Egg quality depends on the ability of the egg to repair DNA and maintain genetic stability throughout its development  – from before you are born right up to ovulation.

An egg cell carries far more than genetic material. It also contains the cellular systems needed to detect and repair DNA damage.

DNA damage happens naturally in all cells. Normal metabolism produces reactive molecules that can affect DNA, and environmental exposures, inflammation, or toxins can add further stress.

To protect the genetic material that will one day be passed to a baby, the egg constantly monitors its DNA. When damage is detected, repair systems remove the affected section and rebuild the sequence using the intact strand as a guide.

This repair activity forms part of the ovary’s natural quality-control system. Eggs that cannot maintain stable DNA are usually removed from the follicle pool before ovulation.

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Egg Development Begins Before Birth

Egg development begins long before adulthood.

When a baby girl is developing in the womb, her ovaries form the full supply of eggs she will carry throughout life. This process occurs roughly between 6 and 20 weeks of pregnancy.

During this stage:

cells that will become eggs multiply rapidly
DNA is copied repeatedly
chromosomes exchange genetic material

This reshuffling of genetic material is a normal part of egg formation, but it requires extremely precise DNA repair systems to ensure the chromosomes reconnect correctly.

Once this stage is complete, the eggs pause in an early stage of development and remain stored in the ovary.

Every egg released during adulthood therefore began its life before birth.

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Ongoing DNA Maintenance Throughout Life

Although eggs remain dormant in the ovary for many years, they are not completely inactive.

Even during this resting phase the egg continues to monitor its DNA and carry out small repairs when necessary.

Over time, some eggs accumulate too much damage. When this happens the ovary removes them through a natural process called atresia.

This gradual filtering process helps ensure that eggs released for ovulation have maintained genetic stability.

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The Final Repair Window Before Ovulation

The most important period for DNA repair occurs in the months before ovulation, when a follicle is recruited to grow.

During this stage the egg becomes metabolically active again. Energy production increases and the egg begins preparing for ovulation.

This phase forms part of the approximately 90-day process of follicle development that leads up to ovulation.

While the follicle is growing, the egg has a final opportunity to detect and repair small areas of accumulated DNA damage before completing maturation.

This is one reason fertility preparation often focuses on the months leading up to conception.

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Factors That Increase DNA Damage in Eggs

The egg’s repair systems are powerful, but they are not unlimited. When DNA damage accumulates faster than it can be repaired, the risk of chromosomal problems increases.

Several factors can increase the amount of damage the egg must manage.

Smoking

Cigarette smoke contains chemicals that directly damage DNA and generate high levels of oxidative stress.

These compounds circulate through the bloodstream and reach ovarian tissue, where they can affect both the egg and the surrounding follicle cells.

Smoking has been associated with increased oxidative damage in reproductive cells and accelerated loss of ovarian follicles.

Vaping

Vape aerosols can contain nicotine, ultrafine particles, trace metals from heating coils, and chemical by-products created during heating.

These substances may increase oxidative stress and place additional strain on cellular repair systems.

Because long-term research is still emerging, most reproductive health bodies recommend avoiding vaping when trying to conceive.

Chronic Inflammation

DNA damage is not only caused by toxins.

Chronic inflammation within the body can increase oxidative stress and raise the number of reactive molecules that interact with DNA.

Common contributors include:

Insulin resistance often linked to PCOS
Ultra processed food
Metabolic instability
Ongoing inflammatory conditions such as endometriosis

Stress and Oxidative Load

Long-term psychological stress can also influence cellular physiology.

Elevated stress hormones are associated with increased inflammatory signalling and oxidative stress, which can increase the burden of DNA damage the egg must repair.

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Nutrients That Support DNA Repair

DNA repair relies on enzymes, structural stability of DNA, and protection against oxidative damage. Several nutrients support these processes.

Zinc

Zinc plays a direct role in DNA repair and replication. Many repair enzymes require zinc to function, and zinc also helps stabilise DNA structure.

In reproductive cells, zinc supports chromosome stability and normal cell division during follicle development.

Folate

Folate provides the building blocks needed to synthesise DNA. When damaged sections of DNA are replaced, the cell must create new nucleotides, which rely on folate-dependent pathways.

Vitamins B6 and B12

These vitamins work alongside folate in methylation pathways that support DNA synthesis and repair.

Selenium

Selenium supports antioxidant enzymes such as glutathione peroxidase, which help control oxidative stress inside cells. By reducing oxidative damage, selenium helps limit the amount of DNA repair required.

Vitamin E

Vitamin E protects the fats that form cell membranes from oxidative damage.

Magnesium

Magnesium acts as a cofactor for many enzymes involved in DNA replication and repair and helps stabilise DNA structures during cellular processes.

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How Age Influences DNA Repair in Eggs

Age is one of the most significant influences on egg quality.

The issue is not simply that eggs become older. Over time, the systems responsible for maintaining and repairing DNA become less efficient.

