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.
Hello Dr,
Iam practising Reproductive medicine consultant from India
Thanks for your posts and webinars,very informative
Do you have any blog for doctors discussion?
I would like your inputs on ERA and EFT(ENDOMETRIAL FUNCTION TEST) What do you recommend?
ERA has its limitations of not identifying a pathological endometrium..what is evidence based and how do u optimise these tests for RIF cases where IID has been ruled out.
thank you
Hi Doctor,
I know of no convincing evidence that ERA testing enhances IVF outcome and as such do not recommend it to my patients. However, for those who are insistent that we do ERA, I do provide and act on the results, it after clearly explaining my personal opinion.
Geoff Sher
HI Dr Sher. Are you familiar with the supplement: pregnenolone? I have been taking 20mg per day for about a year, and it’s helped tremendously with energy , thyroid function as well as overall well being. I began preparing my uterus for FET and am struggling with a thin endometrium – 4.1 mm after 14 days of estradiol. Could the pregnenolone supplemenation while stemming with estradiol be part of the cause for the thin endometrium? Can pregnenolone supplementation cause the endo to thin much like progesterone would? Should I just be taking the pregnenolone once I begin progesterone? TIA!!
P.S. The embryo was created using fresh donor eggs
Hi Jackie,
Very Respectfully, I am not a believer in pregnenelone supplementation.
Geoff Sher
I am a single woman who wants to be a single mother by choice. I have tried 3 medicated IUIs and one IVF and none of them worked. I am currently looking into Embryo adoption and have already found a couple who is willing to donate their embryos to me and have worked with you at your clinic. Dhanashree Dhamal is her name. I live in Omaha and there are no clinics here who does embryo adoption and if they do they need me to go through agencies, etc. I would like to know if your clinic would be able to do the transfer for me and if yes what would be the cost. Please let me know if you have any questions. Any help would be appreciated.
The answer is yes!
Please contact Julie Dahan at 702-533-2691 and set up a Skype consultation with me to discuss.
Geoff Sher
Hello I had a beta of 906 on April 11th, then again on April 16th and it was 2833. Dr said my levels and numbers were good but my hcg doubling rate is slow. I was 5 weeks 5 days on April 16. What does the slowing in my doubling mean?
Forgot to mention gestational sac and yolk sac were present at 5 weeks 5 days.
I predict all is well!…Hope I am right!
Good luck!
Geoff Sher
Gooday Dr Sher,
Greetings from South Africa!
Dr Sher, I was on the contraceptive pill for 11 years, I got married, got pregnant and had a miscarriage, that was 7 years ago and since havent been able to get pregnant again. I did an IUI, 1 full stims, 1 FET and 2 FET cancels due to my thin uterine lining. We tried low dosage stims, down regging and estrogen pills and patches and my lining does not get above 6.9mm I had a hysteroscopy and they found no damage, the uterus was in great condition. I have had to change clinics because my current clinic wont try any blood flow meds to even see if they will work. My new dr wants to try viagra and clexane injections in my cycles to see if that improves the lining. This might be my only hope.
My question is, from years of being on the Pill, could this have thinned my lining? Could that be the reason why I dont respond to estrogen and last but not least could Viagra make a difference in this case?
Im absoloutly desperate
Kind regards
Jo
The BCP will not have been the problem as far as the lining is concerned.
It was as far back as 1989, when I first published a study that examined the correlation between the thickness of a woman’s uterine lining (the endometrium), and the subsequent successful implantation of embryos in IVF patients. This study revealed that when the uterine lining measured <8mm in thickness by the day of the “hCG trigger” (in fresh IVF cycles), or at the time of initiating progesterone therapy (in embryo recipient cycles, e.g. frozen embryo transfers-FET, egg donation-IVF etc.) , pregnancy and birth rates were substantially improved. Currently, it is my opinion, that an ideal estrogen-promoted endometrial lining should ideally measure at least 9mm in thickness and that an endometrial lining measuring 8-9mm is “intermediate”. An estrogenic lining of <8mm is in most cases unlikely to yield a viable pregnancy.
A “poor” uterine lining is usually the result of the innermost layer of endometrium (the basal or germinal endometrium from which endometrium grows) ) not being able to respond to estrogen by propagating an outer, “functional” layer thick enough to support optimal embryo implantation and development of a healthy placenta (placentation). The “functional” layer ultimately comprises 2/3 of the full endometrial thickness and is the layer that sheds with menstruation in the event that no pregnancy occurs.
The main causes of a “poor” uterine lining are:
1.Damage to the basal endometrium as a result of:
a.Inflammation of the endometrium (endometritis) most commonly resulting from infected products left over following abortion, miscarriage or birth
b.Surgical trauma due to traumatic uterine scraping, (i.e. due to an over-aggressive D & C)
2.Insensitivity of the basal endometrium to estrogen due to:
a.Prolonged , over-use/misuse of clomiphene citrate
b.Prenatal exposure to diethylstilbestrol (DES). This is a drug that was given to pregnant women in the 1960’s to help prevent miscarriage
3.Over-exposure of the uterine lining to ovarian male hormones (mainly testosterone): Older women, women with diminished ovarian reserve (poor responders) and women with polycystic ovarian syndrome -PCOS tend to have raised LH biological activity.. This causes the connective tissue in the ovary (stroma/theca) to overproduce testosterone. The effect can be further exaggerated when certain methods for ovarian stimulation such as agonist (Lupron/Buserelin) “flare” protocols and high dosages of menotropins such as Menopur are used in such cases.
