Looking for baby#2. After Csection we try to use same protocol. I use to reach 10-14 in lining very fast. No issues for transfer. Now is been
5FET cycles cancel so far. Endometritis detected on the beginning. Lots of antibiotics. No ovaries. No fallopian tubes. Hsg done. No itsmos.
Estrace pill 8 mg a day. Low thickness 6.9, 5.9, 6.4 its being detected with water (mocus) in lining by 2nd and 3rd check up.
This last cycle start low dosis of estrace, 4 mg a day increased slowly Use mucinex DM drain the mucus in 3 days but came back when I started taking 8 mg again. Lining stop growth. Doctors seems lost. Any suggestions ?
Ask Our Doctors
Supporting Your Journey
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 Patients,
I created this forum to welcome any questions you have on the topic of infertility, IVF, conception, testing, evaluation, or any related topics. I do my best to answer all questions in less than 24 hours. I know your question is important and, in many cases, I will answer within just a few hours. Thank you for taking the time to trust me with your concern.– Geoffrey Sher, MD
Fill in the following information and we’ll get back to you.
Water in lining FET
Name: Ana K
WE should talk. I think I can be of help here. Please call my assistant, Patti Converse at 702-533-2691 and set up an online consultation with me to discuss.
Back in 1989, I conducted a study that examined how the thickness of a woman’s uterine lining, known as the endometrium, affected the successful implantation of embryos in IVF patients. The study revealed that when the uterine lining measured less than 8mm in thickness by the day of the “hCG trigger” in fresh IVF cycles, or at the start of progesterone therapy in embryo recipient cycles (such as frozen embryo transfers or egg donation IVF), the chances of pregnancy and birth were significantly improved. In my opinion, an ideal estrogen-promoted endometrial lining should measure at least 9mm in thickness, while a lining of 8-9mm is considered “intermediate.” In most cases, an estrogenic lining of less than 8mm is unlikely to result in a viable pregnancy.
A “poor” uterine lining typically occurs when the innermost layer of the endometrium, called the basal or germinal endometrium, fails to respond to estrogen and cannot develop a thick enough outer “functional” layer to support optimal embryo implantation and placenta development. The “functional” layer makes up two-thirds of the total endometrial thickness and is the layer that sheds during menstruation if no pregnancy occurs.
The main causes of a “poor” uterine lining include:
- Damage to the basal endometrium due to:
-
- Inflammation of the endometrium (endometritis) often resulting from retained products of conception after abortion, miscarriage, or birth.
- Surgical trauma caused by aggressive uterine scraping during procedures like D&C.
- Insensitivity of the basal endometrium to estrogen due to:
-
- Prolonged or excessive use of clomiphene citrate.
- Prenatal exposure to diethylstilbestrol (DES), a drug given to pregnant women in the 1960s to prevent miscarriage.
- Overexposure of the uterine lining to ovarian male hormones, mainly testosterone, which can occur in older women, women with diminished ovarian reserve, and women with polycystic ovarian syndrome (PCOS) who have increased LH biological activity. This hormonal imbalance leads to the overproduction of testosterone in the ovary’s connective tissue, further exacerbated by certain ovarian stimulation methods used in IVF.
- Reduced blood flow to the basal endometrium, often caused by:
-
- Multiple uterine fibroids, especially those located beneath the endometrium (submucosal).
- Uterine adenomyosis, an abnormal invasion of endometrial glands into the uterine muscle.
“The Viagra Connection”
Eighteen years ago, I reported on the successful use of vaginal Sildenafil (Viagra) in treating women with implantation dysfunction caused by thin endometrial linings. This breakthrough led to the birth of the world’s first “Viagra baby.” Since then, thousands of women with thin uterine linings have been treated with Viagra, and many have gone on to have babies after multiple unsuccessful IVF attempts.
Viagra gained popularity in the 1990s as an oral treatment for erectile dysfunction. Inspired by its mechanism of action, which increases penile blood flow through enhanced nitric oxide activity, I investigated whether vaginal administration of Viagra could improve uterine blood flow, deliver more estrogen to the basal endometrium, and promote endometrial thickening. Our findings confirmed that vaginal Viagra achieved these effects, while oral administration did not provide significant benefits. To facilitate treatment, we collaborated with a compound pharmacy to produce vaginal Viagra suppositories.
