Why It's Impossible to Treat Chronic Gut Dysfunction at the Bacterial Level — Layer 5: The Bile Acid–Mitochondrial Axis Closes the Circuit

This is the layer almost nobody in the gut health space is integrating &#8212; and it&#8217;s one of the most powerful amplifiers of everything above. What the data shows: Secondary bile acid production &#8212; severely reduced. Measured directly at 22 rpkm in one case. Measured indirectly in several others through the microbial signature (dominant bile salt hydrolase producers replacing 7&#945;-dehydroxylators). The bile acid pool has shifted toward primary bile acids and their conjugated forms, and away from the secondary forms (deoxycholic acid and lithocholic acid) that are supposed to dominate a healthy colonic pool. TMA/TMAO at +1,452% above reference. What this means: bile-tolerant organisms that shouldn&#8217;t be dominant are metabolizing dietary choline and carnitine into TMA (trimethylamine), which the liver converts to TMAO. TMAO is directly cardiotoxic, pro-atherogenic, and inflammatory. Why this matters beyond the gut: this is one of the mechanisms linking chronic gut dysfunction to cardiovascular risk, insulin resistance, and kidney strain. Your gut is not a closed system. Fecal fat 5.4 g/100g (reference &lt;3.5). Fecal sugar 4.3 g/100g (reference &lt;2.5). Malabsorption in the presence of a normal pancreatic elastase (522 &#181;g/g) . Why this combination is revealing: the malabsorption isn&#8217;t pancreatic &#8212; the pancreas is producing plenty of enzymes.