When I was in the midst of an IVF cycle I was having ultrasounds every second day or so. You get pretty comfortable with your doctor putting a wand up your vajayjay and looking at your lady parts. My doctor without fail would always say ‘Oooh, you’ve got a beautiful lining, a beautiful beautiful lining.’
We never planned to transfer on a treatment cycle so my lining thickness was irrelevant. My doctor said it to soften the blow before we got to my disappointing ovaries.
I got an email the other day from a lovely lady who wanted to know about thin linings and it really got me curious. So I did what I always do and started digging.
WHAT IS THE UTERINE LINING?
You uterus has three layers and the innermost layer is called the endometrium – it’s the layer that thickens in anticipation of an embryo implantation.
During your period, the top functional layer of your endometrium fragments and sheds. Afterwards, during the first half of your cycle (before ovulation) your ovaries produce estrogen which helps the underlying basal layer of your endometrium reconstruct the functional layer. After ovulation, your body produces progesterone which thickens the endometrium further. This also helps increase the number of blood vessels in the lining, in anticipation of implantation.
If fertilisation doesn’t occur, your progesterone levels drop which causes your endometrium to fragment and shed, and you get your period.
WHAT DOES ‘THIN LINING’ MEAN?
A typical cycle is about 28 days. During this time your endometrial lining should increase, starting at 3mm at the end of your period and, once your oestrogen levels are in full swing, it should thicken by around 1mm a day till it’s at optimum levels. Ideally, the optimal lining thickness is between 10 – 13mm at around day 21 of your cycle, the day implantation is most likely to happen.
Typically, ‘thick’ is considered anything more than 8mm. When the endometrium is thiner than this, the embryo will have problems implanting. If the embryo does implant, a thin endometrium may not be able to supply the necessary nutrients to maintain the pregnancy.
This study (Source) suggests that a thin layer may lead to an abnormally high concentration of oxygen in the epithelial cells, causing a rise in free radicals which can be toxic to cells (and an implanting embryo!)
It’s been shown (Source, Source) that implantation rates are higher when the endometrial thickness is greater than 9mm. This study (Source) showed that a positive beta, ongoing pregnancy and live-birth rates increase significantly with increasing endometrial thickness, independent of the effects of patient age and embryo quality.
In saying that, live delivered pregnancies are possible despite thin endometrial lining (5mm or less) but the pregnancy rate is poor (only 5.7%. Source).
As a personal (and very non-scientific, so take it with a grain of salt) example, in my last round of IVF my lining was measured every few days. Here’s my thickness during the first half of my cycle:
CD 04 – 3.7mm
CD 09 – 9.0mm
CD 11 – 9.8mm
CD 13 – 10.7mm
WHAT CAUSES THIN ENDOMETRIAL LINING?
Low oestrogen/low progesterone
Your cycle is run by oestrogen and progesterone, so if you’re having issues with your lining it could be cause by a lack of oestrogen (pre ovulation) or by low progesterone (after ovulation) (Source).
If you get regular scans and bloods your RE can explain what is happening with your lining. If it’s clear you have a thin lining, your RE might prime your uterus with oestrogen medications during a cycle to see if the endometrium thickens. If it doesn’t, it’s an indication that hormones my not be your problem.
Inadequate blood flow
If there isn’t enough blood flow to your uterus, your lining is unlikely to thicken. This study (Source) found a correlation between issues with blood flow in the uterine radial artery and a thin lining, in comparison with normal lining.
This was also associated with poor growth of the epithelial tissues (they line the cavities and surfaces of blood vessels and organs), poor vascular (blood vessel) development and a decrease in vascular endothelial growth factor (a signal protein produced by cells to create new blood vessels).
Overuse of Clomid
Clomid (Clomiphene citrate) is a drug that helps ovulation, and is often a first line treatment for infertility. It works by attaching to your estrogen receptors which trick your body into thinking your estrogen levels are low. This triggers the production of GnRH (gonadotropin releasing hormone) within the hypothalamus. This, in turn, stimulates the pituitary gland to increase production of follicle stimulating hormone (FSH) which triggers activity in your ovaries to stimulate follicles and induce ovulation. (Source, Source)
Since Clomid is an antiestrogen, using it can cause a blockage in the stimulation of estrogen in your lining. Clomid has two parts. Once you stop taking Clomid, one part leaves the body within a week while the other one remains, acting as an anti-estrogen for up to six weeks.