Research has shown that key DNA repair proteins decline with age. When these repair systems become less effective, more eggs accumulate genetic instability and are removed through the ovary’s quality-control process.

Ageing is also associated with reduced mitochondrial efficiency in eggs. Because DNA repair requires cellular energy, reduced mitochondrial function can limit the egg’s ability to repair damage during its final stages of development.

As repair capacity declines, the likelihood of chromosomal errors during egg maturation increases.

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Why This Biology Matters

Healthy eggs are not simply eggs with intact DNA. They are eggs that still have the cellular energy and repair systems needed to maintain that DNA.

Throughout life the ovary continually filters and selects eggs that maintain genetic stability.

During the months before ovulation, the egg completes its final stage of development, carrying out repair processes that help protect the genetic material it will eventually contribute to the next generation.

A fertility consultation at Now Baby will give you the strategy to support both egg and sperm quality and prepare your uterine environment for successful implantation.

You may have been told your NK cells are high. Your clinic has recommended intralipids — an intravenous fat infusion offered before transfer to calm the immune response that may, the theory goes, be working against your embryo.

The test felt like an answer after so many cycles without one. A measurable marker. An explanation. And now a treatment to address it.

The Human Fertilisation and Embryology Authority, the UK’s independent fertility regulator, formally assesses the add-ons offered alongside standard IVF. Their evidence reviews are used internationally by clinicians and patients trying to understand what the research actually shows.

Intralipids are on that list.

What intralipids are

Intralipids are an intravenous emulsion of soybean oil, egg phospholipids, glycerin and water — originally developed as nutritional support for patients unable to eat. In fertility, they are used off-label as an immune modulator.

The proposed mechanism is that the lipid components of the infusion interact with immune cells — particularly natural killer cells — and suppress their activity around the time of transfer, creating a more tolerant uterine environment for the embryo.

The infusion is administered intravenously, typically in the days before transfer and sometimes repeated in early pregnancy. Unlike IVIG, intralipids are relatively inexpensive and carry a lower risk profile — which is partly why they are offered more readily and earlier in the treatment pathway.

What NK cells actually do

Natural killer cells have a name that implies they are a problem to be solved. In the context of implantation, that framing is misleading.

Uterine NK cells are essential to successful implantation. They are the most abundant immune cells in the uterus during the implantation window and the early stages of pregnancy. They support vascular remodelling — the process by which new blood vessels form to supply the developing placenta. They guide trophoblast invasion — the process by which the embryo embeds into the uterine lining. They contribute to placental formation and help regulate the immune tolerance that allows the embryo to remain without being rejected.

The question is not whether NK cells are present. They should be. The question is whether their activity is dysregulated in a way that interferes with implantation — and that is a different question entirely from whether a blood test shows an elevated count.

The problem with peripheral NK cell testing

The NK cell test most commonly offered before intralipids measures natural killer cells in peripheral blood — a sample taken from the arm.

Peripheral blood NK cells and uterine NK cells are distinct populations with different phenotypes, different functions and different regulatory mechanisms. An elevated count in the blood does not reliably predict elevated or dysregulated activity in the uterus. The two populations do not behave the same way, are not regulated by the same signals, and cannot be read as equivalent.

A high result on a peripheral NK cell test tells you that NK cell levels in your blood are elevated. It does not tell you what your uterine NK cells are doing — or whether intralipids would have any meaningful effect on the environment your embryo is being transferred into.

This distinction is not a minor technical point. It is the reason the evidence for intralipid treatment based on peripheral NK cell testing remains limited.

What the regulator assessment shows

The HFEA reviews each add-on against the evidence for whether it improves the chance of a live birth.

On intralipids, the published assessment is that the evidence is insufficient — there is not enough high-quality trial data to support or reject routine use. Unlike IVIG, which carries a red rating due to safety and efficacy concerns, intralipids sit in grey: the signal is unclear, the safety profile is relatively benign, and the research is ongoing.

The grey rating does not mean intralipids are ineffective. It means the evidence has not yet reached the threshold required to make a reliable recommendation either way.

The clinical situations where intralipids may be considered are specific:

• Recurrent implantation failure where immune dysregulation has been identified by a reproductive immunologist through uterine assessment — not peripheral blood testing alone
• Women with a diagnosed autoimmune condition where immune modulation has a documented clinical rationale
• Women with endometriosis, where chronic pelvic inflammation may contribute to a dysregulated uterine immune environment

If intralipids were offered on the basis of a peripheral NK cell blood test alone, without a reproductive immunologist’s assessment of uterine immune activity, the regulator’s assessment is useful information to bring into the conversation with your clinic.

The regulator’s work is designed to inform that conversation, not replace it.

What intralipids cannot reach

Intralipids modulate the immune environment from outside — delivered intravenously, acting systemically. What shapes the uterine immune environment from within is a different set of inputs entirely.

