What standard fertility care misses about implantation, inflammation, and the reproductive microbiome
If you transferred a “good” or even genetically normal (euploid) embryo and IVF still failed, you were likely told one of three things:
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“It was just bad luck.”
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“Implantation is unpredictable.”
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“You should consider donor eggs.”
None of those explanations are complete.
At Fab Fertile, we work with people who have already done everything “right.” They produced good embryos. Transfers looked perfect. Lining was ideal. And yet, implantation failed.
When this happens, the issue is rarely the embryo alone. It is almost always the environment the embryo was transferred into.
Implantation is a biological process that depends on immune balance, inflammation control, hormone signaling, blood flow, metabolic health, and critically, the vaginal and seminal microbiome.
What “Good Embryo” Really Means (and What It Does Not)
In IVF, a “good” embryo usually means:
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High-grade morphology
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Euploid on PGT-A testing
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Proper blastocyst development and thaw survival
What it does not mean is that implantation is guaranteed.
Embryos implant into a living, responsive system. If that system is inflamed, immune-activated, hormonally misaligned, or microbiologically imbalanced, even excellent embryos can fail.
Structural issues such as fibroids, polyps, or hydrosalpinx can also affect implantation, but in many cases these have already been ruled out before IVF or FET is pursued.
The Two Sides of IVF Success
IVF success depends on two equally important variables:
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Embryo competence
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Endometrial and systemic readiness
Most clinics focus almost entirely on the first.
At Fab Fertile, we see the second overlooked again and again.
1. Immune Dysregulation: When the Body Does Not Tolerate the Embryo
Pregnancy requires immune adaptation. The immune system must allow implantation without triggering excessive inflammation.
When this does not happen, embryos may fail to implant or detach very early.
Functional Immune Markers to Explore
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Antinuclear antibodies (ANA)
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Thyroid antibodies (TPO, TG)
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hsCRP as a global inflammation marker
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Homocysteine as a proxy for immune and methylation stress
What we see at Fab Fertile:
Clients with repeated IVF failure often show subtle immune activation long before it is considered “clinical.” These patterns are rarely addressed unless there are multiple miscarriages.
2. Chronic Inflammation Undermines Implantation
Inflammation interferes with:
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Endometrial receptivity
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Progesterone signaling
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Placental development
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Uterine blood flow
This inflammation is often low-grade and systemic.
Inflammatory Markers Commonly Missed
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hsCRP
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Ferritin (both high and low patterns matter)
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Fibrinogen
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Vitamin D as an immune-modulating hormone
Inflammation frequently originates outside the uterus, particularly in the gut or microbiome.
3. Progesterone Signaling: More Than a Number
Progesterone is essential, but blood levels alone do not guarantee effective signaling.
Problems arise when:
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Progesterone timing is off
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Receptors are downregulated by inflammation
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Cortisol disrupts progesterone response
What we see clinically:
Many Fab Fertile clients were told progesterone was “fine,” yet their symptom patterns and repeated implantation failure suggested otherwise.
4. Blood Flow and Clotting Tendencies Matter
Implantation requires oxygen and nutrient delivery to the endometrium.
Subtle clotting or vascular issues often go undetected.
Markers to Consider
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Fibrinogen
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Platelet patterns
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Iron and ferritin trends
Even mild abnormalities can impair implantation and placental development.
5. Endometrial Receptivity Is Not Just Timing
A lining can look perfect on ultrasound and still be unreceptive.
Receptivity is influenced by:
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Hormonal signaling
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Immune balance
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Inflammation
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Microbiome health
Timing tests alone do not explain why receptivity is impaired.
6. Vaginal and Seminal Microbiome: A Critical and Overlooked Factor
One of the most common reasons IVF fails despite perfect embryos is microbiome imbalance, particularly involving Ureaplasma and Mycoplasma.
Why the Vaginal Microbiome Matters
A healthy vaginal microbiome is typically Lactobacillus-dominant, which supports:
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Optimal pH
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Local immune tolerance
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Reduced inflammation
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Endometrial receptivity
When Lactobacillus is low and inflammatory bacteria are present, implantation rates decline, even with euploid embryos.
Ureaplasma and Mycoplasma: Often Missed, Clinically Relevant
These organisms:
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Are frequently asymptomatic
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Are not reliably included in standard STI screening
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Can trigger chronic local inflammation
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Are associated with implantation failure and early loss
Importantly, IVF does not bypass this issue.
Professional organizations such as the American College of Obstetricians and Gynecologists and the European Society of Human Reproduction and Embryology acknowledge that genital tract infections and altered reproductive tract microbiota are associated with adverse reproductive outcomes, even when embryos are chromosomally normal.
Why the Seminal Microbiome Also Matters
This is where many protocols fall apart.
If the male partner carries inflammatory bacteria:
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Reinfection can occur after treatment
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Vaginal inflammation persists
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Implantation continues to fail
Seminal Microbiome Impact
Inflammatory bacteria in semen are associated with:
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Increased oxidative stress
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Higher sperm DNA fragmentation
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Immune activation in the female reproductive tract
What we see at Fab Fertile:
Repeated IVF failure resolves only after both partners are evaluated, treated, and retested. Treating one partner alone often leads to relapse.
Functional Testing to Explore
From a functional fertility perspective:
Vaginal Testing
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Vaginal microbiome analysis
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Screening for Ureaplasma and Mycoplasma
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Assessment of Lactobacillus dominance
Seminal Testing
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Semen analysis with microbiome evaluation
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Inflammatory and oxidative stress patterns
This is especially important after:
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Failed IVF or FET with euploid embryos
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Recurrent implantation failure
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Unexplained infertility
What we consistently see at Fab Fertile:
When only one partner is treated, inflammation often returns. Successful implantation usually occurs only after both partners are treated, and eradication is confirmed before transfer.
Why Clinics Rarely Address This
Most fertility clinics:
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Test only when symptoms are present
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Do not routinely screen male partners
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Rarely confirm eradication before transfer
Patients are told everything “looked perfect” while low-grade inflammation persists.
Frequently Asked Questions
Can a euploid embryo fail because of infection?
Yes. Euploid embryos can fail to implant in the presence of inflammation or microbiome imbalance, including Ureaplasma or Mycoplasma.
Why wasn’t this tested before IVF?
These organisms are often asymptomatic and not part of routine fertility screening unless there are repeated losses.
Can IVF work if only one partner is treated?
Often no. Reinfection from an untreated partner is common and leads to persistent inflammation.
Does donor egg IVF fix this?
No. Donor eggs do not correct immune imbalance, inflammation, or microbiome issues.
Key Takeaways
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A good or euploid embryo does not guarantee implantation
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Immune balance and inflammation are critical
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Progesterone signaling involves timing and responsiveness
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Blood flow and metabolic health matter
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Vaginal and seminal microbiome imbalance can override embryo quality
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Treating both partners and confirming eradication is essential
The Bottom Line
IVF can fail even with perfect embryos because implantation depends on far more than genetics.
At Fab Fertile, we consistently see success improve when:
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The immune system is regulated
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Inflammation is addressed
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Progesterone signaling is optimized
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The vaginal and seminal microbiome are evaluated and treated
If you have had a failed IVF or FET with a good embryo, the answer is not always another cycle.
Sometimes, the answer is better questions and better testing.