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What you should know about Thin Endometrial Uterine Lining

By Research 21 Comments

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.


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.


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


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. (SourceSource)

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. (SourceSourceSourceSource)

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). (SourceSource, 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.



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.
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

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.

Stem Cells

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. 

Can Vitex help you with low progesterone?

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A friend emailed me the other day – had I heard of Vitex? The information out there is mixed and she wasn’t sure whether to take it or not. I flicked back a quick email with what I knew (which was mostly to avoid it), but after some thought I decided to look into it proper.

What is Vitex?

Vitex Agnus Castus is the berry from a chaste tree, native to the mediterranean. It’s berries are used in herbal medicine, often used for fertility.

What does it do, really?

Taking Vitex can stimulate your hypothalamus to produce more dopamine. High dopamine levels suppress prolactin (Source) which will go on to increase progesterone production.

This is helpful because progesterone is key to your fertility cycle. After ovulation, your LH levels trigger a change in the corpus luteum (the now empty follicle in your ovary) which starts progesterone production to supports the developing embryo.

If the embryo implants successfully, at week 7 the corpus luteum will tag team progesterone production out with the placenta. If pregnancy did not occur, the corpus luteum disintegrates which causes the progesterone production to fall,  triggering the endometrial tissue to break down and your period will start.

In short, progesterone supports the embryo and maintains your uterus lining so the embryo can implant.

Why is low progesterone a problem?

Short Luteal Phases

Your luteal phase is the time post ovulation before your period begins. It should last 11-14 days, which is the lifespan of the corpus luteum. If your luteal phase is shorter than 11 days, it’s likely your corpus luteum did not form as it was supposed to. This is called a luteal phase defect and is associated with low progesterone. (Source)

Early Miscarriages

Up to 35% of women with repeated or habitual miscarriages have a luteal phase defect. This is thought to be a result of an inadequate maturation and development of the endometrium, or the tissue lining your uterus that the embryo implants into. This in part is due to inadequate progesterone levels. (Source)

Low progesterone values are associated with miscarriages and ectopic pregnancies (both considered non-viable pregnancies) and high progesterone concentrations with viable pregnancies. (Source)

How does Vitex help?

By improving progesterone levels, Vitex can help woman with established luteal phase defect (shortened second half of the menstrual cycle) and high levels of the hormone prolactin.

If you have irregular periods, it may normalise your menstruation cycle and encourage regular ovulation (or it may mess it up completely. The research is mixed).

Is Vitex right for me?

Yes, if you have:

  • Low levels of progesterone post ovulation
  • Luteal phase defect
  • High prolactin levels
  • Irregular periods

If you do not suffer from any of these, it’s unlikely Vitex will help you.

Does it Work?

This double-blind, placebo-controlled pilot study (Source) had a small sample of women (30) who had difficulty conceiving take a nutritional supplement containing vitex (chasteberry) and green tea extracts, L-arginine, vitamins (including folate) and minerals.

The monitored their changes in progesterone level, basal body temperature, menstrual cycle, pregnancy rate and any side effects.

After thee months, the supplement group had increased their progesterone levels and increased the number of days with high basal temperatures (indicating ovulation), while the control showed no change. After five months, 33% of the supplement group were pregnant, while the control group had no pregnancies.

This double blind, placebo-controlled study (Source) had a larger sample (93) of women who had difficult conceiving take Fertility Blend, a supplement containing vitex (chasteberry), green tea, L-arginine, vitamins (including folate) and minerals.

The monitored their changes in progesterone level, basal body temperature, menstrual cycle, pregnancy rate and any side effects.

They monitored the same effects: progesterone level, basal body temperature, menstrual cycle length, pregnancy rate and any side-effects.

After three months, the supplement group had increased their progesterone levels and had significantly increased basal temperatures. Women in the supplement group who had either a short (less than 27 days) or long (>32 days) cycles normalized. The control group (N = 40) did not show any significant changes in progesterone levels, basal temps or menstrual cycle length.

After three months, 26% of the supplement group were pregnant (26%) compared to 10% in the control group (10%; p = 0.01).

In short, taking nutritional supplementation may complement conventional fertility therapy.

Is it safe?

There have been several studies (SourceSource) that suggest taking Vitex will have no substantial adverse effects.

This study (Source) suggests that an adverse events are mild and reversible. The most frequent complaints are nausea/gastrointestinal disturbances, headache, menstrual disorders (such as cycle irregularity), acne, itchiness, dizziness and skin rashes.

Where do I get it? How much do I take?

Vitex comes in many forms, loose herbs, capsules, tea, tincture and powder. Capsules and tincture (a liquid extract) ensure you can control the dosage. It’s quite bitter, so a capsule is often preferable to tincture.

For optimal results, Vitex should be taken for three – six months. In regards to dosage, it’s strongly suggested you visit a neuropath or herbalist to discuss what dosage would be right for you.


  • Talk to your doctor. Talk to your doctor. Talk to your doctor. Or even your clinic’s nurse. Or send your clinic an email. It’s always better to ask than to guess. Even better to talk to a medical professional rather than take advice from the internet.
  • As vitex affects hormone levels – if you are pregnant, stop taking it. The level of progesterone may alter the development of your baby.
  • This goes for anything that is particular hormone-sensitive conditions like breast cancer or oral contraceptive use.
  • Don’t combine with fertility drugs or IVF, as it will interfere with your doses.
  • Don’t take it if you’re under 18. At that age, your pituitary-ovarian communication system is still growing.
  • Vitex can make depression worse, and possibly promote suicidal ideation. If you have a history of depression be VERY cautious with it.

As always, I’m not a professional or a doctor – my experience is just that, my experience. I’ve done an awful lot of reading and research which I’m happy to share. If you do have concerns about low progesterone or Vitex, please talk to your doctor.

How to reasearch scientific fertility studies

By Research No Comments

With IVF there is an awful lot of information online and I’m not always sure what is valid and true and what is hearsay.  I’m a UX designer by trade, which means I typically make my decisions based on data, numbers and studies… but I found that most articles didn’t include their sources. They discussed numbers but didn’t follow it up with references. It made it difficult to know what information to trust.

So, I started doing my own research and reading scientific studies. 

It was intimidating at first. I wasn’t sure where to look or how to find studies or how to know if they were statistically significant, or even relevant to me. First things first though. I knuckled down and just started searching.

1. Write out a list of questions

Sometimes it’s hard to find a starting point. There is so much information it can be overwhelming. To make it easier, I like to structure my research with a series of questions. Typically:

  • What is my body supposed to do?
  • What causes x?
  • What can I do so help x?