 

The inflammatory tone of the uterus responds to gut health, metabolic patterns, blood sugar stability, dietary fat quality and micronutrient status. Vitamin D modulates uterine NK cell activity and supports the immune tolerance that implantation depends on. Omega-3 fatty acids reduce systemic inflammatory signalling. Selenium and zinc support immune regulation at the cellular level. These are the nutritional inputs that influence whether the uterine environment is pro-inflammatory or tolerant — and none of them are addressed by an intravenous infusion.

Intralipids act on the immune system from outside. The nutritional environment shapes it from within.

More than 1 in 3 frozen transfers do not result in a live birth. Embryo implantation has 5 distinct phases and each has its own nutrient requirements. Your embryo needs to complete uterine lining preparation, early blood supply, gene expression, placental formation and immune modulation — all before a test can confirm anything. Each of those phases responds to what the body has been given to work with.

The Now Baby FET Implantation Meal Plan was designed around every one of those phases — the nutritional structure for the days your biology is doing its most demanding work. Professionally analysed. Beginning the day after transfer.

You didn’t come this far to wing it.

Get the FET Implantation Meal Plan

If you have spent years trying to get a PCOS diagnosis — or years being told your symptoms were normal, your cycles were just irregular, your weight was the problem — the news that the condition is being renamed may land differently than it does for anyone who hasn’t been through that.

Polycystic ovary syndrome has been officially renamed Polyendocrine Metabolic Ovarian Syndrome — PMOS. The change follows a landmark global consensus study published today in The Lancet, involving more than 50 patient and professional organisations and input from 22,000 people over 11 years. It is not a cosmetic update. It reflects a fundamental shift in how the medical and scientific community understands what this condition actually is.

For the women who knew something was wrong long before anyone believed them, it is also an acknowledgement that was a long time coming.

Why the name mattered — and why it was wrong

The original name — polycystic ovary syndrome — was built around what could be seen on a scan. Cysts on the ovaries. Visible, measurable, nameable.

But the cysts were never the condition. They were a consequence of it. The underlying driver is a complex hormonal and metabolic disruption — affecting how the body processes glucose, regulates hormones, manages inflammation and responds to reproductive signals. The ovarian cysts that gave the condition its name are one downstream effect of a systemic dysfunction that touches almost every system in the body.

Naming it after the cysts was like diagnosing the smoke and missing the fire. It described a symptom and missed the mechanism entirely.

That misidentification had consequences. Women without visible cysts on their scans were told they didn’t have PCOS — despite having every other marker. Women with irregular cycles, elevated androgens, insulin resistance and chronic inflammation were sent away without a diagnosis because the scan looked clear. Women who presented with weight gain were told to lose weight, as if the weight were the cause rather than a symptom of the same dysfunction driving everything else. Women who presented without weight gain were told they couldn’t have PCOS at all. The name set the diagnostic criteria, and the diagnostic criteria excluded the very women the condition was affecting most.

What PMOS changes

Polyendocrine Metabolic Ovarian Syndrome places the hormonal and metabolic complexity of the condition at the centre of the diagnosis where it belongs. It signals that this is not a gynaecological issue with some hormonal features, but a complex multisystem condition with reproductive consequences.

That distinction changes what the right clinical response looks like. A condition named after ovarian cysts invites interventions targeted at the ovaries. A condition understood as polyendocrine and metabolic invites interventions that address hormonal regulation, insulin sensitivity, inflammatory load and the nutritional environment that drives all of them.

It also changes what the woman living with it is entitled to ask for — and what she is entitled to expect her medical team to understand.

What has not changed

The rename does not change the biology. Women with PMOS have the same condition they had last week under its previous name. The insulin resistance, the androgen excess, the disrupted ovulation, the inflammatory drivers — all of it remains. What changes is the framework through which it is understood and, over time, how it is investigated and treated.

It also does not change the gap between what the condition requires and what most women with it have been offered. A condition this complex responds to inputs that address its root causes — nutrition, blood sugar regulation, inflammatory load, hormonal support. That has always been true. The name change makes it harder to ignore.

The women who have spent years managing this condition through diet, blood sugar control, anti-inflammatory eating and lifestyle changes were already doing the right thing — because they understood, even without the language, that this was a hormonal and metabolic issue. The name change gives that work its proper framework.

What this means for fertility

PMOS is one of the most common causes of ovulatory dysfunction and fertility challenges in women of reproductive age. The hormonal and metabolic drivers that disrupt cycle regularity, impair egg quality and create a hostile environment for conception are the same drivers that respond — sometimes significantly — to nutritional and lifestyle intervention.

Insulin resistance affects the hormonal signals that trigger ovulation. Chronic low-grade inflammation impairs egg quality and the uterine environment. Elevated androgens disrupt follicular development. These are not incidental features of the condition — they are the condition. And they are responsive to what the body is being given to work with.

Understanding PMOS as a hormonal and metabolic condition rather than an ovarian one changes where the preparation work sits. It is not about managing symptoms at the point of treatment. It is about addressing the environment that determines whether ovulation, egg quality and implantation can happen at all.

