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BiomeLogic research brief
The Host Capacity Model — condensed brief
Version 1.1 · Last materially reviewed 2026-08-22 · Educational systems-biology analysis, not medical advice
Definition
The Host Capacity Model reads recurrent SIBO, chronic dysbiosis, mast-cell over-reactivity, and post-viral gut syndromes as downstream of a loss of colonocyte bioenergetic capacity — the epithelium's ability to oxidise microbial butyrate and hold the colon's oxygen gradient — rather than as primary microbial pathology.
What the model proposes
- The microbial pattern seen on testing is treated as an indicator of habitat conditions, not as the lesion itself.
- Colonocyte oxidative capacity rests on three pillars: substrate transport, mitochondrial machinery, and regulatory integrity (NAD⁺ / sirtuin signalling).
- When that capacity falls, oxygen availability at the mucosal surface changes, and ecological selection shifts toward facultative organisms.
- Barrier strain, immune and mast-cell amplification, bile-acid signalling changes, and motility instability are read as connected consequences of the same substrate problem rather than as separate diseases.
- Recurrence after antimicrobial pressure is expected when the habitat that selected the organisms is unchanged.
What the model does not establish
- It does not establish that colonocyte bioenergetic failure is the cause in any individual person.
- It does not establish that any treatment, supplement, diet, or protocol restores host capacity or prevents recurrence.
- It does not provide a diagnostic test. No routine assay measures colonocyte oxidative capacity in clinical practice.
- It does not replace, override, or reinterpret a clinician's diagnosis or care plan.
- It does not claim priority over, or refutation of, existing motility, immune, or infection-based models — those remain live competing explanations.
Evidence map
| Mechanism | Tier | References |
|---|---|---|
| Butyrate → PPAR-γ → colonocyte oxygen consumptionColonocytes oxidise microbially derived butyrate, and that oxygen-consuming metabolism maintains the physiological hypoxia of the healthy colonic surface. | Animal / mechanistic evidence | PMID 21531334; PMID 27518564 |
| Epithelial hypoxia → suppression of facultative anaerobesAn intact epithelial oxygen sink restrains expansion of facultative anaerobes such as Enterobacteriaceae. | Animal / mechanistic evidence | PMID 24762973; PMID 30143479 |
| Nitrate respiration → pathobiont advantageHost-derived nitrate provides an alternative respiratory acceptor that favours facultative organisms when the anaerobic niche destabilises. | Animal / mechanistic evidence | PMID 23393266 |
| Colonocyte energy failure → luminal oxygen leakWhen colonocyte oxidative metabolism falls, less oxygen is consumed at the surface and more diffuses into the lumen. | Clinical-pattern inference | PMID 27518564; PMID 21531334 |
| H₂S → inhibition of colonocyte β-oxidationHydrogen sulfide inhibits colonocyte butyrate oxidation, which can reinforce the same energy deficit that destabilised the habitat. | In vitro evidence | PMID 12796484 |
| Bile-acid signalling (FXR / TGR5)Conjugated bile acids restrict small-bowel bacterial overgrowth and act through FXR and TGR5 receptors that also influence motility and immune tone. | Animal / mechanistic evidence | PMID 16473946 |
| LPS translocation → TLR4 → low-grade endotoxemiaBarrier strain permits bacterial lipopolysaccharide translocation, engaging TLR4 signalling and a systemic low-grade inflammatory tone. | Strong human evidence | PMID 17456850 |
| Mast-cell activation → barrier and vagal amplificationMast-cell mediators increase epithelial permeability and modulate visceral afferent signalling, forming a self-reinforcing loop with barrier strain. | Strong human evidence | PMID 32717152 |
| Tryptophan partitioning — AhR / IL-22 barrier signallingTryptophan can be partitioned toward microbial AhR ligands supporting IL-22 barrier signalling, or toward host IDO1 kynurenine metabolism under inflammatory pressure. | Clinical-pattern inference | None — inference |
| ACE2 / B0AT1 amino-acid transportACE2 partners with the B0AT1 transporter in small-intestinal amino-acid uptake, which is why post-viral disruption is discussed alongside tryptophan availability. | Hypothesis | None — inference |
| Motility — MMC and serotonergic (5-HT4) transitMigrating motor complex activity clears small-bowel contents between meals; when transit slows, luminal mixing becomes diffusion-limited. | Clinical-pattern inference | None — inference |
| Cholinergic (α7 nAChR) anti-inflammatory toneVagal cholinergic signalling modulates innate immune tone, which is why autonomic state is treated as a contextual layer rather than a separate disease. | Hypothesis | None — inference |
| CD38 / NAD⁺ / SIRT1–SIRT3 regulatory integrityNAD⁺ availability and sirtuin signalling govern mitochondrial regulation, and the model treats this as one of three pillars of colonocyte capacity. | Clinical-pattern inference | PMID 27518564; PMID 23393266 |
| Fe–S cluster and electron-transport-chain vulnerabilityIron–sulfur cluster integrity is required for electron transport, making it a plausible convergence point for several stressors described in the model. | Hypothesis | None — inference |
| Antimicrobial pressure without habitat change → recurrenceReducing organisms without changing the host habitat that selected them is expected to be followed by re-expansion. | Clinical-pattern inference | PMID 21206488; PMID 32917639 |
| Exogenous butyrate in an energy-failed epitheliumWhere oxidative capacity is impaired, supplying more substrate may not be usable and is registered as a speculative caution rather than guidance. | Speculative | PMID 21531334 |
Limitations
- The integrating model is inference. Its component biology is established; the synthesis is not directly tested in humans.
- Key variables — mucosal oxygen tension, colonocyte NAD⁺, epithelial β-oxidation rate — are not measurable in routine care, so the model cannot be confirmed or refuted at the level of an individual.
- Much of the supporting oxygen-gradient and PPAR-γ work is animal or cell-based.
- Directionality between bioenergetics, motility, autonomic tone, and bile-acid signalling is unresolved; the model asserts an ordering that competing explanations dispute.
- The framework is authored and maintained by one person and has not been peer reviewed.
Suggested citation
Attallah, M. "The Host Capacity Model." BiomeLogic, version 1.1. Last reviewed 2026-08-22. Available at: https://biomelogic.net/host-capacity-model. Self-published educational systems-biology framework; not peer reviewed, not medical advice.
This is a self-published web resource. It is not a peer-reviewed journal article and carries no DOI.