If my research was focused on, say, thin endometrium lining, I’d write down:

  • What part does my endometrium lining play in my cycle (ie, what is it supposed to do?)
  • What counts as thin?
  • What effect does a thin endometrium lining have on my fertility?
  • What causes thin endometrium lining?
  • What can I do to help thin endometrium lining?

2. Brainstorm (ie, Google everything)

At this point you want to start collecting ideas. Not everything will be scientifically correct or have supporting research, but that’s okay. Read wikipedia articles, blogs and clinic websites. Visit forums, and ask questions on instagram. 

For everything you find, write bullet points underneath your questions with what you discover. You’ll get a long list of things, hopefully.

For example, whenever I came across anything that suggested it might cause thin endometrium lining, I’d write it under the ’cause’ heading with a link so I could find it again. 

Here’s the beginning of a list I started when I was researching acupuncture:



3. Verify with Research

This is the tricky bit. For every item on your list you want to verify that there is scientific research supporting the truth of what you’ve got.

Visit NetPubMed. URL:

This is the go-to place for research studies. There are so many journals and scientific research publishers and PubMed is the place all the summaries are consolidated. For everything. Every study, whether about fertility or not. You can put in a search term and hey presto, you’ll get research back. 

Be generous with your search terms, and try several variations. For ‘thin lining’ I might pair the correlation I’m looking for (eg ‘uterine fibroids’) with other variations like: ‘uterine lining’, ‘endometrium thickness’, ‘thin endometrium’, ‘thin uterine lining’, ‘uterine lining growth’. 

You’ll get lots back, often animal studies too. It takes some practice to find what’s relevant and what’s not, and this is where the effort is required – wading through all the research to find what you need. Where possible, filter by human studies.

If there is a correlation, you’ll often find half a dozen studies on the link. Go slow, and make sure to google the medical terms until you understand what each sentence implies. You want to make sure there is a correlation between your subject matter (thin endometrium lining, say) and the cause/fix (eg ‘uterine fibroids’). The study should be explicit in it’s results. 

If it’s not, I wouldn’t take it as a correlation, and I’d strike it from your list. Take your time, this is where you separate the truth of what helps and what is just hearsay. 

For every item in your list, you want to find two or three studies that support it. The studies ideally should be double blind, with a large sample across several different populations. They’re not always going to be like that.  

For each point on your list, see if you can find find studies that support and studies that don’t. You’ll get an idea whether the point on your list can be crossed off as unreliable internet myth or if it has some scientific truth and can be taken to the next point. 

4. Talk to your doctor. 

I think this is the most important. For every study I read, for everything I wanted to try, for every forum thread that sounded interesting, I took a list of questions to my doctor to discuss. I wanted to make sure that anything I tried wasn’t going to cause harm. I wanted to make sure my Doctor  was aware of the possibilities (and she always was, which I found comforting) and I wanted make sure that we were trying everything we possibly could.

We changed up my plan a few times because of my research and lists of questions. It made me feel like I was part of the planning process. It was incredibly helpful to talk it out with someone who was in the fertility profession, who equally wanted the best for me.

So. That’s how I research IVF, and how I come up with almost every research based post there is here. 

What are you favourite IVF research tips? How do you guys make your IVF decisions??


By Research One Comment

There’s a huge learning curve with IVF. I remember being at the very beginning of my journey and completely overwhelmed with all of the information. There were acronyms I didn’t get, I wasn’t sure what the best route for me was, what kind of things I should be doing or not doing… it was tough.

I’m not the kind of person who does well with not-knowing, or not feeling like I have a firm grasp of a situation. As there are so many factors in IVF you can’t control, so I was very keen to educate myself and get a handle on what I *could* control. My kindle was filled with books about IVF. Some were better than others, I have to say.

Here’s my top three.

1. It Starts with the Egg. Rebecca Fett

During my first round when I was at my most determined to ‘beat’ infertility, this book was hands down the most helpful in terms of “what can I do right now?” help. All the advice is based on academic research (and studies are shared in the index).

It gives clear and easy to follow actions of things which will make a difference – the positive AND the negative of all sorts – supplements, lifestyle (think: cleaning and beauty products), diet. It also debunks a few myths (example – turns out there is no evidence to suggest that royal jelly improves egg quality or has a higher incidence of pregnancy).

Overall, pretty interesting and well worth a read for anyone TTC, whether you’re starting out or you’re three IVF rounds in.

(Available on or

2. Get A Life: His and Hers Survival Guide to IVF. Rosie Bray and Richard Mackney

This is such a great book – it’s essentially an IVF 101 guide, with what to expect at each stage of IVF and how best to handle it. It’s written by a wife & husband duo who share their unique perspectives on their three rounds of IVF. For each chapter there is a guys and a girl perspective which helps get your head around how different the experience is for each person. This was super helpful for me with my guy – it took me a long time to understand we were processing at different rates. So when Zee  didn’t want to talk about IVF, or would watch TV instead of fill out his forms – it wasn’t that he uninterested in IVF. He hadn’t processed yet. When I realised, I felt like a light bulb had gone off in my head.

They did a great job of highlighting the ups and downs of IVF. It was quite anecdotal but was very readable. There was just as many giggles as tears and you really felt for them. Their initial IVF experiences weren’t too far from mine and it was comforting to know I wasn’t alone. It also has a handy guide of things to ask at your first appointment.

Well worth a read – especially if you haven’t yet been through a round of IVF and would like to know what to expect.

(Available on or

3. IVF: An Emotional Companion. Brigid Moss

Oh this book. It’s the best example of how not alone we are. There are so many paths that lead to parenthood and this book covers the personal stories of large chunk of them – adoption, IVF, male factor infertility, single mums by choice, gay IVF/adoption, older couples, OHSS, diminished ovarian reserve, giving up on IVF, surrogacy… it shares the real life stories of people who have struggled their way through, and the decisions they’ve made.

It was pretty moving –  it was heartbreaking, uplifting and parts were even pretty gory. I realised how often I’ve read the side effects of IVF and dismissed it as if it couldn’t happen it me. When I read the stories of women who it DID happen to I was shocked at how callous I had been. There were plenty of highs, but a lot of lows too. A very honest look at infertility.

It’s a fantastic resource. Each section has a theme, an honest story and resources to find out more.

(Available on or

Other mentions.

I read many and while I wouldn’t put these in the top three, they were helpful in providing perspective.

The Complete Guide To IVF: An inside view of fertility clinics and treatment. Kate Bain.