At Now Baby we welcome this change and look forward to seeing the benefits it must bring to the patients affected.

Preparation before escalation — that is what this condition has always called for. The name finally says so.

Your embryo is ready for transfer. And your clinic has suggested assisted hatching — a brief laboratory procedure performed on your embryo before it is placed in the uterus.

The idea behind it is straightforward. Your embryo is surrounded by a protective outer shell called the zona pellucida. To implant, it must break free from that shell — a process called hatching. Assisted hatching creates a small opening in the zona to help that process along.

The Human Fertilisation and Embryology Authority, the UK’s independent fertility regulator, formally assesses the add-ons offered alongside standard IVF. Their evidence reviews are used internationally by clinicians and patients trying to understand what the research actually shows.

Assisted hatching is on that list.

Why an embryo might need help hatching

In a natural conception, the zona pellucida softens and ruptures as the embryo grows. In IVF, several factors can make this harder than it should be.

The in vitro culture environment can cause the zona to harden through changes in its protein structure — making it less likely to rupture on its own. Freezing and thawing can affect zona integrity in a similar way, sometimes leaving it thicker or less flexible than it would be in a fresh cycle. Maternal age is also a factor — older eggs tend to produce embryos with a thicker zona pellucida, which can make natural hatching more difficult. And embryos graded with high fragmentation or slower than expected development may also have zona characteristics that make hatching harder.

If any of these apply to your cycle, assisted hatching is being offered for a specific biological reason — not as a routine upgrade.

What the procedure involves

Assisted hatching is performed in the laboratory on the day of transfer, or occasionally a few days before. The timing depends on your cycle — it can be performed on a day 3 embryo at the 6-8 cell stage, on a day 5 blastocyst, or on a frozen-thawed embryo before transfer. The clinical rationale is slightly different at each stage: on day 3, the concern is zona hardening from the culture environment; at blastocyst stage, it is used when your embryo shows signs of delayed or incomplete natural hatching; in frozen cycles, cryopreservation effects on the zona are the primary reason.

Using a precisely controlled laser, the embryologist creates a small opening in the zona pellucida. Your embryo is then returned to culture until transfer. The procedure takes a matter of minutes and does not involve any intervention on your part.

What the regulator assessment shows

The HFEA reviews each add-on against the evidence for whether it improves the chance of a live birth.

The HFEA assessment reflects genuine uncertainty. The Cochrane review of 39 randomised controlled trials involving over 7,200 women found that assisted hatching may slightly improve clinical pregnancy rates — but the evidence for improvement in live birth rates is uncertain. If the live birth rate without assisted hatching is around 28%, the rate with it falls somewhere between 27% and 34% — a range that includes no improvement at all.

There is also a finding the conversation does not always include. The Cochrane review also found a slight increase in multiple pregnancy risk — twins or higher order multiples — without a corresponding confirmed increase in live birth rates. Multiple pregnancy carries its own clinical risks, and this is worth raising with your consultant if it has not been discussed.

The clinical situations where assisted hatching may have a stronger case are specific:

• Older maternal age, where thicker zona pellucida is more common
• Frozen embryo transfer cycles, where cryopreservation may have affected zona integrity
• Embryos graded with high fragmentation or slow development
• Previous IVF cycles where good-quality embryos failed to implant

If your situation matches one of those, the rationale for assisted hatching in your cycle is clearer. If it was offered without that specific clinical picture behind it, the assessment is useful information to bring into the conversation with your clinic.

The regulator’s work is designed to inform that conversation, not replace it.

What hatching alone cannot do

Assisted hatching gets your embryo out of its shell. But if it is struggling to hatch, there may be other factors to consider.

Where hatching is delayed or incomplete, it can indicate that your embryo’s own energy reserves — its mitochondrial capacity — are under pressure. Hatching requires your embryo to expand, generate internal pressure and rupture the zona. If that process stalls, it is often a signal about the metabolic state of the embryo, not just the thickness of its shell. Assisted hatching can open the door mechanically. It cannot supply the energy your embryo needs to complete what follows.

Egg quality determines mitochondrial function in the embryo — and egg quality responds to nutritional and lifestyle inputs in the 90 days before egg collection.

When your embryo attaches, the next step is to embed — establishing the first physical relationship with the maternal blood supply. From there, early blood supply must follow to sustain it. Placental formation must begin. Immune modulation must shift to tolerate your embryo without rejecting it

More than 1 in 3 frozen transfers do not result in a live birth. Embryo implantation has 5 distinct phases and each has its own nutrient requirements. Your embryo needs to complete uterine lining preparation, early blood supply, gene expression, placental formation and immune modulation — all before a reliable test result.  Each of those phases responds to what the body has available to work with.

The Now Baby FET Implantation Meal Plan was designed around every one of those phases — the nutritional structure for the days your biology is doing its most demanding work. Professionally analysed. Beginning the day after transfer.

You didn’t come this far to wing it.