In our initial trial, four women with a history of poor endometrial development and failed conception underwent IVF treatment combined with vaginal Viagra therapy. The Viagra suppositories were administered four times daily for 8-11 days and stopped 5-7 days before embryo transfer. This treatment resulted in a rapid and significant improvement in uterine blood flow, leading to enhanced endometrial development in all four cases. Three of these women subsequently conceived. In 2002, I expanded the trial to include 105 women with repeated IVF failure due to persistently thin endometrial linings. About 70% of these women responded positively to Viagra therapy, with a notable increase in endometrial thickness. Forty-five percent achieved live births after a single cycle of IVF with Viagra treatment, and the miscarriage rate was only 9%. Women who did not show improvement in endometrial thickness following Viagra treatment did not achieve viable pregnancies.
When administered vaginally, Viagra is quickly absorbed and reaches the uterine blood system in high concentrations. It then dilutes as it enters the systemic circulation, explaining why treatment is virtually free from systemic side effects.
It is important to note that Viagra may not improve endometrial thickness in all cases. Approximately 30-40% of women treated may not experience any improvement. In severe cases of thin uterine linings where the basal endometrium has been permanently damaged and becomes unresponsive to estrogen, Viagra treatment is unlikely to be effective. This can occur due to conditions such as post-pregnancy endometritis, chronic inflammation resulting from uterine tuberculosis (rare in the United States), or extensive surgical damage to the basal endometrium.
In my practice, I sometimes recommend combining vaginal Viagra administration with oral Terbutaline (5mg). Viagra relaxes the muscle walls of uterine spiral arteries, while terbutaline relaxes the uterine muscle itself. The combination of these medications synergistically enhances blood flow through the uterus, improving estrogen delivery to the endometrial lining. However, it’s important to monitor potential side effects of Terbutaline such as agitation, tremors, and palpitations. Women with cardiac disease or irregular heartbeat should not use Terbutaline.
Approximately 75% of women with thin uterine linings respond positively to treatment within 2-3 days. Those who do not respond well often have severe inner ( (basal) endometrial lining damage, where improved uterine blood flow cannot stimulate a positive response. Such cases are commonly associated with previous pregnancy-related endometrial inflammation, occurring after abortions, infected vaginal deliveries, or
Viagra therapy has been a game-changer for thousands of women with thin uterine linings, allowing them to successfully overcome infertility and build their families.
_______________________________________________________
PLEASE SHARE THIS WITH OTHERS AND HELP SPREAD THE WORD!!
Herewith are online links to 2 E-books recently co-authored with my partner at SFS-NY (Drew Tortoriello MD)……. for your reading pleasure:
- From In Vitro Fertilization to Family: A Journey with Sher Fertility Solutions (SFS) ; https://sherfertilitysolutions.com/sher-fertility-solutions-ebook.pdf
- Recurrent Pregnancy Loss and Unexplained IVF Failure: The Immunologic Link ;https://drive.google.com/file/d/1iYKz-EkAjMqwMa1ZcufIloRdxnAfDH8L/view
I invite you to visit my very recently launched “Podcast”, “HAVE A BABY” on RUMBLE; https://rumble.com/c/c-3304480
If you are interested in having an online consultation with me, please contact my assistant, Patti Converse at 702-533-2691 or email her at concierge@sherivf.com\
Fertility
Name: Shakema M
Im answering the add that says ivf no cost
Author
Sorry! I have no knowledge of this!
Geoff Sher
I want to get pregnant but I’m 50+
Name: Chinwe O
I want to do IVF for triplets but I’m 50+. I’m still seeing my circle but this April, it came out one day and stopped
Author
Given the natural and inevitable decline in “egg competency and ovarian reserve with advancing age, the chance of conceiving on your own or through IVF with own eggs is remote.
So sorry!
Geoff Sher
Progesterone use throughout pregnancy
Name: Anna L
Hello doctor,
I spoke with your office, and I understand that you do not follow women’s hormones throughout pregnancy. You help women get pregnant and then pass them to an OB. I’m working with a high-risk OB, but because I had two c-sections previously. I did have one miscarriage once before. After that I happened to have a pregnancy while seeing a GP that works based on NaProTechnology and prescribes bio-identical progesterone during pregnancy. I had a successful pregnancy in 2021, but my levels looked good without the hormone, so I stopped taking that at 20 weeks. I’m pregnant now and my GP has been testing my progesterone and it is much lower than my last pregnancy. I did not go to a fertility clinic before, and my high-risk OB wants nothing to do with looking at my levels. I’m really at a loss for where to go to have a conversation about the use of progesterone and maintaining a pregnancy. My GP said, “the progesterone keeps the baby where it is supposed to be.” So basically, if it drops low I could go into pre-term labor. Based on my conversations with the OB, they would only prescribe progesterone if I had multiple miscarriages. It seems weird to me that someone that does not ever track progesterone could even figure out who needs it and who does not. I know this isn’t what you do, but where can I go to get an opinion about continuing to use progesterone? I’m 31 weeks pregnant and my current GP would have me take this dose of 400mg vaginally twice daily until 37 weeks. I live in Flemington, NJ, but I’m willing to travel. I could try and find another OB, but I thought maybe a fertility clinic would know something about what is usually done during pregnancy to reach full term successfully. I have blood work every two weeks before taking my morning dose and I wanted to discuss these levels with a competent doctor or clinic to get a second opinion.
