In October 2025, I got my first full gut test back from Thorne. I'd been dealing with a grab bag of health issues for years and figured a gut test might explain some of it. It explained all of it. And the results were bad.
Staphylococcus at the 99.9th percentile. Higher than 999 out of 1,000 healthy adults in the reference population. My Bifidobacterium (one of the most important keystone species in the human gut) was at the 15.5th percentile. My gut dysbiosis score was 69.8, well above the 66 threshold for severe imbalance. My beta diversity (how similar my overall microbiome was to healthy adults) was at 66%, meaning my gut composition looked nothing like a healthy person's.

At the time, I was already managing Hashimoto's thyroiditis with TPO antibodies over 700 IU/mL (normal is below 9), active Epstein-Barr virus reactivation with early antigen antibodies at 4x the upper limit, and emerging CCP antibodies flagging early rheumatoid arthritis. I had seven genetic mutations affecting methylation, vitamin D reception, and catecholamine clearance. I was 31 years old.
When I saw those gut results, the picture snapped into focus. The gut dysbiosis wasn't a side problem. It was the upstream root cause driving the entire autoimmune cascade.
The Chain I Didn't See for Years
Here's the mechanism, in my case: extreme Staphylococcus overgrowth produces superantigens that dysregulate the immune system. That overgrowth, combined with critically low Bifidobacterium (which normally regulates immune tolerance and suppresses pathogens), created a state of chronic intestinal immune activation. The gut barrier degrades. Bacterial components and pro-inflammatory cytokines (IL-6, TNF-alpha) translocate into the bloodstream. The immune system, now chronically activated and poorly regulated, begins attacking self-tissue through molecular mimicry.
In my case: the thyroid. The joints. And meanwhile, the immune suppression from this chronic activation allowed EBV, a virus that over 90% of adults carry latently, to reactivate.
Gut dysbiosis → leaky gut → immune activation → autoimmune attack → thyroid destruction. That's the chain. And for years, nobody tested my gut. I was managing downstream symptoms (thyroid medication, monitoring antibodies) while the upstream driver kept running.

I Ate Yogurt Every Day for Years. My Gut Was Still a Disaster.
This is the part that still gets me. I wasn't ignoring my gut. I was the guy doing everything the internet said to do. Greek yogurt every morning like clockwork. Kombucha when I felt like it. A generic probiotic from Whole Foods on my shelf. I even considered adding kimchi (every gut health article on the internet tells you to eat fermented vegetables) but I never actually did it. I was the poster child for casual gut health. I genuinely believed I was doing the right thing.

And the entire time, Staphylococcus was at the 99.9th percentile. My Bifidobacterium was cratering. My thyroid was being destroyed by my own immune system. The yogurt did nothing. The kombucha did nothing. The probiotic did nothing. Not because those things are inherently useless, but because they had no relationship to the actual problem. It's like taking Tylenol for a broken leg. You feel responsible. You feel like you're doing something. But the bone is still broken.
I didn't need more fermented foods. I needed to test, find out what was actually wrong, and intervene with precision. Instead I wasted years on generic advice while the upstream driver of my autoimmune cascade ran unchecked.
Why That Advice Would Have Made Me Worse Even If I'd Doubled Down
Here's what makes it worse: if I'd listened harder to the generic advice, eaten more fermented foods, tried a fancier probiotic, it would have actively made things worse. Remember how I considered adding kimchi? I'm glad I didn't.
My gut had an extreme overgrowth of pathogenic bacteria. Adding more bacteria through fermented foods, without knowing what was already overgrown, is like throwing more fuel on a fire and hoping it turns into water. Fermented foods are high in biogenic amines including histamine. With a gut already in dysbiosis, with already elevated Enterobacteriaceae (69th percentile) and Streptococcus (77th percentile) and Enterococcus faecium (89th percentile), the last thing I needed was more microbial metabolites in a system already overwhelmed with them.
And the generic probiotic? Telling someone to “take a probiotic” is like telling them to “take a medicine.” Which one? For what? At what dose? I didn't need random Lactobacillus strains thrown at the wall. I needed to kill the Staphylococcus overgrowth and specifically rebuild my depleted Bifidobacterium population. Those are two completely different interventions, and no off-the-shelf probiotic addresses both.