4.Reduced blood flow to the basal endometrium:
Examples include;
a.Multiple uterine fibroids - especially when these are present under the endometrium (submucosal)
b.Uterine adenomyosis (excessive, abnormal invasion of the uterine muscle by endometrial glands).
“The Viagra Connection”
Eighteen years ago years ago, after reporting on the benefit of vaginal Sildenafil (Viagra) for to women who had implantation dysfunction due to thin endometrial linings I was proud to announce the birth of the world’s first “Viagra baby.” Since the introduction of this form of treatment, thousands of women with thin uterine linings have been reported treated and many have gone on to have babies after repeated prior IVF failure.
For those of you who aren’t familiar with the use of Viagra in IVF, allow me to provide some context. It was in the 90’s that Sildenafil (brand named Viagra) started gaining popularity as a treatment for erectile dysfunction. The mechanism by which it acted was through increasing penile blood flow through increasing nitric oxide activity. This prompted me to investigate whether Viagra administered vaginally, might similarly improve uterine blood flow and in the process cause more estrogen to be delivered to the basal endometrium and thereby increase endometrial thickening. We found that when Viagra was administered vaginally it did just that! However oral administration was without any significant benefit in this regard. We enlisted the services of a compound pharmacy to produce vaginal Viagra suppositories. Initially, four (4) women with chronic histories of poor endometrial development and failure to conceive following several advanced fertility treatments were evaluated for a period of 4-6 weeks and then underwent IVF with concomitant Viagra therapy. Viagra suppositories were administered four times daily for 8-11 days and were discontinued 5-7 days prior to embryo transfer in all cases.
Our findings clearly demonstrated that vaginal Viagra produced a rapid and profound improvement in uterine blood flow and that was followed by enhanced endometrial development in all four cases. Three (3) of the four women subsequently conceived. I expanded the trial in 2002 and became the first to report on the administration of vaginal Viagra to 105 women with repeated IVF failure due to persistently thin endometrial linings. All of the women had experienced at least two (2) prior IVF failures attributed to intractably thin uterine linings. About 70% of these women responded to treatment with Viagra suppositories with a marked improvement in endometrial thickness. Forty five percent (45%) achieved live births following a single cycle of IVF treatment with Viagra The miscarriage rate was 9%. None of the women who had failed to show an improvement in endometrial thickness following Viagra treatment achieved viable pregnancies.
Following vaginal administration, Viagra is rapidly absorbed and quickly reaches the uterine blood system in high concentrations. Thereupon it dilutes out as it is absorbed into the systemic circulation. This probably explains why treatment is virtually devoid of systemic side effects
It is important to recognize that Viagra will NOT be effective in improving endometrial thickness in all cases. In fact, about 30%-40% of women treated fail to show any improvement. This is because in certain cases of thin uterine linings, the basal endometrium will have been permanently damaged and left unresponsive to estrogen. This happens in cases of severe endometrial damage due mainly to post-pregnancy endometritis (inflammation), chronic granulomatous inflammation due to uterine tuberculosis (hardly ever seen in the United States) and following extensive surgical injury to the basal endometrium (as sometimes occurs following over-zealous D&C’s).
Combining vaginal Viagra Therapy with oral Terbutaline;
In my practice I sometimes recommend combining Viagra administration with 5mg of oral terbutaline. The Viagra relaxes the muscle walls of uterine spiral arteries that feed the basal (germinal) layer of the endometrium while Terbutaline, relaxes the uterine muscle through which these spiral arteries pass. The combination of these two medications interacts synergistically to maximally enhance blood flow through the uterus, thereby improving estrogen delivery to the endometrial lining. The only drawback in using Terbutaline is that some women experience agitation, tremors and palpitations. In such cases the terbutaline should be discontinued. Terbutaline should also not be used women who have cardiac disease or in those who have an irregular heartbeat.
About 75% of women with thin uterine linings see a positive response to treatment within 2-3 days. The ones that do not respond well to this treatment are those who have severely damaged inner (basal/germinal) endometrial linings, such that no improvement in uterine blood flow can coax an improved response. Such cases are most commonly the result of prior pregnancy-related endometrial inflammation (endometritis) that sometimes occurs post abortally or following infected vaginal and/or cesarean delivery.
Viagra therapy has proven to be a god send to thousands of woman who because of a thin uterine lining would otherwise never have been able to successfully complete the journey “from infertility to family”.
To be effective, Viagra must be administered vaginally. It is NOT effective when taken orally. We prescribe 20mg vaginal suppositories to be inserted four times per day. Treatment is commenced soon after menstruation ceases and is continued until the day of the “hCG trigger.” While ideally the treatment should be sustained throughout the first half of the cycle, most women will respond within 48-72 hours. For this reason, Viagra can be used to “rescue” a poor lining after the cycle has already started, provided that there is enough time remaining prior to ovulation, egg retrieval or progesterone administration.
Geoff Sher