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.
Dr. Sher,
What is your opinion or thoughts about H.E.R. IVF (3 parent IVF). I read about the recent baby that was born using this process to avoid passing a mitochondrial disorder to the baby. However, I have heard that the clinic that pioneered this new technology is introducing this as a possible treatment for DOR/poor egg quality. Is this bunk science or is this a promising new approach for those of us with DOR/poor egg quality?
Thank you for the time you spend answering questions- I am a regular follower and appreciate your approachability to folks who aren’t even your patients!
Kim
Kim!
Lt me just say that I am VERY skeptical. I think this needs to br proven. Presently it offers a pipe dream to women with DOR. It was first suggested as a possibility >20y ago by Cohen and Munne with so called nuclear cytoplasmic exchange. That did not go very far.
So be cautious in accepting at first glance.
G-d bless!
Geoff Sher
Dr Sher
5 Week blood test yesterday came back at 24000. Today light spotting pink and brown. Is this a cause for concern?
Thank you,
I suggest you have an ultrasound done to exclude a molar pregnancy!
Talk to your doctor.
Good luck!
Geoff Sher
Hi Dr Sher, you talk a lot about biological LH. Are you saying this cannot be tested by a blood test? If someone who has DOR has diminished LH throughout their IVF cycle, how would you measure that? A blood test shows my LH to be close to zero.. Are you saying a blood test is not accurate and you would have to test it every minute to check the rise and falls?
I am saying that LH is released in a pulsatile fashion throughout the day and that there are peaks and vale’s. Before the concentration in the blood rises, the valleys must first “fill up”. Having said this, if the LH is very low, it is much less likely that it will be a problem in your case.
Geoff Sher
Dr. Sher, I’m doing a FET cycle and was wondering if a lining at day 14 of 7.2 is too low and would you think of delaying progesterone intake to potentially thicken lining. Also, does ovulation gets delayed or stopped if you take estrogen from day 2 of cycle? Does progesterone intake start just before ovulation? What if ovulation gets delayed too long? Do they only transfer after confirming ovulation? When do they transfer a day 5 frozen embryo? Many thanks for your insight and feedback.
The transfer is done 5-6 days after starting progesterone. However, there is really no point proceeding if the lining at peak estrogen stimulation is <8mm. The results will be very poor, in my opinion.
About seventeen 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.” For those of you who aren’t familiar with the use of Viagra in IVF, allow me to provide some context.
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, 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”
Treatments such supplementary estrogen therapy, aspirin administration and/or administration of high dosage gonadotropin fertility drugs, aimed at improving endometrial development have all yielded disappointing results.
It was in the 90’s that Sildenafil (brand named Viagra) was 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
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.
It is important to recognize that Viagra will NOT be effective in improving endometrial thickness in all cases. In fact, about one third 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).
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.
Good luck
Geoff Sher
Dear Dr. Sher
I write to you because we have just learned that our 4. IVF/ICSI failed. Background: I´m 33, my husband is 32 yrs old. We have a 3,5 year son conceived naturally on the second try. We startet to try again 2 years ago, I had a chemical pregnancy the 2nd month if trying, then nothing. After 10 months I got impatient and we got testet. It showed my husband only had 1 mio. sperm/ml, <2 % morphology, but no issue with motility, . My blodwork came back normal (normal AMH and FSH in particular).
1. IVF-ICSI : antagonist protocol: 9 eggs, 6 fertilised, Day 2 ET of 1 2-cell (some fragmentation) and one a 3 cell. – unsuccessful.
2. IVF-ICSI: Agonist protocol ( 14 days of down regulating) then 11 days of stim: 15 eggs, 9 fertilised, on day 3 there here 3 great 8 -cells. Tried to grow to blast but they all arrested at morula.
3. IVF-ICSI: Agonist protocol again: 18 eggs, 11 fertilised, again, 4 great 8-cells and two 7 -cells, and two 6 cells. Transferred 1 great 8 cell. Not successful , an neither of the other embryos went to blastocyst.
4. IVF-ICSI but this time 50% donor sperm(IVF), 50% my husbands sperm (ICSI). Lower dosis but again agonist protocol. 11 eggs, 8 fertilised, on day 3: Donor: 2 great 8-cells and 2 3-cells, Husband: 2 great 8 cells, 1 7-cell, 1-6 cell. Went to day 5 to transfer the best. But NONE went to blast (not even the embryos with donor sperm.
Where do we go from here? I´ve read that the egg quality is responsible for the first 3 days and then it is the embryos own genome that kicks in. Can it be that my eggs are good quality but something in my genome that I give to the egg is bad? Will it help if I start taking Inositol and other supplements? Is donor egg our only option now? How is it possible that we both have bad quality egg/sperm but still got our son on the 2nd try? !!
I hope you may have some answers for me, I dont feel I my doctor is very helpful.
Thank you in advance!