When Clomid is used for more than three months in a row, the anti-estrogen isomer build-up causes thinning of the uterine lining. Several studies have found endometrial lining thickness is significantly thinner in women taking Clomid than women not taking Clomid. (Source, Source, Source, Source)
It’s strongly suggested that a thin endometrium caused by Clomid is due to impaired lining growth thanks to the lack of estrogen. This is a major cause of poor pregnancy rates in women who showed a thin endometrium by Clomid treatment. (Source)
Fibroids are growths that can develop in the uterus. They form from muscle cells that grow abnormally. As they grow, they develop into non-cancerous tumours.
It’s not clear what cause fibroids to grow. It appears they’re (at least in part) genetic, so if your mother had fibroids it’s likely you might also (Source). If you’re obese (Source), black (Source) or eat a lot of red meat (Source) you are more likely to get fibroids.
There are several different kinds of uterine fibroids:
- Submucosal fibroids are found inside the uterus.
- Intramural fibroids are found inside the wall of the uterus, typically just underneath the endometrium.
- Subserosal fibroids are outside the uterus.
This study (Source) compared 163 patients with fibroids (in any location) to patients without fibroids, and found no statistically significant differences between endometrial thickness.
However, they did find that some fibroids had an effective on the the pattern of the lining. Typically your endometrium is made up of glands that grow through out your cycle. These glands grow in a kind of pattern as your cycle processes.
They found that patients with fibroids of any size or in any location had glands that grew with a non-proliferative pattern when compared to patients without fibroids. This in turn was associated with less live births.
Intramural fibroids had a 4% nonproliferative rate and a 31.4% live birth rate. Intramural fibroids that was on the edge of the uterus was even more likely to have a nonproliferative endometrial pattern (5.3%) and a significantly reduced live birth rate (19.1%).
Subserosal fibroids appeared to have no effect on endometrial pattern or thickness, as might be predicted. This was also supported by this study (Source) which suggested subserosal fibroids do not appear to have an impact on fertility.
Returning to lining, the current treatment plan for fibroids is to suppress estrogren/progesterone production. It’s thought fibroid growth is associated with estrogen/progesterone, so by suppressing the hormones you suppress fibroid growth. This is shown when a woman enters menopause and her hormones decrease, fibroids tend to shrink in size on their own (Source). However, this will interfere with endometrial development (and the thickness of your lining).
There was also this case study (Source) where a patient had a uterine artery embolization for her fibroids. An artery embolization is where the arteries that supply blood to the fibroids are blocked, causing the fibroids to shrink. However, by blocking these arteries you are blocking the blood supply to the uterus and the endometrium, which could permanently stop your periods and any lining growth.
Oral Contraceptives with Progestin
Progestin is a synthetic progestogen similar to progesterone. It’s the active ingredient in the injected contraceptive Depo Provera (medroxyprogesterone) and the intrauterine device (IUD) Mirena.
It’s also used in oral contraceptive pills. Typically oral contraceptives are pills that contain both estrogen and progestin – they block ovulation and your body is less receptive to a fertalised egg during ovulation. Some oral contraceptives contain only progestin. These pills make the cervical mucus thick, preventing sperm entry to your uterus.
Long term use of progestin, especially at higher doses thins your lining by decreasing the size and number of glands in the endometrium and reducing the spaces inside cells (known as the cytoplasm of a cell). (Source, Source, Pages 40-53).
This study (Source) found that using a oral contraceptive consistently provided a thin endometrium, helpful before a hysteroscopy. Not helpful if you’d like an embryo to implant.
After a dilation and curettage (D&C)
Dilation and curettage (D&C) is a procedure to remove tissue from inside your uterus. It’s performed to diagnose and treat certain uterine conditions — such as heavy bleeding — or to clear the uterine lining after a miscarriage or abortion.
This study (Source) followed 444 women, and measured their lining one day before ovulation, and a 5-7 days after. They split the women into groups, depending on the number of D&C’s they had.
Mean lining measurements 1 day before ovulation:
0 D&Cs – 10.00mm ± 0.58
1 D&Cs – 9.83mm ± 0.47
2 D&Cs – 8.90mm ± 0.92
3 D&Cs – 7.42mm ± 0.18
4 D&Cs – 7.40mm ± 0.07
Mean lining measurements 5-7 days after ovulation:
0 D&Cs – 10.62mm ± 0.68
1 D&Cs – 9.64mm ± 0.49
2 D&Cs – 8.48mm ± 0.96
3 D&Cs – 6.32mm ± 0.15
4 D&Cs – 6.90mm ± 0.04
You can see that the more D&Cs that were had, the smaller the lining thickness. They measured the estrogen and progesterone levels and found no significant correlation in these ladies (indicating it was likely to be the D&C, and not a hormone problem). They also looked at age and found no significant correlation there either.