The Weizmann Institute published research in 2018 showing that after antibiotic treatment, generic probiotics actually delayed the return of the native microbiome by months and promoted the bloom of antibiotic-resistance genes. The wellness world ignored this because it's bad for business.
I needed a targeted protocol. Not vibes.
What I Actually Did: A Two-Front War
Starting in October 2025, I built a 12-week protocol around a simple principle: kill what's overgrown, then reseed what's missing. Two fronts, simultaneously.
Front 1: Targeted antimicrobials. I wasn't trying to sterilize my gut. I was trying to selectively reduce the pathogenic overgrowth, primarily Staphylococcus, E. coli, and Enterococcus faecium.
- Oregano oil (carvacrol), 4x daily with meals. Broad-spectrum antimicrobial with particular efficacy against Staphylococcus aureus and gram-positive pathogens.
- Berberine 500mg twice daily (lunch and dinner). Antimicrobial that also has blood sugar regulation and anti-inflammatory properties. Published data against Staphylococcus, E. coli, and Streptococcus.
- Monolaurin 1,200mg twice daily (morning and night). Derived from lauric acid. Disrupts lipid membranes of gram-positive bacteria and enveloped viruses, relevant for both my Staph overgrowth and active EBV.
Front 2: Precision reseeding. This is where generic advice completely fails. I wasn't deficient in everything. I was specifically deficient in Bifidobacterium at the 15.5th percentile, while my Akkermansia (70th), Coprococcus (61st), and Faecalibacterium prausnitzii (53rd) were adequate. So I targeted Bifidobacterium specifically.
- Bifido Maximus, a high-potency Bifidobacterium probiotic, 4x daily. Not a multi-strain generic blend. A targeted intervention for what my test showed I was missing.
- HMO prebiotic (human milk oligosaccharides), paired with Bifido Maximus every dose. HMOs selectively feed Bifidobacterium species. This isn't generic fiber. It's a precision prebiotic that feeds the exact genus I was trying to restore.
Front 3: Gut barrier repair. With a dysbiosis score of 69.8 and intestinal permeability score of 37.9, my gut lining needed direct support.
- L-Glutamine 20g/day (10g morning, 10g night). The primary fuel source for enterocytes (the cells lining the intestinal wall). At this dose, it provides direct substrate for gut barrier repair.
- BPC-157 500mcg twice daily, empty stomach. A peptide with published evidence for gastrointestinal mucosal healing, angiogenesis, and anti-inflammatory effects in the gut.
- Zinc-Carnosine 16mg with breakfast. Stabilizes the gut mucosa and has clinical trial data for gastric and intestinal lining protection.
- SunButyrate 875mg daily. Direct butyrate supplementation (the primary fuel source for colonocytes) because my own butyrate production was inadequate.
The daily rhythm was simple. I call it 4-2-4-2: HMO + Bifido 4x daily, oregano oil with every meal, BPC-157 morning and night, monolaurin morning and night. Everything else once daily with breakfast. Yes, my kitchen counter looks like a small pharmacy. But the actual daily time commitment is about two minutes. Consistency matters more than perfection.

Why These Things and Not Others
Every intervention in my protocol exists because my test data demanded it. Not because someone on the internet said it was good for “gut health.”
Why Bifido Maximus and not a generic probiotic blend? Because my Bifidobacterium was at the 15.5th percentile. Multi-strain probiotics dilute the dose across many species, most of which I didn't need. The Weizmann Institute research showed that probiotic colonization depends on your existing microbiome (people are either “persisters” or “resisters”) and a high-dose, targeted approach gave me the best chance of actually moving the needle on the genus I was deficient in.
Why oregano oil and not a pharmaceutical antibiotic? Because I wasn't treating an acute infection. I was trying to selectively reduce overgrowth while preserving beneficial species. Pharmaceutical antibiotics are indiscriminate. The Weizmann research showed that after antibiotic treatment, probiotics delayed native microbiome recovery and expanded antibiotic-resistance genes. Botanical antimicrobials like oregano, berberine, and monolaurin have narrower activity profiles and published data showing they can reduce pathogenic bacteria without the same level of collateral damage.