Get the FET Implantation Meal Plan 

The transfer is booked. Your embryo is ready. And somewhere in the paperwork, Embryo Glue has appeared — an addition to the transfer medium that your clinic says may help the embryo attach.

It is a small thing to say yes to. A substance added to the fluid surrounding your embryo at the moment of transfer, designed to make that first contact with the lining more likely to hold. The cost is relatively modest compared to everything else you have spent to get here. And when you have done everything else, saying yes to one more thing — however uncertain the evidence — can feel like the only rational response.

The Human Fertilisation and Embryology Authority, the UK’s independent fertility regulator, formally assesses the add-ons offered alongside standard IVF. Their evidence reviews are used internationally by clinicians and patients trying to understand what the research actually shows.

EmbryoGlue is on that list.

What Embryo Glue is

Embryo Glue is a hyaluronate-enriched embryo transfer medium. Hyaluronate — more commonly known as hyaluronic acid — is not a synthetic additive. It is a molecule that occurs naturally in the body, including in the fluid that surrounds the embryo during its early development and in the uterine lining in the days around implantation.

Levels of hyaluronic acid in the uterus rise naturally at the time of implantation. The body uses it as part of the environment that supports embryo attachment — it is detected by receptors on both the embryo and the endometrium, and plays a role in helping the embryo locate and adhere to the lining.

The Embryo Glue medium concentrates this molecule at a higher level than standard transfer media contain. The embryo is placed in the medium for at least ten minutes before transfer. When it is loaded into the catheter, some of the medium is transferred into the uterus along with it.

The hypothesis is that by raising the hyaluronic acid concentration at the point of transfer, the embryo arrives in a biochemical environment closer to the natural conditions at implantation — and the initial adhesion signals between embryo and endometrium are amplified at the critical moment.

Is it safe?

Hyaluronic acid is naturally present in the body and the reproductive system. No adverse effects from its use in transfer media have been documented in the clinical literature. Some studies have noted a slight reduction in miscarriage rates alongside the improvement in implantation rates, though this has not reached statistical significance across the full data set. The procedure itself is identical to a standard transfer — Embryo Glue adds nothing to what happens physically.

Safety is not the reason the evidence is conflicting. Efficacy is.

What the regulator assessment shows

The HFEA reviews each add-on against the evidence for whether it improves the chance of a live birth.

Embryo Glue carries a yellow rating — meaning the evidence is conflicting. Some studies have shown benefit, others have not. The picture is more positive than most add-ons in the HFEA review, but not consistent enough to support routine use across all patients.

The conflict becomes clearer when fresh and frozen cycles are examined separately. In fresh IVF transfer cycles, studies have shown a consistent signal of benefit — live birth rates rising from around 33% to 40% across a large body of trial data. In frozen embryo transfer cycles, the picture is contradictory — some studies show significant improvement, others show no effect at all. The yellow rating reflects that unresolved picture.

The clinical situations where Embryo Glue has shown clearest benefit are specific:

• Fresh IVF transfer cycles, particularly in women aged 35 and over
• Women with a history of recurrent implantation failure or unexplained infertility
• Women with diminished ovarian reserve where each embryo represents a significant investment — the limited cohort situation where every marginal gain matters
• Situations where the lining environment at transfer has been a concern in previous cycles

If you are preparing for a frozen embryo transfer and do not fit those categories, the conversation worth having with your clinic is what the specific rationale is for recommending it in your case.

The regulator’s work is designed to inform that conversation, not replace it.

What attachment alone cannot do

Embryo Glue supports the moment of transfer. The biology that follows depends on the environment the body is carrying into those days.

When your embryo attaches, the next step is to embed — establishing the first physical relationship with the maternal blood supply. From there, early blood supply must follow to sustain it. The immune environment of the uterus must modulate to tolerate it. The earliest stages of placental formation must begin.

That part is yours.

More than 1 in 3 frozen transfers do not result in a live birth — not because the embryo was wrong, not because the transfer was wrong, but because implantation is a biological process that responds to the environment it meets. That environment is shaped by nutrition, hormonal steadiness, inflammatory load, blood flow and metabolic health. None of those are addressed by what happens in the transfer room.

Embryo implantation has 5 distinct phases and each has its own nutrient requirements,  Your embryo needs to embed into the lining, establish an early blood supply, begin placental formation and negotiate immune tolerance — all before a test can confirm anything. Each of those phases responds to what the body has been given to work with.

The Now Baby FET Implantation Meal Plan was designed around every one of those phases — the nutritional structure for the days your biology is doing its most demanding work. Professionally analysed. Beginning the day after transfer.

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You didn’t come this far to wing it.

Get the FET Implantation Meal Plan 

Before your next transfer, your clinic may have suggested an endometrial scratch.

It is a small procedure, performed in the cycle before transfer. A thin catheter is passed through the cervix and a small area of the uterine lining is abraded — scratched — creating a localised injury. It takes a few minutes and can cause cramping similar to period pain, which usually resolves within hours. The scratch can also be performed during a diagnostic hysteroscopy, where the same instrument used to inspect the uterine cavity creates the injury at the point of withdrawal.

