Why Dysbiosis, SIBO, Hydrogen Sulfide Intolerance, MCAS, and Long COVID May All Be Downstream of a Single Event — Putting it together: the convergence map

No single marker proves the Host Capacity Model. That's not a weakness — it's the nature of systems biology. The model is built by pattern recognition, by watching independent data streams converge on the same story. Here is the convergence I'm looking for when I work a complex case: dysbiosis (loss of butyrate-producers, expansion of Proteobacteria and facultative anaerobes, H₂S organisms) points back to epithelial oxygenation, which points back to butyrate oxidation, which points back to mitochondrial electron flow, which points back to iron-sulfur cluster integrity, which points back to peroxynitrite burden, which points back to iNOS, NADPH oxidase, mast cells, LPS, viral reactivation, and inflammatory signaling. And running in parallel: hydrogen sulfide sits at the intersection of microbial production and mitochondrial clearance; glutathione sits at the intersection of NADPH, FAD/riboflavin, selenium, and lipid peroxidation; NAD⁺ is drained by CD38 even as the chain that needs it is failing; SLC5A8 silencing locks the colonocyte out of its own fuel. The data I read to test this convergence includes stool / microbiome testing (loss of butyrate-producing ecology, expansion of facultative anaerobes and Proteobacteria-like patterns, sulfide-associated organisms, plus host-inflammation markers — calprotectin, secretory IgA, occult blood, pancreatic elastase, bile-acid clues); or