Why HMO prebiotics and not inulin or generic fiber? Because not all fiber feeds all bacteria equally. HMOs are selectively utilized by Bifidobacterium species. Inulin feeds a broader range of organisms, including some I was trying to suppress. A 2024 study in Nature Medicine (the ZOE METHOD trial) showed that dietary interventions have different effects depending on your existing microbiome composition. High-fiber diets improved glucose metabolism in people with Prevotella-dominated guts but did nothing for those with Bacteroides-dominated guts. The same food helping one person and doing nothing for another. My prebiotic needed to match the bacteria I was trying to grow, not feed everything indiscriminately.
Why SunButyrate supplementation if butyrate is naturally produced? Because by January 2026, my butyrate production had collapsed from the 72nd to the 18th percentile. The antimicrobial protocol, while successfully reducing pathogens, also disrupted some butyrate-producing species. My Roseburia dropped from the 96.5th to the 11.6th percentile. Direct butyrate supplementation bridges the gap while those populations rebuild. This is the kind of tradeoff that generic advice never prepares you for.
Three Months of Data: What Changed
In January 2026, I retested. You can see my full biomarker tracking, including every gut marker, on my biomarkers page. Here's the summary.

The wins were real:
- Bifidobacterium: 15.5th → 75.3rd percentile (+385%). From severely deficient to above average. The single most important improvement. This was the Bifido Maximus + HMO protocol working exactly as intended.
- Staphylococcus: 99.9th → 67.5th percentile (−32%). Still elevated, but no longer at the extreme. The antimicrobial stack reduced it meaningfully.
- Beta diversity: 66% → 35% (−47%). My overall microbiome composition moved dramatically closer to healthy reference populations.
- Prevotella: 87.8th → 72.4th percentile (−18%). This is an RA-associated bacterium. I'm watching it closely given my positive CCP antibodies.
- Veillonella: 68.2nd → 26.9th percentile. Staphylococcus aureus: 60.9th → 35.4th percentile. Multiple pathogenic species trending in the right direction.
But gut healing is not a straight line:
- Butyrate production: 72nd → 18th percentile (−75%). This is the biggest concern. The antimicrobial protocol reduced pathogens but also hit butyrate-producing species. Roseburia collapsed from the 96.5th to the 11.6th percentile. Butyrate is the primary fuel for colonocytes, the cells lining the colon, and its loss degrades gut barrier integrity. This is why I'm supplementing SunButyrate directly while rebuilding those populations.
- Blautia: 58.4th → 96.4th percentile (+65%). This is an autoimmune-associated bacterium linked to molecular mimicry and T-cell dysregulation in rheumatoid arthritis. It bloomed into the ecological niche left by suppressed species. More on this below. It's become the central problem of my next phase.
- Total fungi: 77.1 → 88.1 percentile (+14%). When you reduce bacterial populations, fungi expand into the space. This is a known consequence of antimicrobial protocols and needs to be addressed.
- Citrobacter freundii: 1st → 94.6th percentile. An opportunistic pathogen that dramatically expanded. The antimicrobial protocol created an ecological niche and C. freundii filled it. This is what happens when you disrupt an ecosystem. You don't just remove what you targeted.
- B vitamin production declined across the board. B3 (niacin) dropped from the 46th to the 5th percentile. B6 from 74th to 30th. Folate from 66th to 34th. The bacteria that produce these vitamins were impacted by the protocol.
This is why I keep saying: gut health is not simple. My protocol achieved exactly what it was designed to do (crush the Staph overgrowth, rebuild Bifidobacterium, shift beta diversity toward healthy) and it also created new problems that I now need to address. It's like fixing a leak in your roof and discovering the plumbing is shot. Anyone who tells you there's a clean, linear path to a “healthy gut” hasn't actually tracked the data.
The Blautia Problem: Why “Good for Gut Health” Can Be Terrible for Your Gut
This is my favorite example of why gut advice has to be personalized, and why it makes me a little crazy when people oversimplify this stuff. Blautia is not a pathogen. It's commensal. It's supposed to be there. At normal levels it participates in carbohydrate fermentation and produces short-chain fatty acids. Some studies even list it as beneficial. Go ahead, Google “Blautia gut health.” You'll find articles calling it a good bacterium.