Author
With very few exceptions. I am not a believer in their being any benefit through progesterone supplementation throughout pregnancy.
Geoff Sher
donante
Name: barbara a
como puedo hacer para ser donante de ovulos
Author
Please re-post in English!
Geoff Sher
Protocol Question
Name: Avery C
I am writing to ask for advice on the proper protocol for me.
Background: I am 32 years old, with a normal BMI. My AMH is 0.11, and my AFC is 3. My husband has male-factor infertility that requires IVF.
For my first round, I stimmed for 23 days. The doctor used 50 mg Clomid (morning/night), Dexamethasone (morning), 300 Gonal (morning), 150 Menopur (PM), and Cetrotide (at night, starting day 17). On day 11 of my first cycle, I was not showing any growth, so the doctor had me discontinue Gonal and Menopur but continue Clomid and Dexamethasone. On day 15, the doctor had me add Menopur back in. This round resulted in 3 eggs being retrieved, resulting in Day 6 5AA and Day 7 5BB embryos, with 1 embryo testing PGT-A normal.
For my second round, my doctor removed Gonal completely and prescribed 50 mg of Clomid (morning and night), Dexamethasone (morning), 150 mg of Menopur (PM, starting day 6), and Cetrotide (starting day 9). This round was canceled on day 10 as I had only 1 lead follicle.
I have spoken with my doctor, and he wants to stay with the same protocol as the failed round 2 and try stimming for longer.
This is the last round that insurance will cover, so I want to maximize my outcome. Do you have any suggestions on a protocol that may be beneficial for my circumstance?
Author
Respectfully, I do not think you were on optimal stimulation protocols. I suggest you call my assistant, Patti (702-533-2691)and set up an online consultation with me to discuss in detail.
Understanding the impact of ovarian reserve on the success of in vitro fertilization (IVF) is crucial when it comes to reproductive health. This article aims to simplify and clarify these concepts, emphasizing their significance in the selection of ovarian stimulation protocols for IVF. By providing you with this information, we hope to shed light on the importance of considering these factors and making informed decisions regarding fertility treatments.
- The Role of Eggs in Chromosomal Integrity: In the process of creating a healthy embryo, it is primarily the egg that determines the chromosomal integrity, which is crucial for the embryo’s competency. A competent egg possesses a normal karyotype, increasing the chances of developing into a healthy baby. It’s important to note that not all eggs are competent, and the incidence of irregular chromosome numbers (aneuploidy) increases with age.
- Meiosis and Fertilization: Following the initiation of the LH surge or the hCG trigger shot, the egg undergoes a process called meiosis, halving its chromosomes to 23. During this process, a structure called the polar body is expelled from the egg, while the remaining chromosomes are retained. The mature sperm, also undergoing meiosis, contributes 23 chromosomes. Fertilization occurs when these chromosomes combine, resulting in a euploid embryo with 46 chromosomes. Only euploid embryos are competent and capable of developing into healthy babies.
- The Significance of Embryo Ploidy: Embryo ploidy, referring to the numerical chromosomal integrity, is a critical factor in determining embryo competency. Aneuploid embryos, which have an irregular number of chromosomes, are often incompetent and unable to propagate healthy pregnancies. Failed nidation, miscarriages, and chromosomal birth defects can be linked to embryo ploidy issues. Both egg and sperm aneuploidy can contribute, but egg aneuploidy is usually the primary cause.
- Embryo Development and Competency: Embryos that develop too slowly or too quickly, have abnormal cell counts, contain debris or fragments, or fail to reach the blastocyst stage are often aneuploid and incompetent. Monitoring these developmental aspects can provide valuable insights into embryo competency.
