

The carnivore diet has earned a passionate following, especially for those seeking to relieve autoimmune symptoms, stabilize blood sugar, or eliminate digestive triggers. Carnivore is very different from a ketogenic diet which is more heavily weighted to fats and has more balance. Carnivore, on the other hand, it purely a meat/protein-based diet. Removing all plant matter, including fiber and polyphenols, often results in dramatic short-term improvements in an inflamed gut. But behind the anecdotal success lies a deeper systems-level question: what happens to the microbiome on a meat-only diet—and is that change healing, harmful, or both?
This blog explores the complexities of carnivore eating through the lens of microbial ecology, toxic metabolite production, and long-term host resilience.
What carnivore gets right — short term benefits
A zero-fiber, meat-only diet can act as a metabolic and immunological reset. This is how carnivore has been used in the work of Ben Azadi with his Keto Kamp Academy, as a tool in the healing toolkit but not as a long term dietary strategy. Many people report relief from bloating, skin rashes, migraines, and brain fog. Mechanistically, this makes sense:
- It removes fermentable carbohydrates that feed overgrown microbes.
- It starves problematic Gram-negative and FODMAP-sensitive species.
- It reduces microbial fermentation, which can lower intestinal gas and pressure.
- It limits exogenous plant antigens that can provoke immune reactions.
For individuals with SIBO, post-infectious IBS, histamine intolerance, or poorly regulated immunity, this can feel like a miracle. But a short term “miracle” is not always a foundation for long-term health. Some similar results can been obtained from a longer fast but fasting for extended periodics of time is not likely to maintain health.
Where carnivore starts to break the terrain
Long-term, carnivore diets may promote microbial shifts that compromise resilience, increase toxic burden, and reduce immune tolerance. The most concerning observations from data from a recent 90 day carnivore diet include:
- A consistent depletion of Bifidobacteria, key early-life and adult immune modulators, from an already very low level
- A drop in anaerobic SCFA producers such as Faecalibacterium and Roseburia.
- A rise in Gram-negative, bile-resistant organisms like Bacteroides, Bilophila, and Alistipes, often associated with protein fermentation and inflammatory metabolites. But beneficial metabolizers of secondary bile acids
- Persistent low levels of Akkermansia, important for mucin maintenance and metabolic signaling and very sensitive to oxygen in the gut
These aren't just compositional changes — they're functional shifts that affect ammonia production, redox balance, and systemic signaling pathways.
Not all diversity is healing
I learned this from my Parkinson’s microbiome research where in a number of studies the PD gut actually had greater diversity, but not a good bacteria. A common misconception in microbiome interpretation is that more species always means better health. But diversity in itself isn’t protective if the composition favors organisms adapted to stress, starvation, or inflammation.
In the post-carnivore microbiome profile, we saw a slight uptick in species richness, but without the return of keystone mutualists like Bifidobacteria, Akkermansia, or Faecalibacterium. These missing players are critical for barrier support, redox regulation, and metabolite cross-feeding. Their absence undermines true resilience, even if the overall species count increases. However, there were signs of butyrate production via non-traditional species that may have countered this lose.
Functional diversity matters more than raw diversity.
Ammonia and toxic metabolites: the hidden byproducts
When fermentable fibers disappear from the diet, microbes shift toward protein and amino acid fermentation. This process produces a host of metabolites that may be harmful in excess, especially over longer periods of time:
- Ammonia: Raises intestinal pH, increases epithelial permeability, and disrupts mitochondrial function. Produced by urease-expressing bacteria that also produce amino acid deamination.
- Phenols and p-cresol: Formed from tyrosine and phenylalanine. Associated with epithelial damage and oxidative stress. p-cresol is particularly toxic to mitochondria and has been found elevated in Parkinson’s and Austism microbiome research.
- Indoles and indoxyl sulfate: From tryptophan fermentation. Some indoles are beneficial in moderation, but others are linked to uremia, systemic inflammation, and neurotoxicity.
- Hydrogen sulfide (H₂S): Produced by sulfur-metabolizing microbes like Desulfovibrio and Bilophila. Can impair mitochondrial respiration and damage the colonic epithelium in excess. H₂S is a free radical scavenger and can be beneficial at low concentrations but is toxic at higher concentrations and is associated with SIBO.
These aren’t always flagged in stool or blood labs, but their production can be inferred from the overrepresentation of specific species and the absence of buffering organisms and substrates.
Protein Fermentation, Hydrogen Sulfide, and Methane
One of the underappreciated consequences of a carnivore diet is what happens when large amounts of protein reach the colon. Unlike fiber, which microbes ferment into short-chain fatty acids (SCFAs) such as butyrate that nourish and protect the gut lining, protein undergoes putrefactive fermentation. This process produces a very different set of byproducts: ammonia, phenols, indoles, branched-chain fatty acids, and large amounts of hydrogen gas (H₂).
What happens to that hydrogen determines whether your gut tips toward toxic hydrogen sulfide (H₂S) or methane (CH₄) production:
- H₂S pathway: Sulfate-reducing bacteria (Desulfovibrio, Fusobacterium, certain Clostridia) consume sulfur amino acids like cysteine and methionine, or taurine from bile salts, and convert them to H₂S. At low levels, H₂S acts as a signaling molecule. At higher levels, it becomes toxic — blocking butyrate oxidation in colonocytes, damaging the glycocalyx, and compromising the gut barrier.