The procedure has a more layered biological rationale than it first appears.

Why the scratch is offered

The theory behind the endometrial scratch operates on several levels.

The first is the repair response. When tissue is injured, the body sends resources to fix it — increased blood flow, growth factors, immune activity. The theory is that this repair activity leaves the lining in a more receptive state when the embryo arrives the following cycle.

The second is that the scratch may trigger a process that prepares the lining to receive and hold an embryo — helping it form the right environment for attachment, controlling how deeply the embryo embeds, and supporting the immune tolerance that allows the embryo to stay rather than be rejected.

The third is timing. IVF stimulation can push the lining ahead of where the embryo is — the two are slightly out of sync at the point of transfer. The scratch in the previous cycle may help reset that timing.

These are plausible biological reasons for the procedure. The question the regulator addresses is whether they translate into more live births.

What the regulator assessment shows

The HFEA reviews each add-on against the evidence for whether it improves the chance of a live birth.

On the endometrial scratch, the published assessment is that the evidence does not currently support its use as a routine add-on for the general IVF population. Earlier studies suggested benefit, particularly in women with recurrent implantation failure, and the procedure became widely used on that basis. Larger, better-designed trials have not confirmed that benefit across the broader population. For women with recurrent implantation failure specifically, the picture remains less settled — some studies show signal, others do not.

The distinction matters. The HFEA assessment covers the general IVF population. If you have had multiple failed transfers, your situation sits in the subgroup where the evidence is more actively debated — and where a consultant’s specific rationale for the procedure carries more weight than a general recommendation.

The clinical situations where the scratch may still be considered are specific:

• Recurrent implantation failure where standard preparation has not produced a successful transfer and a consultant has a specific rationale for the procedure
• Individual cycle histories where the endometrial response has been atypical
• Where a diagnostic hysteroscopy is already planned and the scratch can be incorporated without additional intervention

If your recommendation came with that specific clinical picture behind it, the conversation with your consultant is a different one. If it was offered as a routine next step, the assessment is useful information to bring into that conversation.

The regulator’s work is designed to inform that conversation, not replace it.

What the repair response needs

The scratch creates the stimulus. Nutrients activate the response.

Each of the mechanisms the scratch is intended to trigger — repair, immune modulation, the preparation of the lining for attachment — draws on what the body has available. Zinc is a documented cofactor in cell proliferation and the formation of new tissue. A body well-supplied with the nutrients these processes depend on responds differently to the same stimulus than a depleted one. This is a gap that you can fill.

These are the same inputs implantation depends on when transfer comes.

The two-week wait is not neutral — it is biologically active. Receptivity, early blood supply, placental formation, immune modulation — each stage has its own specific nutrient requirements.

The Now Baby FET Implantation Meal Plan was built for targeted implantation support. Professionally analysed. Beginning the day after transfer.

You didn’t come this far to wing it.

Get the FET Implantation Meal Plan

The Human Fertilisation and Embryology Authority, the UK’s independent fertility regulator, is one of the few public bodies anywhere in the world that publishes plain-English evidence reviews on the optional tests, treatments and laboratory techniques offered alongside standard IVF. They look at the trials, weigh the data, and tell patients and clinicians what the research currently shows. Their assessments are widely referenced internationally, regardless of where treatment is taking place.

PGT-A testing — preimplantation genetic testing for aneuploidy — is one of those add-ons, and one of the most widely offered.

What PGT-A is

PGT-A testing is performed on embryos before transfer. A small number of cells is taken from each blastocyst and analysed for the expected number of chromosomes. Embryos with the typical count are described as euploid. Those with an extra or missing chromosome are described as aneuploid.

The aim is to give clinicians better information when deciding which embryo to transfer first.

Where PGT-A has a clear clinical role

The strongest evidence for PGT-A testing sits in specific clinical situations.

Women in their late thirties or forties, where chromosomal errors in eggs become more common with age. Couples who have had multiple miscarriages where chromosomal causes have already been identified. Repeated cycles where good-looking embryos have failed to implant. Severe male factor infertility, where sperm-related chromosomal errors are more likely.

The reason age and egg-related factors dominate that list is biological. More than 90% of embryo aneuploidies originate from errors during egg development, not sperm. The egg sits in arrested meiosis for decades before ovulation, and that long pause is what makes it uniquely vulnerable. This is why PGT-A’s clinical case strengthens with maternal age, and why egg quality in the months before stimulation matters in any cycle, with or without testing.

In these situations, PGT-A is doing what it was designed to do. It identifies which of the available embryos carry the expected number of chromosomes, so transfer decisions can be made on better information. The relief of hearing this one is normal after a miscarriage, after multiple failed cycles, is real. The clarity matters.

What the regulator assessment shows

The HFEA reviews each add-on against the evidence for whether it improves the chance of a live birth.

