The Same Barrier Collapses Everywhere: Why Dysbiosis Causes ADHD, Brain Fog, Anxiety, Depression, and Chronic Fatigue Simultaneously—And Why You Can't Treat Them Separately The Discovery That Changes — Part 6: The Clinical Framework—How to Actually Diagnose and Treat This Properly

Diagnostic Step 1: Screen for Dysbiosis-Associated SCFA Deficiency Standard microbiota sequencing tells you composition. It doesn&#8217;t tell you metabolic function. You need: Quantitative SCFA analysis via gas chromatography-mass spectrometry (GC-MS): Fecal acetate: healthy baseline 20-100 mM Fecal propionate: healthy baseline 5-20 mM Fecal butyrate: healthy baseline 5-15 mM ADHD/anxiety/depression typically show: Acetate: &lt;10-15 mM (50-75% reduction) Propionate: &lt;2-5 mM (60-75% reduction) Butyrate: &lt;2-5 mM (60-80% reduction) Microbiota composition via 16S sequencing: Look specifically for depletion of SCFA-producing taxa: Faecalibacterium prausnitzii Roseburia spp. Eubacterium hallii Akkermansia muciniphila Look for overgrowth of dysbiotic taxa: Proteobacteria (especially if &gt;5% of total) Pathogenic Clostridium Veillonella Streptococcus Functional assessment: KEGG pathway analysis &#8594; look for reduced butyrate production pathway genes PICRUSt2 functional prediction &#8594; compare observed SCFA pathway genes to expected If SCFA production is &lt;30% of normal and dysbiotic taxa are prominent, you have the diagnosis: dysbiosis-driven SCFA deficiency. Diagnostic Step 2: Assess Barrier Integrity Biomarkers of barrier dysfunction: Intestinal barrier: Zonulin (serum): elevated zonulin indicates tight junction protein degradation; normal &lt;0.9 ng/mL, dysbiotic ty