This book has a good overview of the IVF process and a brief look at the various causes . It was a great behind the scenes look at how clinic’s operate, and what happens outside of the rooms we typically get to see in. I also really enjoyed the technical breakdown of the processes (like ICSI) but wished it could have taken it a step or two further. I wouldn’t call it a complete guide, as it discounts lifestyle choices (like diet) as irrelevant and not helpful. It didn’t provide the tips or the details/studies I was looking for. Side note, it was published in 2010, so parts of it (like freezing) are a little out of date.

(Available on and

The Baby Making Bible. Emma Cannon.

This was a pretty interesting read. Essentially it talks through Eastern Medicine (think: Chinese herbs and philosophy with acupuncture, diet and visualisations) with Western Medicine. While it does have a few nods towards research studies, a lot of the supporting evidence was anecdotal. I enjoyed the ‘look after yourself’ message, as often when trying to conceive there is pressure on the ‘conception’ segment but very little thought given to the rest of your cycle. The idea is that you remove that pressure to conceive and spend some time building up your body. I’m not sure I understood the Chinese type casting and found it quite difficult to take in. I also got the impression that this book is essentially an ad for her clinic.

(Available on and

The Fertile Female. Julia Indichova

I… struggled with this book. I’m very scientifically driven and like data and research and studies. The Fertile Female is not like that – it’s very spiritual. If IVF is about taking care of the medical side of things, this book provides insight into how to take care of your emotional/spiritual side. I found it difficult when I first approached IVF, because I wanted to know what I could do physically to improve my chances. It wasn’t until much later (Round #3) that I cycled back to this book and gave it some proper thought. It encourages you to trust your body and advocate what is best for you. Our doctors often take a very medical approach and it’s up to us to take care of our lifestyle approach.

The most telling for me is that I read this study about how visualising an exercise can make a significant difference. With that in mind, spending the time to visualise what was happening with my body seemed like a good use of time.

(Available on and

The Essential Fertility Guide. Professor Robert Winston.

This is a good beginners book, if you’re new to the world of infertility. He does a great breakdown of what to expect and what to ask, over several different types of infertility. I think the best bit is that Professor Robert Winston suggests you really understand what is happening with your body before you jump to IVF. He mentions the great costs (and thus potential profits) associated with IVF now that it’s so commercialised and provides the information so you can advocate for yourself.

(Available on and

How to Improve Egg Quality: The Smart Way to Get Pregnant. Darja Wagna. 

I really wanted to like this book. I did. It seemed great at first – clear and concise actions you can take to improve egg quality. However there wasn’t enough scientific evidence to back up what she was sharing and I found that parts of what she was suggesting didn’t go into enough detail. An example would be call to take the supplement CoQ10. Yes, you absolutely should take it, but the book didn’t mention that you should be taking the form ubiquinol (and NOT ubiquinone, which is the cheaper and more widely available).  I found it difficult to trust what was being advised.

(Available on and

The Four Hour Body. Tim Ferris. 

This book has nothing specifically to do with fertility. It’s more about about understanding the relationship you body has with food in a weight loss context. Bonus, the low carb diet is pretty IVF friendly, too – because there are some pretty strong correlations between BMI and fertility. I thought it might be relevant. I lost 15kg with the four hour body method, and found it relatively easy to stick to. Essentially, you cut out carbs, dairy and sugar (easier than it sounds, promise!) for 6 days out of 7. .

(Available here on and

GM-CSF Media Improves Embryo Development

By Research No Comments

We’re on round four, so when I sat down with my RE to plan out this last and hopefully final round of IVF I wasn’t expecting anything new. I asked anyway: was there anything we could do to improve the quality of our blastocysts that we weren’t already doing?

I was pretty shocked when she came back with GM-CSF Media. How had I not heard about it before? (That’s always my response – if it helps, why didn’t we do it in the first round?)  Still, I checked it out and was easily convinced – it should help our embryos make it to blastocyst stage. We’re definitely incorporating it this next round.

I couldn’t find a lot of information online that was easily digestible, so I wrote up my notes in the hope it helps someone else.

What is GM-CSF Media?

GM-CSF stands for Granulocyte Macrophage Colony-stimulating factor. Check out that mouthful. As I understand it (and remember, I’m not a doctor or a scientist in anyway shape or form) the GM part – granulocyte macrophage – is a protein that contains a type of white blood cell that protects your body by eating any foreign cells. The last bit, colony-stimulating factor is because this protein is important in cell signalling – it’s released by cells and affects the behaviour of other cells. I think, anyway. The literature is all written in extreme scientist. 

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 helps embryo growth and survival as it cleaves, all ready for implantation.

Why use it with IVF?

Typically, an embryo is naturally exposed to a large number of hormones, proteins and growth factors that are present in a woman’s reproductive system. We know that with IVF, a petri dish is not as good as a uterus. Part of that is because the nutrients in the body can’t always be replicated in vitro. Without the right nutrients there is an effect on the development (Source) and quality of embryos. The lack of these nutrients in the culture medium contribute to the high rates of implantation failure and miscarriage with IVF.

In some clinics, proteins like GM-CSF are considered just fine-tuning agents which can be omitted in the lab.  But, the research shows the lack of growth factors like GM-CSF in the culture embryos are incubated in is a major cause of environmental stress. We know that embryos are highly sensitive to their environment – any stress is bad. If the cells are severely stressed, it will alter the rate of cell division or kill the cell, causing the blastocyst to arrest. 

As GM-CSF prevents cell stress, by adding GM-CSF to the culture which the embryos are stored in, it’s thought that the embryos have a better chance of survival. 

What does the research say?

First things first – adding GM-CSF to the culture does no harm to the embryos. This multicentre, prospective placebo-controlled and double-blinded study (Source) found that embryos incubated in a solution of GM-CSF, they had the same chromosomal composition and similar number of top quality embryos and development on day three than embryos incubated in a solution without GM-CSF. That’s good to know – essentially, there was no increase in chromosomal abnormality in embryos cultured with GM-CSF.

Several studies have found that by adding GM-CSF to the culture, you’re likely to get a two fold increase in the number of embryos that develop into blastomeres (Source).  Embryos cultured in the with GM-CSF reached blastocyst stage on average 14 hours quicker and contained approximately 35% more cells (Source).  

In one study (Source), they took a sample of cells from the uterus lining and added it to the culture with the embryos. The tissue secreted GM-CSF and this was measured post transfer. They found the more GM-CSF that was secreted the more likely a successful pregnancy was after embryo transfer.

This large scale study (1332 patients across 14 fertility clinics in Sweden and Denmark – Source) found that there was a significant increase in the number of embryos that implanted and survived to week 12 (23% for GM-CSF vs 18.7% for control).  It also found that of a subgroup of 327 women who had previously miscarried, the women who had GM-CSF media had a much higher ongoing implantation rate (24.5% for GM-CSF and 17.0% for control). 