On PGT-A testing, their published assessment is that the evidence does not currently support its use as a routine test for the average IVF patient. For some groups, the data suggest it may even reduce the chance of a live birth, because chromosomally normal embryos can still be discarded based on a biopsy that is not always representative of the whole.

This is not a verdict against the test. It is a statement about who the evidence supports, and who it does not.

If your clinical situation matches one of those above, the case for PGT-A testing in your cycle may be stronger than the general-population review suggests. If it does not, the assessment is useful information to bring into the conversation with your clinic about whether testing is the right next step.

The point of the regulator’s work is not to override clinical judgment. It is to give patients and clinicians a shared evidence base to discuss.

What no add-on can change

Whatever you and your clinic decide about PGT-A testing, one thing remains constant.

PGT-A does not improve the embryo you transfer. It selects from what is already there.

By the time the test can be performed, your cycle is largely already written. Stimulation has happened. Eggs have been collected. Some have fertilised and developed; some have not. Whatever number of blastocysts is left at biopsy is the group PGT-A acts on.

The number of eggs collected, how well they matured, the integrity of the sperm at fertilisation, the rate of attrition through the lab — those are shaped in the months before the cycle, by biology that responds to nutrition, hormonal signalling, sleep, stress and metabolic health.

Once a euploid embryo is selected and transferred, what happens next has nothing to do with the test either. Implantation depends on a body that is ready to receive the embryo. Pregnancy depends on the embryo’s own continuing development inside that body.

Even with a chromosomally normal embryo, more than 1 in 3 frozen transfers do not result in a live birth. The endometrial environment during the two-week wait is the variable that remains within your influence.

 

Evidence-based peace of mind for the two-week wait

The 2 Week Wait is not neutral, it is biologically active.

The Now Baby FET Implantation Meal Plan is structured to support each stage of implantation — secure embedding, early circulatory development, balanced immune signalling, and the early hormonal and metabolic conditions that pregnancy depends on. Every meal has been professionally analysed using clinical nutrition software so the macronutrient and micronutrient profile is balanced and consistent.

What it gives you is a decision already made. You are not standing in the kitchen during the most important fortnight of your cycle wondering whether what you are eating is helping. The plan has been designed for these specific days, by a fertility nutritionist, against the physiology of implantation. Your job is to follow it.

That is what evidence-based peace of mind looks like during the two-week wait. A clear nutritional structure to follow, designed for the biology you are in.

You didn’t come this far to wing it.

Get the FET Implantation Meal Plan 

The embryos were good. The transfers were done correctly. And each time, your embryo didn’t make it.

If you have been through this more than once, you already know that recurrent implantation failure is one of the hardest places to be in fertility treatment — because it explains almost nothing about why. Something is preventing implantation. The question of what is rarely answered clearly.

When it isn’t, the immune system is frequently proposed as the reason. And steroids — prednisolone or dexamethasone, prescribed to modulate immune activity around the time of transfer — are among the most commonly offered next steps.

The Human Fertilisation and Embryology Authority, the UK’s independent fertility regulator, is one of the few public bodies anywhere in the world that formally assesses the add-ons offered alongside standard IVF. Their evidence reviews are used internationally by clinicians and patients trying to understand what the research actually shows.

Steroids for recurrent implantation failure are on that list.

What the immune theory is based on

Implantation requires the maternal immune system to do something counterintuitive. It must partially suppress itself — tolerating an embryo that carries paternal antigens it would ordinarily identify as foreign.

The theory behind immune add-ons is that this balance is harder to achieve in some women. The immune environment remains more active than implantation requires. Steroids, as anti-inflammatory and immune-modulating agents, are offered to support that shift.

The reasoning has a biological basis. The question the HFEA addresses is whether intervening in that signalling produces more live births.

What the regulator assessment shows

The HFEA reviews each add-on against the evidence for whether it improves the chance of a live birth.

The evidence for steroids in recurrent implantation failure is weak. Routine use across the general population of women with implantation failure is not currently supported.

The clinical situations where the case for steroids may be stronger are specific:

• A diagnosed autoimmune condition — rheumatoid arthritis, lupus, thyroid autoimmunity — where immune dysregulation is already documented
• Endometriosis, where chronic peritoneal inflammation is part of the clinical picture
• Elevated inflammatory markers identified in blood tests that a consultant is specifically responding to
• A reproductive immunologist has reviewed the full picture and identified a specific immune pattern worth addressing

If your recommendation for steroids came with that level of clinical rationale behind it — a named condition, a specific test result, a specialist assessment — the conversation is a different one. The regulator’s assessment covers the broader population. Your situation may sit within the narrower group where the evidence is more supportive.

If steroids were offered as a general next step after failed transfers, without that specific clinical picture behind them, the assessment is useful information to bring into the conversation with your consultant about what the reasoning is and whether it applies to you.

The regulator’s work is designed to inform that conversation, not replace it.