- Diminished Ovarian Reserve (DOR): As women advance in their reproductive age, the number of remaining eggs in the ovaries decreases. Diminished ovarian reserve (DOR) occurs when the egg count falls below a certain threshold, making it more challenging to respond to fertility drugs effectively. This condition is often indicated by specific hormone levels, such as elevated FSH and decreased AMH. DOR can affect women over 40, but it can also occur in younger
Why IVF should be regarded as treatment of choice for women who have diminished ovarian reserve ( DOR):
Understanding the following factors will go a long way in helping you to make an informed decision and thereby improve the chances of a successful IVF outcome.
- Ovarian Reserve: While chronological age plays a vital role in determining the quality of eggs and embryos [there is an increased risk of egg aneuploidy (irregular chromosome number) in eggs, leading to reduced embryo competency. Additionally, women with declining ovarian reserve (DOR), regardless of their age, are more likely to have aneuploid eggs/embryos. Therefore, it is crucial to address age-related factors and ovarian reserve to enhance IVF success.
- Excessive Luteinizing Hormone (LH) and Testosterone Effects: In women with DOR, their ovaries and developing eggs are susceptible to the adverse effects of excessive LH, which stimulates the overproduction of male hormones like testosterone. While some testosterone promotes healthy follicle growth and egg development, an excess of testosterone has a negative impact. Therefore, in both older women or those who (regardless of their age) have DOR, ovarian stimulation protocols that down-regulate LH activity before starting gonadotropins are necessary to improve egg/embryo quality and IVF outcomes.
- It is possible to regulate the decline in egg/embryo competency by tailoring ovarian stimulation protocols. Here are my preferred protocols for women with relatively normal ovarian reserve:
- Conventional Long Pituitary Down Regulation Protocol:
- Begin birth control pills (BCP) early in the cycle for at least 10 days.
- Three days before stopping BCP, overlap with an agonist like Lupron for three days.
- Continue daily Lupron until menstruation begins.
- Conduct ultrasound and blood estradiol measurements to assess ovarian status.
- Administer FSH-dominant gonadotropin along with Menopur for stimulation.
- Monitor follicle development through ultrasound and blood estradiol measurements.
- Trigger egg maturation using hCG injection, followed by egg retrieval.
- Agonist/Antagonist Conversion Protocol (A/ACP):
- Similar to the conventional long down regulation protocol but replace the agonist with a GnRH antagonist from the onset of post-BCP menstruation until the trigger day.
- Consider adding supplementary human growth hormone (HGH) for women with DOR.
- Consider using “priming” with estrogen prior to gonadotropin administration
- Protocols to Avoid in Women with DOR: Certain ovarian stimulation protocols may not be suitable for women with declining ovarian reserve:
- Microdose agonist “flare” protocols
- High dosages of LH-containing fertility drugs such as Menopur
- Testosterone-based supplementation
- DHEA supplementation
- Clomiphene citrate or Letrozole
- Low-dosage hCG triggering or agonist triggering for women with DOR
Preimplantation Genetic Screening/Testing for aneuploidy (PGS/PGTA): PGS/PGTA is a valuable tool for identifying chromosomal abnormalities in eggs and embryos. By selecting the most competent (euploid) embryos, PGS/PGTA significantly improves the success of IVF, in women with DOR.
Understanding the impact of declining ovarian reserve on IVF outcomes is essential when making decisions about fertility treatments. Diminished ovarian reserve (DOR) can affect egg quality and increase the likelihood of aneuploid embryos with resultant IVF failure. By considering this factor, you can make informed choices and work closely with fertility specialists to optimize your chances of success. Remember, knowledge is power, and being aware of these aspects empowers you to take control of your reproductive journey.
PLEASE SHARE THIS WITH OTHERS AND HELP SPREAD THE WORD!!
Herewith are online links to 2 E-books recently co-authored with my partner at SFS-NY (Drew Tortoriello MD)……. for your reading pleasure:
- From In Vitro Fertilization to Family: A Journey with Sher Fertility Solutions (SFS) ; https://sherfertilitysolutions.com/sher-fertility-solutions-ebook.pdf
- Recurrent Pregnancy Loss and Unexplained IVF Failure: The Immunologic Link ;https://drive.google.com/file/d/1iYKz-EkAjMqwMa1ZcufIloRdxnAfDH8L/view
I invite you to visit my very recently launched “Podcast”, “HAVE A BABY” on RUMBLE; https://rumble.com/c/c-3304480
If you are interested in having an online consultation with me, please contact my assistant, Patti Converse at 702-533-2691 or email her at concierge@sherivf.com\