In a nutshell?

Adding GM-CSF to the medium embryos are cultured in:

  • Doesn’t hurt your embryos in anyway.
  • Has been shown to protect embryos from cell stress.
  • The research suggests it helps embryo development and implantation.
  • May improve the chances of implantation in women who have miscarried in the past. 

Overall, adding GM-CSF to the medium embryos are cultured in may help establish a successful pregnancy and increase the chances of a healthy infant.


  1. Granulocyte-macrophage colony-stimulating factor (GM-CSF) acts independently of the beta common subunit of the GM-CSF receptor to prevent inner cell mass apoptosis in human embryos. (link)
  2. Granulocyte-macrophage colony-stimulating factor promotes human blastocyst development in vitro. (link)
  3. Culture of human oocytes with granulocyte-macrophage colony-stimulating factor has no effect on embryonic chromosomal constitution. (link)
  4. Granulocyte macrophage-colony stimulating factor production by autologous endometrial co-culture is associated with outcome for in vitro fertilisation patients with a history of multiple implantation failures. (link)
  5. A randomized clinical trial to evaluate the effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) in embryo culture medium for in vitro fertilization. (link)


When to use an embryoscope

By Research No Comments

After egg collection comes the week of wait-and-see. You wait and see how many of your eggs fertilise, how many cleave at the right time and grow into blastocysts. They’ll often be graded at this point, based on how even the cell sizes are, and what kind of fragmentation they have.

I’ve gotten pictures on all these days – pictures of my little embryos. It’s a hard week, as often the number of eggs you start with is not the number of blastocysts you get at the end.

This last round we’ve decided to use an embryoscope, in the hope that it’ll help our embryos get to blastocyst level.

What is an Embryoscope?

Typically your eggs and embryos are placed in a special incubator that maintains the environmental conditions necessary for embryos to grow. Every day, at set time points an embryologist will remove your embryos from the incubator to take photos and ensure they’re developing on time. This has to be done quickly, because any environmental stress can potentially damage the embryos.  Based on these observations, an embryologist will grade your embryos to tell which embryos are most likely to result in pregnancy and will select an embryo that develops along a set timescale.  **

An embryoscope is an incubator that maintains the environmental conditions – just like a standard incubator. It has an incorporated time lapse camera system – it will take a picture every 20 minutes. This means your embryologist can monitor embryo development while the embryos are still in the incubator – they won’t have to remove the embryo to examine it, making for more stable culture conditions. 

It also means an embryologist can make more informed decisions, particularly with embryo selection as there is more information to consider.  Time lapse observation is more thorough way to understand what is happening with the embryo. Embryo cells aren’t static – they move. With a single static observation per day it’s difficult to judge correctly what stage the embryo is at. For example, an embryo that has just cleaved and is pulling itself back together at the time of observation may be misjudged for extreme fragmentation.  With more information, embryologists can can better tell which embryos will have a better chance at success.

Who should use an embryoscope?

An embryoscope is an expensive piece of equipment, adding to an already hefty IVF price tag.  You’ll want to weigh up the advantages of using an embryoscope with the cost.

– People who have lots of eggs/embryos for selection.

As using an embryoscope provides more information about an embryos development, there is a more informed chance of selecting a viable embryo for transfer. ** 

– People who would like more information about the embryo, when past cycles have not gone as expected.

Sometimes more information about an embryo is helpful in situations where there is repeated implantation failure, advanced maternal age or a history of recurrent miscarriage. It can help people make informed decisions about future treatment plans or sometimes bring closure.

– People who have a limited number of rounds.

IVF is such an expensive treatment and many of us can only afford a handful of rounds, if that. By ensuring a more stable culture environment you know you’re doing everything you possibly can to help your embryos along. 

What does the research say?

Unsurprisingly there has been loads of research around embryoscopes – they provide so much more information and have been used in a fair number of studies.  

This study (Source) found that culturing embryos and selection improves reproductive outcomes. While there was no significant difference in pregnancy rate (the beta taken after the 2 week wait), the ongoing pregnancy rate (where there was a heartbeat at 12 weeks) was much better with the embryoscope than standard incubation. Implantation rates were also better with embryos selected from the embryoscope, and that early pregnancy loss was much less likely to happen.

This French report (Source) found that better embryo selection (according to embryo movement parameters and better observation of abnormal cleavages, along with greater quality control and flexibility) lead to an overall increase in success rates in IVF cycles.

This study (Source) echoes a similar message. by providing more accurate information about the embryo potential, it allows for better selection of embryos with high reproductive potential. This study (Source) goes on to suggest that by selecting embryos with good morphology and normal cleavage rates, they could, one day, provide the basis of a qualitative algorithm for embryo selection.

Should you use an embryoscope?

Essentially, there is no harm in using an embryoscope. It only offers positives – a more stable culture environment and more information about your embryos. If you can afford it, perhaps talk to your doctor about incorporating it into your cycle plan. 


** Side note: While an embryo that cleaves on time, has little fragmentation and whose cells are symmetrical might look good – it still might chromosomally abnormal which will not result in a healthy pregnancy. More on chromosomal quality here. How an embryo looks is not the be all and end all, so if your embryos grade poorly please take it with a grain of salt.


By Research 2 Comments

During that last round of IVF I felt like I was fighting an uphill battle. Diminished Ovarian Reserve, Poor Responder, High FSH levels. All of the odds were against me, and I knew it. That didn’t stop me from hoping, though. From reading all the research and taking all the supplements, using all sorts of relaxation techniques, standing outside on a full moon downing royal jelly (okay, not that last one!).  You get the idea. I was doing everything I could. 

We tried a new protocol, I’d be on DHEA + we added in human growth hormone to my protocol. Woop! We were in! My follicles grew, and by the time egg collection came we retrieved 12 eggs!! TWELVE! I was considered a normal responder!! We were over the moon, and I was quietly patting myself on the back for a job well done.

The thing with celebrating early is that you leave yourself open to all the other hurdles. Like fertilisation.

Of our 12 eggs, only 5 eggs fertilised. All my eggs were mature. The sperm sample was good. And less than half, only 41% fertilised. Sucker punch to the belly – I felt like all my hard work was for naught. My disappointment shouldn’t be mistaken for ungracious – I am grateful we that had five little embryos, and that five is better than none. I’m grateful for that.

However, I’m a determined person and want to increase my odds however I can. I’m looking for something more than 41%. The biggest thing for me was should I have asked for ICSI, rather than IVF?

