What causes recurrent SIBO?

The Host Capacity Model identifies colonocyte bioenergetic failure as the upstream driver of recurrent SIBO. When colonocyte mitochondrial respiration fails, oxygen leaks into the lumen and reshapes the ecology toward facultative and sulfidogenic overgrowth—so antimicrobials clear the symptom but not the cause.

How is MCAS different from other mast cell conditions?

BiomeLogic stratifies MCAS into Pattern A/B/C/D activation phenotypes based on upstream drivers (barrier, neuroimmune, infectious, or connective-tissue mediated). Treatment differs by pattern, which is why generic mast-cell stabilizers fail in many patients.

Do you provide medical care or diagnoses?

No. BiomeLogic provides independent systems-biology consultation and mechanistic case analysis. It is not medical care, not a diagnosis, and does not replace your physician.

Public framework governance

Governance.

Stability, contradictions, revisions, and terminology drift — surfaced transparently. Trust is engineered by exposure, not by suppression.

Concepts tracked

Open contradictions

Deprecated terms

Logged revisions

Concept stability matrix

Concept	Tier	Stability	Evidence	Last reassessed
host-capacity-model	Framework principle	evolving0.57	0.72 developing	2026-05-11
colonocyte-bioenergetics	Framework principle	foundational0.88	0.85 mature	2026-04-15
oxygen-gradient-failure	Framework principle	foundational0.88	0.80 mature	2026-04-15
dysbiosis-ecological-adaptation	Framework principle	evolving0.68	0.70 developing	2026-04-20
inflammatory-bioenergetics	Mechanistic hypothesis	evolving0.68	0.60 developing	2026-04-15
nitrate-respiration	Framework principle	foundational0.93	0.82 mature	2026-04-15
mitochondrial-barrier-failure	Mechanistic hypothesis	evolving0.60	0.55 developing	2026-04-15

Recent revisions

2026-04-15evidenceinflammatory-bioenergetics— Weakened by partial non-replication of immunometabolism findings in human mucosa.
2026-04-15definitionmitochondrial-barrier-failure— Refined definition to reference ATP throughput rather than concentration.
2026-04-15evidencehost-capacity-model— Strengthened by replication of butyrate-driven O2 consumption study.
2026-02-10scopehost-capacity-model— Explicit non-scope: structural lesions and primary IEMs.
2026-01-20scopeinflammatory-bioenergetics— Restricted scope to mucosal immunometabolism; excluded systemic generalization.
2025-11-10terminologymitochondrial-barrier-failure— Deprecated 'mitochondrial leaky gut' framing.
2025-09-01deprecationoxygen-gradient-failure— Deprecated 'oxygen collapse' and 'gut oxygen leak syndrome' phrasings.
2025-08-15terminologyhost-capacity-model— Deprecated 'host capacity theory' in favor of 'Host Capacity Model'.

Terminology drift

oxygen collapse → oxygen-gradient failure
Ambiguous; conflates gradient loss with absolute O2 changes.
gut oxygen leak syndrome → oxygen-gradient failure
Pseudo-clinical framing implying a discrete disease entity.
host capacity theory → Host Capacity Model
'Theory' overstates current evidence maturity.
dysbiosis is normal → dysbiosis as ecological adaptation
Misrepresents the ecological-adaptation framing.
mitochondrial leaky gut → mitochondrial barrier failure
Compresses two distinct mechanisms into a slogan.

Tracked contradictions

Dysbiosis-first vs Host-first causationstructural · unresolved
The dominant clinical narrative places dysbiosis upstream; HCM places host bioenergetics upstream. Both frames have partial empirical support and partial explanatory failure.
Junctional vs bioenergetic primacy in barrier failuremoderate · monitoring
Junctional-protein-centric models frame barrier failure as a primary structural lesion; the bioenergetic frame treats it as downstream of ATP capacity.

← Flagship frameworks