But at the 96th percentile, which is where mine is, it's associated with molecular mimicry, T-cell dysregulation, and autoimmune progression. Specifically rheumatoid arthritis, which is the exact condition I'm trying to prevent given my positive CCP antibodies. A bacterium that is genuinely good for most people is, at this level, actively dangerous for me. This is the entire point: what's healthy in one context is pathological in another. You cannot know which without testing.
And here's how it got this bad: I killed butyrate producers (Roseburia crashed to the 11th percentile) while the antimicrobial protocol left an ecological niche. Blautia, an opportunist, filled it. The same intervention that fixed my Staph overgrowth created a new problem that is specifically dangerous for someone with my autoimmune profile. For someone without CCP antibodies, a Blautia bloom might be a non-issue. For me, it's a priority. Rebuilding Roseburia and other competitors is as important as directly suppressing Blautia. You can't just keep killing things without rebuilding what competes with them.

What feeds Blautia:
| Substrate | Notes |
|---|---|
| Simple sugars | Fructose, glucose |
| Refined carbs | Even gluten-free grains |
| Certain fibers | FOS, inulin (avoid these specifically) |
| Alcohol | Even occasional |
What suppresses Blautia:
| Intervention | Mechanism |
|---|---|
| Pomegranate extract | Selective polyphenol inhibition (I'm on this) |
| EGCG / green tea extract | Same mechanism (I'm on this) |
| Berberine | I reduced this. May need to keep a low dose specifically for Blautia |
| Time-restricted eating | Starves overgrowth |
| Lower carb intake | Reduces substrate |
I'm already on pomegranate extract and EGCG. It may not be enough. I'm considering adding short 5-day pulses of low-dose oregano oil (I stopped it entirely, but pulsing may help without the same collateral damage to butyrate producers) and allicin (garlic extract), a selective antimicrobial. I also need to cut high-fructan foods like whole onion and garlic. Ironic, since allicin extract is fine while the whole food feeds the problem.
But here's the real insight: Blautia won't normalize until Roseburia recovers and competes for the niche. You can't just suppress the opportunist. You have to rebuild the competitors. That's why I'm on PHGG and arabinogalactan to selectively feed butyrate-producing species, supplementing Clostridium butyricum (a spore-forming butyrate producer), and continuing direct butyrate via SunButyrate to bridge the gap. Timeline: 8–12 weeks, then retest.
No generic protocol would tell you any of this. No influencer would know that the inulin they're recommending for “gut health” specifically feeds the bacterium that's driving your autoimmune risk. No off-the-shelf probiotic would address a problem this specific. This is what personalized gut health actually looks like: understanding which organisms are problems for you, what feeds them, what suppresses them, and what competitors need to be rebuilt. It's not a food trend. It's ecology.
The Next Phase
Based on the January 2026 results, I'm adapting. This is the part generic advice never covers: what happens when your first intervention creates second-order effects.
I'm continuing the Bifido Maximus + HMO protocol because it worked. My Bifidobacterium is now in a good range and I want to maintain that. I'm scaling back the broad antimicrobials since the primary Staph overgrowth is reduced, and the continued pressure was contributing to the butyrate producer decline and fungal expansion. But I may keep low-dose berberine for Blautia suppression specifically.
The fungal expansion (77th → 88th percentile) needs its own intervention. Saccharomyces boulardii and possibly antifungal strategies are on the table. When you reduce bacterial populations, fungi expand into the space. This is a known consequence of antimicrobial protocols, and ignoring it just trades one dysbiosis for another.
I'll retest in three months. Then adjust again. That's the process. Test, intervene based on data, retest, adapt. There is no endpoint where you're “done.” But it works.
What This Taught Me About Gut Health Advice
Look, I get it. I used to be the person who would've taken the generic advice and felt good about it. Eat kimchi. Drink kombucha. Take a probiotic. Maybe throw in some bone broth for good measure. It sounds reasonable. It sounds scientific-ish. And for someone with a healthy baseline microbiome, it might even be fine.