It took me a while to understand the subtleties between the two:

Fertilisation by IVF

With IVF the eggs are placed in a fancy liquid into a glass petri dish and the washed sperm sample is added to the dish near the egg. The sperm hopefully find their way to the egg, burrow in past the shell and cause a chemical reaction (which stops other sperm from joining the party). The sperm kicks off a round of meiosis to bring the chromosomes together and causes fertilisation. 

Fun side note, IVF stands for In Vitro Fertilisation – turns out In Vitro means “in glass”.

Fertilisation by ICSI

An embryologist will select a single sperm from the washed sample. This sperm will be put into a needle which is then carefully advanced through the outer shell of the egg and the egg membrane. The sperm is injected into the inner part (cytoplasm) of the egg, allowing fertilisation to take place. 

Most clinics will only use ICSI if there is an issue with male factor infertility (such as low sperm concentrations, motility or poor sperm morphology), where the benefits are clear. They might also, at a stretch use ICSI for couples who have had pervious IVF rounds with low or no fertilisation with mature eggs that should have fertilised. 

There are some risks with ICSI. In IVF natural selection takes care of things – the fastest and fittest sperm wins the race. However, with ICSI it’s not nature that makes the selection, but an embryologist. If the sperm has a chromosomal abnormality or a genetic defect, this might be passed on to the embryo. In some cases, the chromosomal abnormality may result in a miscarriage.  However, this is also possible when fertilisation is done by IVF. Chromosomal abnormalities aren’t specific to ICSI. 

One concern is that ICSI requires the removal of cell-to-cell communication structures.  When oocytes are processed for ICSI an embryologist will remove the outer cumulus cells around an egg. These cells have little extensions which penetrate through the shell of the egg and touch the egg itself, forming a little communication network between the surrounding cumulus cells and the egg within. 

With ICSI the cumulus cells are dissolved with an enzyme, and helped away with a little shearing of the pipette. This helps the embryologist see inside the egg to check that it’s mature (which is to say that it’s thrown out the excess maternal DNA in the polar body). It also ensures that ICSI is done in a relatively empty area of the egg, rather than through any maternal chromosomes.

While the cumulus cells typically falls off naturally over after fertilisation, with ICSI the communication between the egg and cumulus cells is removed well before fertilisation.  It’s been shown that this effects the fertilisation rate and subsequent embryo quality negatively.  (Source)

There have also been some animal studies in mice that show that with ICSI some genes can be imprinted incorrectly, suggesting that removing the communication network between the cells and the eggs could interrupt a gene printing process. (Source)

Another risk is the introduction of PVP into the egg and the effect it has to both the egg and the sperm.  In some ICSI cycles an embryologist will use PVP (polyvinylpyrrolidone, which is a thick syrupy polymer) to slow down the sperm so they can be easily managed with the pipette. Without PVP sperm are fast and would be impossible to catch and manage for fertilisation.

However, there is research that suggests PVP causes significant damage to sperm membranes  (Source, Source) and are associated with chromosomal abnormalities (Source). 

One study (Source) reported that exposure to PVP prior to ICSI damages the sperm plasma membrane, allowing thiol-reducing agents to gain access to the sperm nucleus (not a good thing).  It’s also possible that PVP loosens the make up of the sperm nucleus, which will eventually condense into cells. 

It’s suggested that fertilisation rates and clinical pregnancy rates could be improved by using a PVP- free solution with ICSI. (Source). That instead of using PVP, an embryologist should use a hyaluronate solution (hyaluronate is naturally found in the reproduction tract) instead. (Source)

Another risk is that the success doesn’t just ride on the quality of your eggs and sperm but on the skill of the individual performing the procedure and the overall quality of the laboratory. It’s a pretty hefty chance to take, so fingers crossed for an amazing embryologist. You might want to have a conversation about your clinic’s embryologist experiences. 

Heavy stuff. 

Alright, here are the questions I had:

  • Is there a better fertilisation rate with ICSI over IVF?
  • Exactly what happens with ICSI?
  • Will ICSI effect the embryo quality?
  • Is there a better transfer rate and pregnancy rate  with ICSI over IVF?
  • What is Rescue ICSI, and does it have a better fertilisation rate?
  • What is IMSI? Does that have a better transfer rate than ICSI?

I did an awful lot of reading and googling, and here is what I found.


  1. Immediately after egg collection, the oocytes (eggs) are evaluated to see how mature they are. Eggs that are clearly not mature are discarded.
  2. Cumulus cells are removed from the oocyte. First with a enzyme solution and then by moving through a pipette to shear the cells off.
  3. The oocytes are evaluated again to assess how mature they are and their integrity to ensure they’re suitable for ICSI.
  4. Sperm are washed with a viscous medium, and analysed. One sperm is selected.
  5. The selected sperm is immobilised by breaking it’s tail, and aspirated into the needle.
  6. The oocyte is held in place with suction to the holding pipette, and the injection pipette is pushed against the oocyte shell. Once at the centre a break occurs in the membrane, which pushes a flow up into the injection pipette.
  7. The sperm is injected into oocyte.



I really struggled to find clear studies on this. I wanted something concrete, a proper study rather than a clinic’s promotional success rates – most spout something along the lines of 70-85% of eggs fertilise.  The tricky thing with that amazing rate is it’s a bit biased. ICSI is often used to treat male-factor infertility where fertilisation is the main hurdle. This means that the eggs used in ICSI cycles are typically high quality and collected from young fertile women – a very different skew from the typical IVF patient range.  

I did find one study, done in the Netherlands in 2005.  It’s called Conventional in vitro fertilization versus intracytoplasmic sperm injection in patients with borderline semen: a randomized study using sibling oocytes. (Source). Definitely a mouth full but had some interesting results.

At first I discounted it as being 10 years old, but when I realised that it was one of the few studies I could find that was relevant and that rates could only have improved as the technology has, I took a look.

Here’s how it worked: each couple in study had a selection of their eggs split into two groups: Those to be fertilised by IVF, and those to be fertilised by ICSI. This get’s around the ICSI bias, as the eggs are likely to be the same quality across both methods. 

Some couples eggs only fertilised with ICSI, and some with both ICSI and IVF, and the results are split along those lines:

Group IVF-
Couples whose eggs only fertilised with ICSI and not IVF. 
This group is likely to include those couples with male factor infertility.

Group IVF+
Couples whose eggs fertilised both the ICSI AND with IVF.

Down to business, how’d they do?


Group IVF – 
IVF Fertalisation Rates – Of the eggs in the IVF group, 0% fertilised.
ICSI  Fertalisation Rates – Of the eggs in the ICSI group, 51% fertilised.

