Claim Ledger

Colonocyte β-oxidation of microbial butyrate contributes to physiological epithelial hypoxia in the colon.

Demonstrated in vitro (Donohoe 2011) and in animal models (Byndloss 2017). Mechanism well-supported across independent groups.

Chronic dysbiosis may persist when host epithelial bioenergetic capacity remains impaired, regardless of antimicrobial intervention.

Inferred from documented high relapse rates after antibiotic therapy for IBS-SIBO and from mechanistic work on host bioenergetics.

SIBO, MCAS, and long COVID may share an upstream host-capacity substrate in some complex overlapping cases.

Pattern-level synthesis across published mechanistic work on epithelial bioenergetics, mast cell biology, and post-viral mitochondrial dysfunction.

Excess hydrogen sulfide may simultaneously contribute to SIBO-pattern symptoms and mast cell activation through colonocyte energy failure.

Built on established H₂S inhibition of cytochrome c oxidase plus pattern observation in clinical cases.

Gut dysbiosis can impair oocyte competency through follicular LPS/TLR4 signaling that suppresses aromatase, even when serum estradiol appears normal.

Built on in vitro work showing TNF-α suppresses FSH-induced aromatase in granulosa cells, plus established LPS translocation biology.

Lactulose and glucose breath testing for SIBO show poor specificity against jejunal aspirate culture.

Documented in clinical guidelines and multiple validation studies.