Reference · 33 terms
Glossary
Every concept, molecule, pathway, and process that appears across the BiomeLogic framework — with the same canonical definition we use internally. The framework terms anchor the Host Capacity Model; the rest are the mechanistic building blocks behind every article.
A
- ATPmolecule
- Cellular energy currency.
B
- Butyratemolecule
- Four-carbon SCFA; primary mitochondrial fuel for colonocytes.
- Also: short-chain fatty acid, scfa
C
- CD38pathway
- NADase upregulated by inflammation; collapses mitochondrial NAD⁺ pools.
- colonocyte bioenergeticsframework
- Colonocyte bioenergetics describes how colonic epithelial mitochondria oxidize butyrate to maintain steep epithelial oxygen consumption, sustaining the lumen's near-anaerobic state that selects for obligate anaerobic commensals.
- Also: epithelial bioenergetics, colonocyte energy metabolism, colonocyte ATP economy
- CYP19A1 (aromatase)pathway
- Granulosa-cell aromatase; suppressed by inflammatory cytokines.
D
- dysbiosis as ecological adaptationframework
- Rather than a primary microbial disease, dysbiosis is interpretable as ecological succession to a host-derived disturbance: shifted oxygen, nitrate, mucin, and bile-acid availability reshape the niche, and the community tracks the new substrate.
- Also: ecological dysbiosis, adaptive dysbiosis, dysbiosis ecology
E
- Epithelial O₂ consumptionprocess
- Mitochondrial O₂ sink that maintains luminal hypoxia.
F
- FXRpathway
- Bile acid–activated nuclear receptor; controls bile acid pool, FGF19, motility, immunity.
H
- HIF-1αpathway
- Hypoxia-inducible factor; epithelial barrier and metabolism regulator.
- Histaminemolecule
- Mast cell mediator and dietary biogenic amine.
- Host Capacity Modelframework
- The Host Capacity Model (HCM) holds that recurrent SIBO, MCAS, post-viral illness, and persistent dysbiosis are downstream consequences of failing host bioenergetic capacity at the gut epithelium — not primary microbial diseases.
- Also: HCM, host capacity framework, host-capacity model
- Hydrogen sulfide (H₂S)molecule
- Microbial metabolite; toxic to mitochondrial complex IV at excess.
- Also: h2s, sulfide
I
- IL-22molecule
- Cytokine that supports epithelial regeneration and antimicrobial defense.
- inflammatory bioenergeticsframework
- Inflammatory bioenergetics describes the bidirectional energy coupling between activated immune cells, epithelial mitochondria, and microbial respiration — including iNOS-derived nitrate that fuels Enterobacteriaceae nitrate respiration.
- Also: immunometabolism of mucosal inflammation, inflammation energy economics
L
- Lipopolysaccharide (LPS)molecule
- Gram-negative endotoxin; TLR4 agonist driving systemic low-grade inflammation.
- Also: endotoxin
- Luminal oxygenmolecule
- Trace O₂ in the colonic lumen; rises with colonocyte ETC failure.
M
- Mast cell degranulationprocess
- Mediator release from mast cells; histamine, tryptase, prostaglandins, cytokines.
- MCT1 / SMCT1pathway
- Colonocyte transporters for butyrate uptake.
- Migrating motor complex (MMC)process
- Cyclic small-bowel motility that prevents bacterial colonization.
- mitochondrial barrier failureframework
- Mitochondrial barrier failure positions tight-junction loss as a downstream consequence of epithelial ATP insufficiency, not as a primary lesion — barrier integrity tracks bioenergetic capacity.
- Also: mitochondrial epithelial failure, barrier energy collapse
- Mitochondrial β-oxidationprocess
- Catabolism of fatty acids to acetyl-CoA in the mitochondrial matrix.
N
- NAD⁺molecule
- Central redox cofactor; substrate for SIRT3 and PARP1.
- NF-κBpathway
- Master inflammatory transcription factor.
- Nitrate (NO₃⁻)molecule
- Inflammation-derived terminal electron acceptor used by Enterobacteriaceae.
- nitrate respirationframework
- Nitrate respiration enables Enterobacteriaceae to outcompete obligate anaerobes when iNOS-derived nitrate becomes available — a hallmark of inflamed, low-capacity gut habitats.
- Also: microbial nitrate respiration, anaerobic nitrate use, nitrate-driven blooms
O
- oxygen-gradient failureframework
- Oxygen-gradient failure is the collapse of the colonocyte-maintained oxygen sink, raising luminal pO2 and licensing facultative-anaerobe (Proteobacteria) blooms — a pivotal hinge in the Host Capacity Model.
- Also: O2 gradient collapse, epithelial hypoxia loss, loss of mucosal anaerobiosis, oxygen gradient collapse
P
- PARP1pathway
- DNA-damage NAD⁺ consumer; depletes redox capacity under oxidative stress.
- PPAR-γpathway
- Nuclear receptor maintaining colonocyte β-oxidation and luminal hypoxia.
S
- SERT (serotonin transporter)pathway
- Mucosal serotonin reuptake; impaired in inflammation.
- SIRT3pathway
- Mitochondrial NAD⁺-dependent deacetylase governing ETC and SOD2.
T
- TGR5pathway
- Membrane bile acid receptor; modulates GLP-1, energy expenditure, immunity.
- Tight-junction assemblyprocess
- Energy-dependent assembly of occludin, claudins, ZO-1 at the epithelial junction.
- TLR4pathway
- Pattern recognition receptor for LPS; primes innate immune and mast cell activation.