Group IVF+
IVF Fertalisation Rates – Of the eggs in the IVF group, 51% fertilised.
ICSI Fertalisation Rates – Of the eggs in the ICSI group, 51% fertilised.

Pretty consistent results, right? ICSI fertilisation rate is consistent with IVF, if your eggs and sperm are able to be fertilised by IVF. If your eggs/sperm aren’t able, you may loose all your eggs to trying IVF. 

I guess this up to you – if you think it’s worth taking the chance, then IVF and ICSI have pretty similar fertilisation rates. If you’re in the borderline group, you can avoid unnecessary fertilization failure with ICSI. 


In the study, embryos were put into four buckets (1 – 4) based on the number of cell divisions and the fragmentation. They were looking for the best: Type 1 embryos with equal sized cells with no fragmentation and Type Two, with equal sized cells and less than 20% fragmentation.

It’s important to remember this is only a visual guide, and an embryo that looks good may also be chromosonally abnormal, and thus not viable. 

Group IVF – 
Of the embryos that fertalised in the ICSI group, 77% were Type 1/2.

Group IVF+
Of the embryos that fertalised in the IVF group, 72% were Type 1/2
Of the embryos that fertalised in the ICSI group, 83% were Type 1/2

I was surprised by this, but glad to see that ICSI didn’t harm embryo quality anymore than IVF does. In fact, ICSI embryos had consistently better visual quality than IVF.


These two are the proper indicators of success – how many resulted in a BFP at the first beta, 15 days post egg retrieval (which I’m calling pregnancy rate) and how many resulted in a positive pregnancy, with a heartbeat at week 12 (ongoing pregnancy rate). 

Group IVF – 
Of the embryos that fertilised in the ICSI group, the pregnancy rate was 54%.
Of the embryos that fertilised in the ICSI group, the ongoing pregnancy rate was 42%.

Group IVF+
Of the embryos that fertilised in the IVF group, the pregnancy rate was 43%.
Of the embryos that fertilised in the IVF group, the ongoing pregnancy rate was 36%.

Of the embryos that fertilised in the ICSI group, the pregnancy rate was 53%.
Of the embryos that fertilised in the ICSI group, the ongoing pregnancy rate was 50%.

Here is the most convincing evidence for me – both ICSI groups has a higher pregnancy rate AND a higher ongoing pregnancy rate than IVF.


There is a third option, which is Rescue ICSI. If no eggs are fertilised via IVF, some clinics will take those eggs and use ICSI to fertilise them. This comes with risks, because if a sperm is already inside the egg the resulting embryo will have chromosomal abnormalities. 

The research is also not clear. Some studies (like this one) suggest it might be worth a shot if none of the eggs that should have fertilised did. Other studies (like this one) suggest the odds aren’t worth the cost as the success rate is so small. 


With ICSI an embryologist will do a sperm morphology analysis and sperm selection at a magnification of 400x.  With IMSI, it’s thought that bigger is better, and this is done at an extremely high magnification (8000x). If you want to see what the difference looks like, here is a youtube video.

This is relevant particularly during sperm selection, as IMSI shows finer details and it is easier to see sperm that have head vacuoles or other abnormalities. One study (Source) found that between ICSI and IMSI the fertilisation rate was the same, but the pregnancy rate was higher and the miscarriage rate was lower for IMSI than ICSI.


It’s a pretty personal choice.

  • ICSI and IVI have the same fertilisation rate when you discount the male factor bias. However ICSI has the better pregnancy rate, but it depends on the clinic (and whether they use PVP in their ICSI process).
  • There’s the concern that by removing the cumulus cells in ICSI alters the gene imprinting process. 
  • If you are going to go the ICSI route, push for IMSI instead – as it has an even better pregnancy rate since the embryologists can see the sperm better during sperm selection. 

Personally,  I’m leaning towards either half and half or full ICSI/IMSI the next round. The benefits of ICSI I think well outweigh the risks of conventional IVF not fertilising… It’s a tricky choice! It’s hard to know what the right choice is. Hopefully my body will cooperate and the next round will be soon. I plan to discuss it with my RE, anyway. 


  • Does the clinic offer ICSI, even if you don’t have male factor infertility?
  • What are your fertilisation and pregnancy rates like for half ICSI, half IVF fertilisation method? 
  • Do you use a PVP-free solution in your sperm selection process?
  • Do you have the tools to offer IMSI?
  • How experienced is the embryologist who will be performing ICSI on my eggs? How many ICSI procedures have they performed?  
  • Do you offer Rescue ICSI, and this is an option for me?

As always, I’m not a professional or a doctor – my experience is just that, my experience. I’ve done an awful lot of reading and research which I’m happy to share. If you do have concerns about IVF vs ICSI, talk to your doctor. 

Everything you need to know about AMH and Ovarian Reserve

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When my doctor told me I may be infertile, I told her she was lying. It wasn’t a great day, to be honest. It was a gut reaction, and turns out that she wasn’t lying. I even got my own copy of the blood test results. My AMH levels were low, she said. AMH is an indication of ovarian reserve and mine waI was at the end of my fertility season, she said.

It was definitely a shock and took me a while to understand what she was saying. There’s a hormone in your blood that can be used to give an indication of how fertile you are, called AMH. AMH stands for Anti-müllerian hormone, which is secreted in the granulosa cells of follicles. Follicles are the cavities in your ovaries that eggs grow in.  Your AMH levels starts high, when you’re at your most fertile age and as you get older, declines as your ovarian reserve does.  It’s measured with a simple blood test, typically included with the regular Day 3 blood work if you’re doing an IVF round. 

To confirm, AMH typically correlates to your antral follicle count. That is to say, how many antral follicles you have on Day 3 (measured with an ultra sound). It’s another method to confirm your fertility potential.

It used to be that FSH (Follicle Stimulating Hormone) was used to gauge ovarian reserve, but FSH fluctuates a lot throughout your cycle as it’s used to kickstart your ovaries into action. AMH on the other hand is a fairly stable measure that doesn’t have the same fluctuation from month to month and is considered a much more accurate guide.

What my not-lying doctor was trying to say was that at age 30, I had an AMH level of 6.4. I had a low ovarian reserve, also known as diminished ovarian reserve, or low fertility. Essentially, I don’t have that many eggs left.