Where your influence sits

Waiting isn’t neutral

Implantation unfolds in stages.

Each stage responds to the nutritional and metabolic environment around it. These are the variables that remain within your influence.

More than 1 in 3 frozen transfers do not result in a live birth. The physiological environment during the two-week wait is within your capacity to support.

From the moment of transfer, your body is working. 

The Now Baby FET Implantation Meal Plan was built around every one of them. Professionally analysed. Beginning the day after transfer.

You didn’t come this far to wing it.

Get the FET Implantation Meal Plan 

A failed transfer of a good-quality embryo is one of the hardest things to make sense of. The clinical numbers said the embryo was strong. The lining looked right on the scan. The protocol was followed. And still, no pregnancy.

When that happens, the conversation often turns to whether the timing of transfer was actually correct for your body. Whether your personal window of receptivity is shifted from the standard. Whether a more bespoke approach to progesterone timing would change the next outcome.

That is the question the ERA test was designed to answer.

The ERA test — endometrial receptivity analysis — examines the genetic activity of the uterine lining at the moment of biopsy, with the aim of identifying a personal window of implantation that may differ from the standard.

It is also one of the add-ons formally reviewed by the Human Fertilisation and Embryology Authority, the UK’s independent fertility regulator. The HFEA publishes evidence reviews on the optional tests and procedures offered alongside standard IVF, and their assessments are widely used internationally by clinicians and patients trying to decide what is worth doing next.

What the ERA test is

The ERA test is a biopsy of the uterine lining, taken during a mock cycle that mimics the timing of a frozen embryo transfer. Around 200 genes associated with endometrial receptivity are analysed, and the lining is classified as receptive, pre-receptive or post-receptive at the moment of biopsy.

If the result is pre-receptive, the next transfer may be done with more hours of progesterone before transfer. If post-receptive, fewer. If receptive, standard timing is confirmed.

The aim is to personalise the implantation window for women whose cycles have not produced a pregnancy on standard timing.

Where the ERA test has a clearer clinical role

The strongest case for the ERA test sits in a narrow group.

Women who have had multiple failed transfers of chromosomally tested or otherwise high-quality embryos, where standard endometrial preparation has not resulted in implantation, and where a shifted window of receptivity is being investigated as a possible explanation.

In a small subset of these patients, the ERA test does identify a receptivity window outside the standard timing. For those women, adjusting the hours of progesterone before transfer is a logical clinical response.

That is the corridor where the test was originally designed to be useful.

What the regulator assessment shows

The HFEA reviews each add-on against the evidence for whether it improves the chance of a live birth.

On the ERA test, the published assessment reports that high-quality randomised trials have not shown that ERA-guided timing improves live birth rates for most patients — including, in the largest study available, women with recurrent implantation failure, the group the test was originally designed for.

This is not a finding that timing does not matter. It is a finding that the test, as currently performed, has not yet been shown to identify the timing change that leads to more live births in the patients it is most often offered to.

If your situation matches the narrow corridor above, the ERA test may still be worth discussing with your clinic. If it does not, the assessment is useful information to bring into that conversation about whether testing or a different approach makes more sense as your next step.

The point of the regulator’s work is not to override clinical judgment. It is to give patients and clinicians a shared evidence base to discuss.

What no add-on can change

The ERA test identifies a window. It does not prepare the lining that is offered up at that window.

By the time the test or transfer takes place, the receptivity of the endometrium has already been shaped — by lining thickness, blood flow to the uterus, hormonal steadiness, glucose regulation, inflammatory load, thyroid function, micronutrient status, and the broader gut and vaginal microbiome.

These are the variables that determine whether a transferred embryo, at any timing, has a body that is genuinely ready to receive it.

A receptive result on a mock cycle does not guarantee the same receptivity months later in the actual transfer cycle. A non-receptive result guides timing but does not address the underlying physiology that produced the result in the first place.

Even with personalised timing and a good-quality embryo, more than 1 in 3 frozen transfers do not result in a live birth. The endometrial environment during the two-week wait is the variable that remains within your influence.

The Now Baby FET Implantation Meal Plan is a fourteen-day, practitioner-designed nutritional protocol to follow from the day after transfer.

Evidence-based peace of mind for the two-week wait

The FET Implantation Meal Plan is structured to support each stage of implantation — secure embedding, early circulatory development, balanced immune signalling, and the early hormonal and metabolic conditions that pregnancy depends on. Every meal has been professionally analysed using clinical nutrition software so the macronutrient and micronutrient profile is balanced and consistent.

What it gives you is a decision already made. You are not standing in the kitchen during the most important fortnight of your cycle wondering whether what you are eating is helping. The plan has been designed for these specific days, by a fertility nutritionist, against the physiology of implantation. Your job is to follow it.

That is what evidence-based peace of mind looks like during the two-week wait. Not a promise about outcome. A clear nutritional structure to follow, designed for the biology you are in.

You didn’t come this far to wing it.

Get the FET Implantation Meal Plan