs from the ovaries prior to ovulation, fertilizing these outside of the body and then transferring the resulting embryo(s) to the uterus, bypasses the toxic pelvic environment and is therefore is the treatment of choice in cases of endometriosis-related infertility.
I am not suggesting that all women with infertility-related endometriosis should automatically resort to IVF. Quite to the contrary…. In spite of having reduced fertility potential, many women with mild to moderate endometriosis can and do go on to conceive on their own (without treatment). It is just that the chance of this happening is so is much lower than normal.
In young ovulating women (< 35 years of age ) with endometriosis, who have normal reproductive anatomy and have fertile male partners, expectant treatment is often preferable to IUI or IVF. However, for older women, women who (regardless of their age) have any additional factor (e.g. pelvic adhesions, ovarian endometriomas, male infertility, IID or diminished ovarian reserve-DOR) IVF should be the primary treatment of choice. 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.
•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!
•Endometriosis and Infertily
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.
Hello Dr Sher
I am reposting my question here as I believe it got burried below.
Thanks for letting me know you don’t recommend Fragmin for protein c deficiency. I asked because I have come across conflicting opinions- one RE said to use Fragmin w/the prot c def, while another one said it won’t make a difference, so I didn’t know what to do. I’m 6 weeks pregnant and already using it but considering switching RE/going off since I don’t want to be considered “high risk” bc of Fragmin if it’s unecessary to take. Why do you advise against it? I really respect your opinion.
Also are there any safe diuretics that you recommend to your patients using steroids? My ND said dandelion and alphalpha tea are safe but I’m not sure I should trust herbs during pregnancy?
Thanks
I have responded to this post earlier tofay!
Geoff Sher
Do you see that AMH levels fluctuate between cycles? One woman had a 2.7 and another time 9.0?
It does fluctuate but if measured correctly this should be within a small and relatively inconsequential range.
Anti-Müllerian hormone also known as AMH is a protein that, is encoded by the AMH gene located on chromosome 19p13.3,. There is an important interaction between AM and its receptor AMHR2 on chromosome 12. AMH is a glycoprotein hormone secreted by Granulosa cells in developing follicles. AMH blood levels in a woman’s blood is an indicator of the remaining quantity of eggs (ovarian reserve) and potentially the number of fertile years the woman may have left and thus provides a valuable tool by which to strategically design a safe and individualized protocol for ovarian stimulation, one that will optimize both egg quantity and quality, AMH levels do does not change during the menstrual cycle, so the blood can be done at any time of the month – even while using oral contraception.
In males: AMH inhibits the development of the Müllerian (paramesonephric) ducts (i.e. embryological rests that develop into the female reproductive apparatus. In males AMH is responsible for irreversible regression of the Müllerian ducts (that are programmed to develop into uterus, Fallopian tubes, cervix and upper two thirds of the vaginal canal) a process that is vital to male sex differentiation. Albeit infrequent, mutations of the AMH gene and certain AMH receptors sometimes lead to failure of the Mullerian system to regress and their subsequent persistence in affected male concepti resulting in failed virilization and phenotypic intersexuality, undescended testes, rudimentary uterus and cryptorchidism.AMH is produced by Sertoli cells in the testicles where it helps facilitate spermatogenesis.
In Females: AMH is produced by ovarian (Granulosa) cells present in early primary follicles that advance from the primordial follicle stage. AMH production decreases and then ultimately eases off as follicles grow beyond 8mm, becoming virtually undetectable in larger follicles . AMH production is greatest in preantral and in small antral stages of < 5mm in diameter. Evidence points to the fact that the size of the cohort of recruited (growing) available follicles in a given cycle is strongly influenced by the size of the remaining pool of primordial (sleeping) follicles. It is against this background that AMH blood levels reflect the size of the remaining egg supply or OR.” A normal blood concentration of AMH points towards a good OR, an abundance of remaining eggs and primordial follicles, that menopause is not imminent and to robust follicular response to ovarian stimulation. A high AMH suggests (often seen in women with irregular menstruation, those with polycystic ovarian syndrome and in very young women) the presence who have very many primordial follicles and are at risk of over-responding to gonadotropin stimulation, placing them at risk of developing very severe ovarian hyperstimulation syndrome (and thus require low dosage stimulation protocols, in readiness for “prolonged coasting”). Below normal AMH levels on the other hand, point to a diminishing ovarian reserve (DOR) suggest an acceleration in the march towards ovarian failure (menopause) , that response to ovarian stimulation with gonadotropins (FSH) is likely to be blunted and accordingly that a more robust stimulation protocol with gonadotropins is called for. It follows that any suggestion that women with DOR (low AMH) might benefit from using “low or mini” stimulation protocols is my opinion, illogical, counter-intuitive and misinformative. AMH levels probably do not reflect egg competency” This is more a function of the woman’s age, intraovarian environment impacted by the underlying cause of infertility and the protocol used for ovarian stimulation (see elsewhere on this blog the article; “IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation”). This having been said, harvesting more eggs at egg retrieval provides the opportunity for a greater number of eggs to fertilize.. However, this does not always translate into more good quality embryos. Nor does it in any way translate into better quality embryos. When it comes to fertilization rate and embryo quality (the rate limiting factor in IVF outcome) egg quality plays the most important role and here, the selection and implementation of a strategic and individualized approach to ovarian stimulation is vital to optimizing IVF outcome. if the person being measured is vitamin D deficient. The table below provides guidelines. Cut-offs are not necessarily as exact as suggested by the compartments below AMH-LEVEL (NTERPRETATION) High (often seen PCOS)> 3.0 ng/ml> 21pmol/L
Normal2.0-3.0 ng/ml14-21pmol/l
Low Normal Range1.0 – 2.0 ng/ml7-14pmol/l
Low0.5 – 1.0 ng/ml3-7pmol/l
Very Low<0.5 ng/ml<4pmol/l
•Low blood Vitamin D levels can falsely lower AMH
•AMH can be measured any time in the cycle.
AMH is not the only test that measures ovarian reserve. Measurement of basal FSH, inhibin B and the antral follicle count should also be considered.
Recommended complementary articles for reading on my blog, to be found on my website, www. sherIVF.com
1.Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
2.Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
3.Ovarian Stimulation for IVF: Comparing “conventional” use of GnRH antagonists to the Agonist/Antagonist Conversion Protocol (A/ACP)
4.IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
5.The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
6.Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
7.Launching Ovarian Stimulation with a BCP: How Does it Affect Response?
Geoff Sher
What do you recommend patients to take as supplements for TTC and is it the same for women over 40? Maca ? DHEA? ,Fish oil, b complex, CQ10
also I wanted to add herbs to this question….?
Thank you Dr Sher
Optimalutrition 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.
Geoff Sher