AVERAGE AMH LEVELS (across all ages, pmol/L)
Optimal Fertility: 40.04 – 67.9
Satisfactory Fertility: 21.98 – 40.04
Low Fertility: 3.08 – 21.97
Very Low/Undetectable Fertility: 0.0 – 3.07

Age 25 – 24
Age 30 – 17.5
Age 35 – 10
Age 40 – 5
Age 45 – 2.5

Source: Lister Fertility Clinic

At first I thought low ovarian reserve was the be all and end all of our fertility journey. We’re done before we even started – I was never having a baby. That’s actually not the case – I still have some eggs left even if not very many, and we were reassured that pregnancy was still possible. Having this information was helpful for planning our IVF cycles as AMH can help predict your response to stimulant drugs during IVF.

If you have a low ovarian reserve (like me) you might need some help developing more eggs and require a higher dose of stimulants. If you have a high ovarian reserve, you may have a very high level of fertility and require a much lower dosage of stimulants.

Because AMH is just a hormone, it’s unlikely that increasing the hormone levels will also raise your ovarian reserve. In saying that, there are a few interesting cases that do effect AMH level.

  1. Vitamin D deficiency is linked with falsely low AMH. In fact, it was found that AMH levels decreased by 18% depending on the season, and these effects were mitigated with the supplementation of Vitamin D.  If you’re concerned, get your Vitamin D levels checked.
  2. DHEA has been shown to help with women with low AMH. DHEA (Dehydroepiandrosterone) is a hormone produced by the adrenal glands and ovaries and is involved in the production testosterone and estrogen. As DHEA levels tend to decline naturally with age, it’s thought that supplementation can help with fertility. 
    Source  (If it helps, I used Fertinatal DHEA, available here on Amazon
  3. Smoking has been shown to decrease AMH levels. 
  4. Occasionally there can be minor fluctuations within the bounds of lab error. If you’re unsure, insist on a second test.


I will say this though – learning about my low AMH levels kicked off this sense of urgency. I didn’t have that many eggs left and I was only losing more as each month ticked by. Because of this we got into IVF right away and we didn’t necessarily take a considered approach. 

What I’d say now is if you’re faced with a low AMH level, even though it feels like it’s best to rush – take some time and consider your situation and what you want to do. We’ve been a year in our IVF journey and my AMH levels haven’t changed. We’ve learnt that taking a month or two to research and understand our situation and emotionally come to terms with low fertility levels is an option, even if it doesn’t feel like it. 

As always, I’m not a professional or a doctor – my experience is just that, my experience. I’ve done an awful lot of reading and research which I’m happy to share. If you do have concerns about AMH, talk to your doctor. 

A TTC Acronym Glossary

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When I first stumbled across the #ivf tag on instagram, I was ecstatic – here were people who UNDERSTOOD!  I was not alone! I found my tribe of people!! I did a dance I was so happy. It was a comfort to know I wasn’t the only one.

The next emotion was less happy – my tribe were speaking in a language of acronyms I did not understand. Not even in the slightest. It was intimidating and confusing. It made me feel small. 

It took some time, but with some googling, determination and many questions I soon understood what was being said. Here’s a quick glossary to help you understand the #TTC acronyms.

2 Week Wait. It’s that time between post IVF transfer and taking a beta test to prove pregnancy. It’s a nervous time, hoping the transfer is successful.

Aunt Flo, After Flo, Period, or Menstrual Cycle.

Assisted Hatching. It’s an IVF term, where an embryologist will create a small hole in the embryo shell before transfer. It’s thought that embryos who have assistance hatching are more likely to implant. 

Artificial/Assisted Insemination. Where semen is injected into the vagina or uterus.

Assisted Reproductive Technology. Essentially any conception assistance that isn’t sex. Examples would be IVF or IUI. 

Anti-Mullerian Hormone. The hormone that predicts ovarian reserve (that is, the number of eggs you have left in your ovaries).

Baby Aspirin. There is some thought that taking a single baby aspirin can improve pregnancy outcomes with IVF by improving the blood supply to various organs, like ovaries.

Baby Dust
That magic something that ensures the whole pregnancy process goes as planned.

Basal Body Temperature. Helpful for temperature charting to predict ovulation.

Birth Control Pills.

Baby Dance, otherwise known as sex.

The beta is a pregnancy test taken after the 2WW. It measures the levels of the hormone beta-hCG via a blood test, as it is the first measurable sign of implantation.

Big Fat Negative. When you take a pregnancy test and you’re not pregnant. Sad face.

Big Fat Positive. What we’re all looking for – when you take a pregnancy test and it is positive. High five! 

Bloodwork. Getting bloods drawn is a fairly frequent occurrence if you’re working with assisted reproduction.

Cycle Buddy. When you have a friend with a similar cycle to you, and you both run through similar IVF/IUI journeys at the time.

Cycle Day. The day of your cycle. The first day of your period is CD1.

Cervical Mucus. Your body produces a mucus around the cervix. It’s typically used to prevent any bacteria moving between the vagina to the uterus. When you’re ovulating estrogen alters the mucus to become sperm friendly, which allows the sperm to move quickly through the uterus to the fallopian tubes.

Dear Husband. 

Dihydroepiandrosterone is a hormone that can be taken as a supplement. It’s naturally occurring in most women and converts into androgens (like testosterone). It’s used to improve outcomes for women experiencing Diminished Ovarian Reserve.

Diminished Ovarian Reserve. A condition where a woman will have a low number of eggs in her ovaries, or impaired development of existing eggs. It’s thought to be one of the main causes of infertility.

Days Post-Ovulation.

Days Post-Egg Retrieval.

Days Post-Transfer. Often it will have a number in front – 5DPT would be 5 days post transfer.

Days Post 3-Day Transfer. This refers to an embryo that was transferred on Day 3 after egg retrieval. 

Similar to the above, except a 5 Day old blastocyst was transferred.

Dear Wife.

Estradiol. Estradiol is the primary female sex hormone. Most importantly, as your follicles grow it triggers hypothalamic-pituitary events that lead to a luteinizing hormone surge which induces ovulation. It will be one of the hormones measured frequently during an IVF round.

Endometriosis is a common condition where tissue that behaves like the lining of the womb is found outside the womb.

Egg Retrieval. Where, after being stimulated with hormones during an IVF cycle, the eggs are retrieved from the ovaries.

Embryo Transfer. Where, after being fertilised and allowed to cleave during an IVF cycle, the embryo is transferred to the uterus. 

Egg White Cervical Mucus. The kind of cervical mucus where, around ovulation, it takes on a consistency like egg whites.

Frozen Embryo Transfer. Where a frozen embryo is thawed and transferred to the uterus.

Fertility Friend is an app for tracking fertility.

Is a frozen embryo.

Follicle-Stimulating Hormone promotes the formation of eggs in an ovary. It is used as a guide to indicate the quality of eggs on CD3, which can be used to predicate whether an IVF round should go ahead or not.