This study (Source) followed 1400 women through their IVF cycles. 13 women had persistently thin endometrium linings of 7mm or less. They found that when a persistently thin endometrium was because of D&Cs, even if the thickening of the lining eventually occurred, the pregnancies that resulted in a live birth were few.
This could be because of resulting scar tissue, leading to Ashermans Syndrome.
Ashermans syndrome/Intrauterine adhesions
Also known as: uterine/cervical atresia, traumatic uterine atrophy, sclerotic endometrium, endometrial sclerosis, and intrauterine synechiae.
Asherman’s syndrome is characterised by adhesions or scar tissue in the endometrium. Adhesions are bands of tissue that can form between organs (like your uterus, fallopian tubes or ovaries) or between your organs and the wall of the abdomen
This typically is caused by a D&C (dilation and curettage) on a recently pregnant uterus where the uterine wall was scraped with too much force damaging both the functional layer and the underlying basal layers of the endometrium. (88% of cases, Source)
Asherman’s syndrome can also be caused after the removal of polyps and fibroids from the uterus, or even a cesarean (Source) or a uterine bacterial/inflammation infection.
If your endometrium is scarred and blocked with adhesions, your lining is unlikely to respond to the estrogen, which means your lining is unlikely to thicken. You may find your periods are shorter and less heavy (Source). If the adhesions are not removed, it’s likely they’ll block the flow of blood from your period and could cause endometriosis (Source).
One study (Source) discovered a correlation between Müllerian/Paramesonephric duct anomalies and uterine adhesions. Like other organs, your reproductive organs take shape when you’re a fetus. Your uterus and fallopian tubes develop from two ducts known as the Müllerian/Paramesonephric ducts.
During normal development, these ducts fuse together forming a single uterus with an open cavity and two fallopian tubes. Sometimes these don’t form like they should, and these are called Müllerian/Paramesonephric duct anomalies.
It’s thought that because women with Müllerian/Paramesonephric duct anomalies are predisposed to miscarriages, they are likely to have a higher rate of D&Cs performed which leads to a higher incidence of Asherman’s syndrome.
In-Utero exposure to diethylstilbestrol (DES)
Diethylstilbestrol is a synthetic, non-steroidal estrogen that was created in 1938 (Source).
From about 1940 to 1971, DES was given to pregnant women in the mistaken belief it would reduce the risk of pregnancy complications and losses. In 1971, DES was shown to cause clear cell carcinoma, a rare vaginal tumor in girls and women who had been exposed to this drug in utero. Follow-up studies have indicated that DES also has the potential to cause a variety of significant adverse medical complications during the lifetimes of those exposed, like that of a decreased endometrial thickness (Source).
Note: I’ve included this, as the book does explicitly confirm the link, but it doesn’t provide sources and I couldn’t find any explicit studies. In saying that, there is a close structural similarity between DES and clomid, which has been shown to cause thin linings could explain why the administration of clomiphene to DES daughters is more likely to result in a thin lining.
SK3 – Calcium activated potassium channel 3
This may be a bit of a stretch, but in the interest of providing as much information I can I’m including it. It’s quite scientific, and took me a while to understand. Inside the structure of a cell, there are potassium channels. These channels are membrane proteins that control the flow of ions across the membrane to control electrical signals, and they’re found in virtually all living organisms.
Calcium activated potassium channels are potassium channels gated by calcium. Calcium ions are important for cell signalling, as once they enter cytoplasm (thick solution that fills each cell) they regulate some of the enzymes and proteins.
SK3 is a calcium activated potassium channel that belongs to a family of small conductance channels. We know these channels exist in the endometrium lining. This study (Source) found that a reduced number of SK3 was associated a thin endometrium and unsuccessful pregnancies.
The idea is that with less SK3 in the endometrium meant a rise a cytosolic calcium – the amount of calcium in the cytoplasm – and an increase in membrane hyperpolarization. This is where the membrane potential is negative, and inhibits cell events. The membrane requires a larger stimulus to get it moving again. In chemical speak: membrane hyperpolarization is induced by thapsigargin, a Ca(2+)-ATPase inhibitor, cell migration, and F-actin assembly.
