Cycle 1

The Baseline: Evvy Metagenomic Results

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Cycle 1, Day 2. Test date: April 2, 2026.

The Evvy results are back, and they paint exactly the picture I expected: a microbiome that hasn't had any reason to organize itself yet.

The Scores

Evvy reports three summary metrics. Mine are all flagged "Out of Range":

  • Protective Score: 2% (target: >46%)
  • Diversity Score: 2.9 (target: <1.5)
  • Disruptive Score: 96% (target: <5%)

If you're not familiar with vaginal microbiome scoring (as I was prior to doing this test), the results look pretty alarming. A healthy vaginal microbiome is typically low diversity and high Lactobacillus dominance. The opposite of what you want in your gut. My results show the inverse: high diversity, almost entirely composed of anaerobic bacteria associated with bacterial vaginosis.

But here's the thing. I don't have BV. Evvy's own affiliated clinician didn't diagnose an infection. No odor, no irritation, no abnormal discharge beyond what's expected from peritoneal tissue (which produces more serous fluid than keratinized skin by design).

What's Living in There

The community is dominated by Prevotella. Five different Prevotella species account for about 40% of the total relative abundance:

  • Prevotella sp. (12.42%)
  • P. disiens (9.61%)
  • P. timonensis (8.87%)
  • P. buccalis (4.97%)
  • P. bivia (3.47%)
  • P. amnii (1.19%)

The rest is a mix of other BV-associated anaerobes: Peptoniphilus duerdenii (11.76%), Atopobium deltae (7.60%), Porphyromonas bennonis (7.19%), three species of Gardnerella (totaling ~10.4%), and Fannyhessea vaginae (3.27%).

This is a polymicrobial anaerobic community. It's disorganized, it's not protective, and it's exactly what the literature describes for vaginal microbiomes that lack Lactobacillus dominance.

The Important Part

Lactobacillus crispatus is present. At 2.29%, it's not dominant, but it's there. L. iners is also present at 1.53%.

This matters. L. crispatus is the species most strongly associated with a stable, low-pH vaginal environment. It's the one you want to see. The fact that it's detectable at all in peritoneal tissue that's less than a year post-op, before any targeted probiotic intervention, is the data point I care about most in this entire report. It means colonization is possible. The tissue can support it. Now I need to give it a competitive advantage.

L. iners is the more common but less protective Lactobacillus species. It tends to show up during transitional states and can coexist with disruptive bacteria. It's not a negative finding, but it's not the foundation I'm building on either.

What's Not There

The negatives are actually reassuring:

  • No Candida species (no yeast)
  • No E. coli
  • No Ureaplasma or Mycoplasma
  • No Staphylococcus aureus
  • All STI panels negative

These are organisms that would complicate the picture or require treatment. Their absence means the path forward is about competitive displacement, not infection clearance.

Antimicrobial Resistance

One resistance gene detected: tetracycline. This is common and not surprising in a polymicrobial community. The more relevant finding is that no macrolide resistance was detected, which means clindamycin (the first-line topical treatment for BV if it ever becomes clinically relevant) would remain effective.

No resistance detected for carbapenems, methicillin, quinolones, or vancomycin.

What This Means for the Protocol

This swab was collected on Day 2 of Cycle 1. The VagiBiom probiotic suppository loading phase hadn't started yet. The vaginal estradiol cream hadn't really been done either at this point (scheduled for Wednesdays and Fridays now). So this represents a true pre-probiotic baseline with early estradiol exposure.

The strategy from here is straightforward: continue the VagiBiom loading phase to introduce L. crispatus directly into the vaginal environment, maintain the estradiol cream schedule to support epithelial maturation and glycogen production (which Lactobacillus feeds on), and let the cyclic hormone protocol do its work on the tissue.

The next check will be the Juno Bio 16S rRNA interim at roughly six weeks, followed by the Evvy 12-week confirmation around July. That confirmation swab is the one that matters. It'll show whether the combination of direct probiotic inoculation, topical estrogen, and cyclic hormones actually shifted the community structure.

The Bigger Picture

There is almost no published data on vaginal microbiome composition in peritoneal flap vaginoplasty patients. What data exists is mostly from penile inversion, and it consistently shows skin-flora-dominant communities (Corynebacterium, Staphylococcus, Streptococcus). That's not what this looks like. This is an anaerobic community that, while not yet protective, at least resembles the type of community found in natal vaginal tissue, just without the Lactobacillus dominance that would make it healthy.

Whether that's a function of the peritoneal tissue itself, the estrogen exposure, or both, I can't say from a single time point. That's what longitudinal tracking is for.

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