Gonadotropin-Releasing Hormone is also known as a luteinizing hormone which is responsible for the release of FSH and LH from the anterior pituitary gland. 

The Glucose Tolerance Test is a tool used to diagnose high blood glucose during pregnancy, otherwise known as gestational diabetes.

Human Chorionic Gonadotropin is a hormone produced in a placenta during pregnancy. It tells the ovary to continue producing estrogen and progesterone which help the lining of your uterus stay intact.

Human Menopausal Gonadotropin (also known as Menotropin) is hormonally active medication used to treat infertility. It contains equal amounts of LH and FSH and is used to help stimulate ovulation

Home Pregnancy Test.

Hysteroscopy is a procedure used to examine a womb for fibroids, polyps or adhesions by inserting a narrow camera through the cervix. 

Hysterosalpingogram is a procedure to ensure the fallopian tubes are clear. It’s done by injecting a dye into the cervical canal and then taking an xray as the dye moves around the uterus into the fallopian tubes.

Intracervical Insemination is an artificial insemination procedure, which involves placing sperm directly into the reproductive tract to improve the chances of pregnancy. 

Intra-cytoplamic Sperm Injection. This is where a single sperm is inserted into an egg to aid fertilisation. 

Intra-uterine Insemination is a form of assisted conception. Sperm is placed in the uterus near the egg at the time of ovulation.

In Vitro Fertilization. This is a form of assisted conception, where an egg is removed from an ovary and fertilised with sperm in a laboratory. The embryo is then transferred to the womb to grow and develop.

Luteinizing Hormone is released to encourage your ovary to ovulate. 

Luteal-Phase is the second half of a menstrual cycle that occurs after ovulation. It’s the phase where fertilisation and implantation are likely to happen. 


Male Factor Infertility.




Oral Contraceptives.

Ovarian Hyperstimulation Syndrome is an occasional side effect of IVF. Your ovaries overreact to the stimulants and produce too many follicles.

Ovulation Predictor Kit/Ovulation Predictor Test. Both work by measuring the amount of luteinzing hormone (LH) in your urine. A surge of LH is an indicator of ovulation.

Over the Counter. Typically refers to medication.

Polycistic Ovarian Syndrome/Polycistic Ovarian Disease is a hormone imbalance which interferes with periods and other fertility aspects. It’s thought to be the leading cause of infertility. 

Pre-implantation Genetic Diagnosis/Pre-implantation Genetic Screening. This is where an embryo that has grown to Day 5, blastocyst level is sampled and the cells are tested for chromosomal abnormalities.

Pre-menstrual Syndrome.

Pee On A Stick. Typically associated with pregnancy tests or OPKs. 

Reproductive Endocrinologist.

Semen Analysis. A sample is taken and a few different factors are checked to rule out male infertility. 

Thyroid Stimulating Hormone is a hormone secreted by the pituitary gland. It plays a significant role in reproduction and pregnancy. There has shown to be an increase in miscarriages when the TSH levels are off the scale. 

Trying To Conceive. 

Why should worry about Egg Quality if you’re doing IVF

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There’s a lot of speculation that fertilisation is the crux of getting pregnant. Take one good swimmer plus an egg and boom – nature will take it’s course and produce a healthy little baby. So to fall pregnant all you need to do is introduce an egg to the sperm, right? 

Often when trying to conceive there is a huge focus on fertilisation. There are some complicated ovulation prediction methods to help get the timing right. Like temperature charting and OPKs – peeing on sticks to compare the lines from previous days. The hope is having sex at the right time, the sperm and egg will meet and fertilise. 

Turns out it’s a bit more complicated than that. Truth is,  Fertilisation is only a small part the equation. Only around a third of fertilised embryos will survive and grow in a healthy baby (1). 

Let’s take a moment to process that. Miscarriages are more common than we think, occurring in about 10-15% recognised pregnancies (2). The important part there is “recognised pregnancies”. Most miscarriages happen before you even realise you’re pregnant (3).  In fact, it’s thought that up to 70% of pregnancies end in miscarriage (1).

So despite getting past fertilisation a large number of pregnancies won’t grow to term. It’s been found that the key to getting pregnant (and staying pregnant) is egg quality. That is, whether your egg has the right number of chromosomes or not.  

Each egg starts with four sets of chromosomes. Shortly before ovulation (4) your egg will go through a process of aligning two sets of chromosomes.  Once matched, your egg will dispose of the extra set. It does this twice and if all goes as planned your egg ends up with one copy of each chromosome, ready to ovulate. This process is called meiosis.

Meiosis will define whether your egg will have the right number of chromosomes. This is important, because an egg with the wrong number of chromosomes could result in a miscarriage, or even have difficulty fertilising. If a chromosomal abnormal embryo does grow to term it’s likely to have a genetic disorder. Down’s Syndrome, or Turners for example. 

Chromosomal abnormalities are surprisingly common. In women over 40, it’s thought that more than half her eggs may be abnormal (5), possibly even as high as 70%-80% (6). For women under 35, in one study it was found that up to a quarter of her eggs will have an abnormal number of chromosomes (6).

Putting that in context: for every month that a woman under 35 ovulates hoping to become pregnant, one month of four  it’s unlikely she’ll be able to conceive. If she does, she’s likely to miscarry.

During IVF there is an optional process called PGS – Pre-Genetic Screening. Once fertilised embryos reach blastocyst level they can be screened to check the number of chromosomes. Only chromosomal normal embryos will be transferred back for implantation.

It’s a heartbreaking decision to make. With PGS there is a possibility all the embryos may be abnormal. There may no-viable embryos to transfer. If that’s the case it’s likely even without PGS the outcome would not result in a healthy pregnancy.

There have been several interesting studies (7, 8, 9) on the impact of using PGS with IVF. The most interesting – pregnancy rates increase dramatically when using PGS screened eggs. Embryos that have been checked and are chromosomal normal are more likely to produce a successful pregnancy. 

In one study, the successful implantation rate for ladies between 40-43 years old went from 19.0% to 45.5% when using only screened embryos. The number of ladies in that age bracket who became mothers more than doubled. (7).

Another study repeated in both Beijing and LA found that 69% of IVF patients who used PGS screening and selected only chromosomal normal eggs became pregnant. In the control group (who did not use PGS to select chromosomal normal eggs) had only 41% of IVF patients fall pregnant. (9)

It’s clear that having chromosomal normal eggs – good quality eggs – is fundamental in having a successful pregnancy, and a happy healthy baby, more so than fertilisation. To put it simply: Egg Quality is everything.

The question then becomes, can Egg Quality be changed? If so, how?  Stay tuned for more posts. 🙂


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