Essentially – the less SK3 channels found in the endometrium, the more likely you are to have a thin endometrium. The same study found similar results in SK3 channels in mice.
Other Causation Notes:
I looked into a link between pelvic inflammatory disease/chronic bacterial infections and lining. Essentially, it’s a bacterial infection in the uterus, fallopian tubes and ovaries that could cause scarring in the fallopian tubes (most likely) but in extreme cases can cause scarring of the endometrium, which may prevent the lining from growing. At that point, it’s essentially Ashermans Syndrome.
I also looked into a link between a retroverted (tilted) uterus and thin lining, but I couldn’t find any research to indicate a correlation between the two.
I also couldn’t find any research that linked a sedentary lifestyle with a thin endometrium. While I understand the theory (being active increases blood pumping around your body, which should increase the blood moving to the uterus) I couldn’t find any scientific research linking the two.
While there is some research that covers studies where the patient had both premature ovarian failure and a thin lining, there isn’t any research indicating that premature ovarian failure causes thin lining.
WHAT HELPS THICKEN ENDOMETRIAL LINING?
hCG stands for Human Chorionic Gonadotropin. It’s a hormone produced by an embryo after implantation. It’s hCG that is detected in pregnancy tests. LH stands for Luteinizing Hormone. When your eggs are mature you’ll get a spike of LH in your cycle, which triggers ovulation and helps your follicles/ovaries produce oestrogen/progesterone.
It’s thought that in your endometrium lining there are LH/hCG receptors. This small study (Source) was a proof of concept study, and hypothesised that if hCG was given early in your cycle, when your eggs and follicles are growing and maturing it might help your endometrium.
They gave 17 patients with previous implantation failures and resisting thin endometrium oestrogen, and part way through, 7 days of hCG. This was used to prime the lining before progesterone was started. They found the endometrial thickness increased from 5.2mm to 6mm. A third of the patients had a 20% thickness increase after HCG priming. Unfortunately, 29% had no change. Surprisingly, seven of the women became pregnant after, which suggests that receptivity of the uterine lining may have normalised.
hMG stands for human menopausal gonadotropin – it’s a synethetic medication extracted from the urine of post menopausal women. It’s used because it reflects the state of menopause, with high levels of FSH and LH. FSH stands for Follicle Stimulating Hormone, it helps control your menstrual cycle and the production of eggs by the ovaries. LH is Luteinizing Hormone – when your eggs are mature you’ll get a spike of LH in your cycle, which triggers ovulation and helps your follicles/ovaries produce oestrogen/progesterone.
This study (Source) had women with a lining thickness of less than 6mm on the cycle days 6-10 split into two groups. One took hMG daily, and the other oestrogen (known as micronized 17beta-estradiol). They did ultrasounds every few days to measure the lining. They also measured the number of follicles and how many eggs were mature at the time of retrieval.
In both groups the lining thickened. However, low-dose hMG resulted in larger follicles and a significantly higher number of mature eggs (15.1% vs. 10.5%).
Progynova patches contain estrdiol (a version of estrogen). They’re applied to the skin release around 100 micrograms of estradiol every 24 hours. This is called ‘transdermal therapy’ as the medication is absorbed via the skin. This case study (Source) had a patient that improved her endometrial thickness to 7.6mm, and was able to carry twins. This particular case should be taken as grain of salt though, as it’s a single patient and may not work for everyone.
Increasing uterine radial artery blood flow.
(via Vitamin E, L-arginine and Viagra)
The radial aterty are the secondary veins that supply blood into the endometrium. By increasing the blood flow through the radial arteries, the theory is that it will improve the endometrial lining.
This study (Source) measured 61 patients who had a lining thickness of less than 8mm, and a high radial artery resistance.
This a measure of blood flow. Essentially, blood flow through a vessel (like a vein, or the uterine radial artery) has a particular pattern that can be seen with an ultrasound. This pattern is caused by two different pressures – one from the heart as it beats blood through your body and the other pulled by the organ it supplies blood too. Most of the peripheral resistance is offered by arterioles (smaller blood vessel that branches out from an artery and leads to capillaries, like the radial artery) because of changes in the vessels wall muscles (Source).
A high radial artery resistance indicates a low rate of blood through through the vessel, to the endometrium.
These patients were given several supplements to help widen the radial artery. They were split into three groups: Vitamin E (which can act as an anticoagulant, which thins the blood and prevents it from clotting (Source), L-arginine (is an amino acid, which is converted into nitric oxide inside the body. This causes blood vessels to open wider for improved blood flow) and Viagra (which enhances signalling through the nitric oxide pathway, improving blood flow when taken vaginally).