- Methane pathway: Methanogenic archaea (Methanobrevibacter smithii) use hydrogen to reduce CO₂ into methane. Methane itself is not directly toxic, but it slows intestinal motility and is strongly linked to constipation-predominant IBS.
These two microbial guilds — sulfate reducers and methanogens — compete for hydrogen as a fuel source. Which pathway dominates depends on the balance of your microbiome. If sulfate reducers win, H₂S rises and barrier toxicity increases. If methanogens win, methane rises and bowel transit slows. Either way, the outcome diverges sharply from the protective SCFA environment we see with fiber fermentation.
For someone following a strict carnivore diet, this means:
- A high sulfur amino acid load from meat can push toward more H₂S.
- A low-fiber, low-SCFA environment leaves colonocytes without their protective fuel, making them more vulnerable to gas toxicity.
- Depending on your microbial makeup, you may develop either a H₂S-dominant terrain (inflammation, barrier damage) or a methane-dominant terrain (slowed motility, constipation).
- This is why two people can follow the same carnivore diet and have completely different gut outcomes. Ben Azadi's microbiome results may reflect a snapshot of his microbial guild balance at that moment, but the deeper question is how this terrain evolves over time — and whether the loss of fiber fermentation leaves the system less resilient in the long run.
The overlooked role of Bifidobacteria
In both early and later carnivore stool samples, Bifidobacteria are nearly absent. This is not surprising: Bifidobacteria require fibers like XOS, GOS, and arabinoxylans to thrive — substrates completely missing from meat-based and ketogenic heavy diets.
Why does that matter?
- Bifidobacteria are essential for immune training and mucosal tolerance.
- They produce acetate and other metabolites that nourish epithelial cells and support gut barrier function.
- They contribute to the microbial network involved in plasmalogen biosynthesis — lipids essential for mitochondrial membrane integrity, neural signaling, and redox control. See my substack on Dr.Dayan Goodenowe’s work.
Contrary to some earlier views, Bifidobacterium longum and Bifidobacterium bifidum do produce plasmalogens directly, as shown in recent studies:
Nagao et al., 2020. “Production of Plasmalogens by Bifidobacteria.”
Yamashita et al., 2017. “Plasmalogen levels and Bifidobacteria abundance correlate with cognitive resilience in elderly.”
Our Sugar Shift probiotic contains B. longum, a known plasmalogen producer. But in a fiber-depleted gut, these organisms can’t thrive or function optimally — they are metabolically active but underfed. Adding some of their favorite fibers in to a daily shake could go a long way to restoring these important strains.
When carnivore evolves — the Saladino example
Even staunch carnivore advocates have shifted. Dr. Paul Saladino, once a strict meat-only proponent, now includes fruit and honey in his daily intake. This shift isn’t just about glucose availability — it’s about feeding the microbiome.
Fruits contain soluble fibers, polyphenols, and fermentable sugars that:
- Support Bifidobacteria and Lactobacillus growth.
- Provide substrates for SCFA production.
- Restore redox balance through flavonoids and prebiotic compounds.
This change mirrors what we see clinically: once carnivore has done its work as an elimination tool, the next step is targeted reintroduction of fermentable plant material to rebuild microbial ecology.
Terrain change, not collapse
It’s inaccurate to describe the post-carnivore microbiome as collapsed — but it is shifted toward a stress-adapted, protein-metabolizing, bile-tolerant state. Some organisms persist, others emerge, but the balance is altered in ways that are hard to detect without understanding functional pathways and metabolite outputs. If we look at the research of the Hadza in Africa, it may provide some clues. This indigenous population eats a carnivore heavy diet part of the year and flips to a carbohydrate - root veggies and honey - diet in the opposite season. Their microbiomes adapt and adjust back and forth between the two. So this may provide some clues about how to restore a gut that has been too long without sufficient fiber sources.
We need to support the return of immune-supportive, SCFA-generating, mucin-feeding microbes,so that the system can regenerate.
With gratitude,
Martha Carlin, is a “Citizen Scientist”,
systems thinker, wife of Parkinson’s warrior, John Carlin, and founder of The BioCollective , a microbiome company expanding
the reach of science and BiotiQuest, the first of it’s kind probiotic line. Since John’s diagnosis in 2002,
Martha began learning the science of agriculture, nutrition, environment, infectious disease, Parkinson’s
pathology and much more. In 2014, when the first research was published showing a connection between the gut
bacteria and the two phenotypes of Parkinson’s, Martha quit her former career as a business turnaround expert
and founded The BioCollective to accelerate the discovery of the impact of gut health on all human disease. Martha was a speaker at the White House 2016 Microbiome Initiative launch, challenging the scientific
community to “think in a broader context”. Her systems thinking background and experience has led to collaborations
across the scientific spectrum from neuroscience to engineering to infectious disease. She is a respected out of the
box problem solver in the microbiome field and brings a unique perspective to helping others understand the
connections from the soil to the food to our guts and our brains.

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