But for me, with Staphylococcus at the 99.9th percentile, Bifidobacterium at the 15.5th, an autoimmune cascade actively destroying my thyroid, and seven genetic mutations affecting how my body processes everything from folate to catecholamines, generic advice would have been, at best, useless. At worst, actively harmful. Fermented foods would have added histamine load to a system already overwhelmed with microbial metabolites. A generic probiotic would have added random species while doing nothing about the overgrowth that was the actual problem.
The Stanford 2024 fingerprint study proved what my data already told me: your microbiome is unique to you. The bacteria that persist most stably are those most particular to the individual. The Weizmann researchers showed that probiotic colonization depends on your baseline microbiome. The ZOE PREDICT studies, across thousands of participants, demonstrated that personalized dietary programs significantly outperform standard guidelines.
None of this is theoretical for me. I lived it. I have the before-and-after data. The generic approach failed silently for years while my autoimmune markers climbed. The data-driven approach moved Bifidobacterium by 385% in three months.
What I'd Tell Someone Starting From Where I Was
Get tested before you do anything else. A Thorne Gut Health Test uses shotgun metagenomics to identify which microbes are present and their genetic potential. A GI-MAP uses quantitative PCR for specific pathogen detection. Neither is perfect. scientists haven't yet defined a consensus “healthy” baseline microbiome, and your microbiome changes throughout the day. But a snapshot with data is infinitely better than flying blind on influencer advice.
Work with a functional medicine practitioner who can interpret the data. Only 28% of primary care providers feel confident prescribing specific probiotic strains. If most doctors aren't confident interpreting this data, an Instagram account with a kombucha affiliate link definitely can't.
Target your interventions to your data. If you're deficient in Akkermansia, Pendulum Therapeutics has a formulation with actual clinical trial data showing a 0.6% HbA1c reduction. If you're low in Bifidobacterium like I was, Bifido Maximus with HMO prebiotics specifically feeds that genus. If you have SIBO, you need to address the overgrowth before adding more bacteria. The intervention has to match the problem.
Expect second-order effects and plan to retest. My antimicrobial protocol worked beautifully for its primary targets and simultaneously created a butyrate production collapse, a Blautia bloom, and fungal expansion. This is how complex ecosystems work. You don't just remove something and call it done. You intervene, measure, and adapt. Plan for at least three testing cycles over a year.
Be skeptical of anyone giving universal gut advice. If someone tells you a single food, supplement, or protocol is good for everyone, they're either selling something or repeating what someone selling something told them. The global probiotic industry is worth $72–90 billion. The incentive structure is broken: companies sell generic supplements, influencers promote them for affiliate revenue, consumers buy them without testing, most feel no benefit, and the industry grows anyway.
I track every biomarker publicly. My full gut microbiome results, blood work, autoimmune markers, and supplement protocol are all available on my biomarkers page. I do this because I think transparency about what's actually working, and what isn't, is more valuable than another confident voice telling you to eat sauerkraut.
My gut was destroying me from the inside out for years. Generic advice didn't catch it. Testing did. Data-driven intervention moved the numbers. And the work isn't done. It's iterative, messy, and full of tradeoffs. But at least now I know what I'm actually fighting.
That's the real story of gut health. Not the clean version the wellness internet sells.
References
- Zeevi, D. et al. “Personalized Nutrition by Prediction of Glycemic Responses.” Cell, 163(5):1079-1094 (2015).
- Zmora, N. et al. “Personalized Gut Mucosal Colonization Resistance to Empiric Probiotics Is Associated with Unique Host and Microbiome Features.” Cell, 174(6):1388-1405 (2018).
- Suez, J. et al. “Post-Antibiotic Gut Mucosal Microbiome Reconstitution Is Impaired by Probiotics and Improved by Autologous FMT.” Cell (2018).
- Sonnenburg, J. et al. “Gut-Microbiota-Targeted Diets Modulate Human Immune Status.” Cell (2021).
- ZOE METHOD Trial. “Personalized dietary program improves cardiometabolic health.” Nature Medicine (2024).
- Stanford Medicine. “The microbiome is as unique as a fingerprint, Stanford study finds.” (2024).
- NIH Human Microbiome Project (2012). 242 healthy volunteers, 5,000+ samples, 3.5 terabytes of data.