Please be aware before I share the numbers, that the sample sizes were small (approximately 12 patients per group).
Vitamin E improved the lining (for 52% of patients) and the radial artery resistance (72%). This group also had samples of their endometrium examined in a few patients (5) and they found Vitamin E improved the glandular epithelial growth, the development of blood vessels, and vascular endothelial growth factor protein expression in the endometrium.
L-arginine improved the lining (for 67% of patients) and the radial artery resistance (89%).
Viagra improved the lining (for 92% of patients) and the radial artery resistance (92%).
The control group, only one person (10%) improved in either the lining or the radial artery resistance.
Improving Blood Flow with Pentoxyfylline + Vitamin E
This retrospective (Source) looked at how blood flow to the endometrium could be improved with Pentoxyfylline and Tocopherol (otherwise known as Vitamin E).
Pentoxyfylline is tablet typically used to improve circulation. It’s a hemorrheologic agent that helps blood flow through narrowed arteries. Tocopherol is a family of Vitamin E compounds. Naturally sourced vitamin E is called d-alpha-tocopherol.
20 women who hadn’t responded to conventional hormonal stimulation and linings 6mm or less were prescribed both Pentoxyfylline and Tocopherol. As it was a retrospective study, all the women took the medication from anywhere between 1-18 months. However, 73.7% of women showed an improve in endometrial thickness, moving from a mean thickness of 4.37 mm (+/-1.5 mm) to 6.05 mm (+/-1.83 mm) after the treatment. 40% went on to become pregnant.
Acupuncture to improve blood flow
There are a small number of acupuncture studies with variable quality, so it’s not clear how effective acupuncture is, exactly. There have been some basic research studies which suggest that acupuncture can help regulate the blood flow of different organs, like the heart (Source, Source) the skin, and muscles (Source, Source) in both animals and humans.
This study (Source) measured the spread of blood flow before and after acupuncture. They found that acupuncture increased blood flow.
There was only one study I could find that mentioned endometrial thickness explicitly. The study (Source) looked at how acupuncture effected the endometrium and hormone levels of rats who were taking clomid (a drug that stimulates your ovaries to release eggs). They found no significant differences in endometrial thickness between the acupuncture and no acupuncture groups.
Other studies looked at uterine blood flow. We know that if there isn’t enough blood flow to your uterus, your lining is unlikely to thicken. This study (Source) found a correlation between issues with blood flow in the uterine radial artery and a thin lining, in comparison with normal lining.
It’s thought that the positive effect of acupuncture is because it changes the uterine blood flow and momentarily calms down your central nervous system’s tendency for flight or fight by sending endorphins (caused by the stress/slight pain of acupuncture). Relaxation and stress reduction is also thought to help (Source).
This clinical trial (Source) looked the pregnancy rate and uterine artery blood flow in 44 patients. They were split into two groups – acupuncture or no acupuncture. They measured the pulsatility index of both the left and right arteries in the patients uterus before and after acupuncture.
Pulsatility index is a measurement of the blood pressure in your arteries. When your heart beats it contracts and pushes blood through your body, which creates pressure on the arteries. This is called systolic blood pressure. Your diastolic blood pressure is the pressure in your arteries when your heart rests between beats. By taking your peak systolic and minimum diastolic measurements and dividing them by the velocity of a full heartbeat cycle you get the pulsatility index.
This study (Source) showed that Uterine Artery resistance (shown with a Pulsatility Index measurement) goes down during the middle a cycle to prepare for implantation, regardless of age or parity.
Returning to the clinical trial, they found that while there was no difference in pregnancy rate between the two groups (had acupuncture group 30%; no acupuncture group, 28.6%). The mean pulsability index of both uterine arteries was significantly reduced after acupuncture (left uterine artery, 2.3 to 2.0; right uterine artery, 2.4 to 2.2). There was no significant change in PI in the group with no acupuncture (left uterine artery, 2.5 to 2.3; right uterine artery, 2.4 to 2.3). So, acupuncture is helpful for improving blood flow to the uterus but looking forward, did not increase the pregnancy rate.
This study (Source) ran a similar 10 women study, but they down-regulated their patients to exclude any hormonal effects. Their patients had acupuncture sessions twice a week for four weeks. A baseline pulsability index was measured before the first treatment and subsequent measurements after the eighth treatment, and then again 10-14 days after.
They found that the mean pulsability index was significantly reduced after the eighth treatment and lingered 10 – 14 days after treatment.
This study (Source) found that electrical stimulation of acupuncture helped improve pulsatility index in uterine ateries to normal levels. It also helped induce ovulation.
GM-CSF stands for Granulocyte Macrophage Colony-stimulating factor. Granulocyte macrophage is a protein that contains a type of white blood cell that protects your body by eating any foreign cells. Colony-stimulating factor is a protein is important in cell signalling – it’s released by cells and affects the behaviour of other cells.
Typically it’s secreted into the fallopian tubes and the uterus a few days after ovulation – when fertilisation is due to take place. The level of GM-CSF will fluctuate throughout your cycle, but is typically at it’s highest in the mid-luteal phase (a few days after ovulation).
GM-CSF is key in early pregnancy, particularly in embryo development and implantation. It’s thought that GM-CSF inhibits the stress response of the embryo cells, stopping cells from dying due to stress (Source).
This study (Source) is a small but positive one. They flooded the uterine with G-CSF of 4 women who couldn’t increase their thickness. These women had already tried estrogeon and medication to widen their blood vessels. Within 48 hours of the infusion all four women had their thickness increase to 7mm, and all four conceived.
This study (Source) was an extension of the previous GM-CSF study. Still small, and uncontrolled but worth a look. It was a pilot of 18 months that followed 21 women with thin lining (anything under 7mm) on the day of their IVF trigger. They’d all tried other treatments which were unsuccessful.
During the next cycle, the day before the trigger GM-CSF was flooded into the uterus with a catheter by slow infusion. If their lining had not reached at least a 7-mm within 48 hours, they got a second infusion after egg retrieval. The mean lining thickness increased from approximately 6.4mm to 9.3mm. The ongoing pregnancy rate was 19.1%.
Hysteroscopic adhesiolysis is the where uterine adhesions (like that caused by Ashermans Syndrome) are broken down, using either microscissors or extreme heat/cold.
This study (Source) followed 187 patients whose uterus was blocked by adhesions. The type of adhesions were varied in severity: mild/filmy adhesions, moderate/fibromuscular adhesions and severe connective tissue adhesions. After treatment, normal mensturation was restored in 88.2% of patients who had menstrual abnormalities (like amenorrhea, hypomenorrhea and dysmenorrhea). Of the 187 patients, 143 women achieved pregnancy, and of those 114 (79%) achieved a live birth.
They found the outcome correlated with the type of adhesions and the extent of the blockages. Patients who had a mild adhesions had a pregnancy rate of 81.3%, while those with severe adhesions had a 31.9% pregnancy rate.
This is a bit a of a reach, but in the interest of sharing everything I’m including it. Generally speaking, stem cells are like a base cell that can grow into any other kind of cell. Some might differentiate and become specific to their task, and some return to the stem cell population to be used again.
An embryo is made up of stem cells, and you’ll often find stem cells in bone marrow. As stem cells have specific markers so they can be identified. It’s thought that the endometrium has a layer of these cells that allow for the lining to regenerate after your period.
This study (Source) followed a women with severe Asherman’s Syndrome, whose lining was perpetually at 3.2mm. When conventional methods failed, they isolated stem cells from her bone marrow and placed them in her endometrium. She was given high rounds of estrogen (pre ovulation) and progesterone (post ovulation) to stimulate the growth of her lining. Her endometrium grew to 7.1mm with good vascularity on transfer day. The embryo implanted and the study followed her pregnancy to week 8.
I’d be wary, as this is a single report with a single patient. I’d want to to see several fleshed out, rigorous scientific studies to understand that the results are repeatable and due to the stem cells.
Other Treatment Notes:
There was no research to indicate that low-dose asprin of baby asprin improved lining thickness. This study (Source) found that there was no demonstrable increase in endometrial thickness in the group that had aspirin. However, there was a statistically significant increase in implantation rates in the aspirin-treated group (24% versus 9%) and also an increase in clinical pregnancy rates in the aspirin-treated group when the final endometrial thickness reading was greater than 8 mm. This study (Source) found similar results.
This study (Source) found no change in endometrial thickness when taking clomiphene citrate or the aromatase inhibitor letrozole.
As always, I’m not a doctor, or a scientist or an expert in anyway. I’m someone who has looked at the research available on the internet (from published scientific journals) and presented what I’ve found. If you have any questions or doubts please please talk to your doctor.