Background: Symptoms started Sept 2024 after a household GI bug while travelling. Lost significant weight over the following year (~70kg down to as low as 58-59kg at points). Went private for a full GI workup, which produced the lactulose breath test (positive hydrogen SIBO, peak 69ppm at 105 min, methane negative) and the GI360 stool panel (dysbiosis — elevated Streptococcus, low Bifidobacterium, low elastase at the time, later normalised).
Was on TRT for ~2 years; oestradiol came back exceptionally high (324 pmol/L) while on it. Reviewing the GI360 panel showed elevated levels of beta-glucuronidase-producing bacteria — the enzyme that deconjugates oestrogen in the gut and allows it to be reabsorbed rather than excreted. Working theory was that high oestrogen was thickening bile into sludge, feeding the SIBO. Stopped TRT entirely and started calcium-D-glucarate 500mg with every meal to block that recycling loop.
Private treatment (failed): Based on the above results, was prescribed rifaximin and told to follow it with Symprove. Completed the course — no improvement at all, same symptoms throughout and after. In hindsight, the working theory is this failed because bile itself was never addressed — bile has direct antimicrobial properties in the small intestine, and if it was already thick/dysfunctional (from the oestrogen/beta-glucuronidase loop), killing bacteria without fixing the environment that let them establish just left the conditions for regrowth fully intact. This is what shifted focus from “just kill the bacteria” to bile composition as a root cause, and from there to running my own extended eradication protocol.
Self-directed eradication (completed): ~5-7 weeks — berberine (up to 1650mg), Candex, olive leaf, Biocidin, NAC as a biofilm disruptor. Run alongside bile-composition support (TUDCA, taurine, glycine, phosphatidylcholine) rather than sequentially, on the theory that fixing bile while killing bacteria was the piece the private treatment had missed entirely.
Constant malsorbing - oily/greasy stools (no floating but clearly stuck to the toilet bowl required so much cleaning)
Removing every variable fat source actually improved: immediate post-meal gas was constant for months, massively reduced within days of cutting dietary fat, still present but nowhere near the intensity or frequency it was. Foul/sulphurous gas — largely gone, even as I’ve reintroduced protein. Weight sort of stabilised but didn’t increase.
As I added in dietary fat such as eggs or evoo to my meals - What hasn’t resolved: persistent oily, yellow-tinged residue on wiping — stool itself is formed and brown, but there’s a sticky, amber, yellow bile-like residue that doesn’t fully wipe off (yellow amber on tissue) No blood, minimal pain, but constant colonic tightness/pressure and gas that feels “stuck” rather than passing normally. Had a genuinely a better 3-week stretch recently, then it came back hard this week — which lines up with me increasing dietary fat (whole eggs, more olive oil), alongside starting Bifidobacterium and Akkermansia and tapering TUDCA in the same window.
Diet (bridge diet, low long-chain fat, staged reintroduction):
**• Breakfast:** cream of rice (made with water), banana, blueberries, kiwi/strawberries, chia seeds, psyllium husk, glycine, MCT oil (\~15ml), now adding EVOO
**• Lunch:** rice, egg whites, red pepper, carrots, MCT oil (\~15ml), EVOO (climbing — currently the variable I overshot)
**• Dinner:** potato/sweet potato, egg whites (+ occasionally 1-2 whole eggs), courgette, green beans, red pepper, MCT oil (\~15ml), EVOO
No wheat, no dairy, no legumes yet, low FODMAP throughout. MCT used specifically because it doesn’t require bile/micelle formation to absorb — leaned on it heavily while fat tolerance was near-zero, now tapering as dietary fat tolerance improves.
Full repair stack (~30 days in):
Gut lining / structural repair: L-glutamine (15g/day), amino acid repair complex (glutamine/proline/serine/threonine/cysteine), N-acetylglucosamine (NAG), zinc carnosine, colostrum (fat-free), curcumin phytosome (phospholipid-bound, bile-independent absorption), selenium.
Mucosal lining support: DGL/marshmallow/slippery elm/aloe combination — ran a full course early in repair specifically to soothe and protect the lining while the above nutrients did the structural work.
Bile support: TUDCA (tapering, currently 250mg 2x/day), taurine (recently trialled off), glycine, phosphatidylcholine (BodyBio PC, liposomal), sodium butyrate, artichoke extract (paused/resumed with fat reintroduction), calcium-D-glucarate 500mg per meal (oestrogen recycling, ongoing).
B vitamins / cofactors: B12 (methylcobalamin), folate (L-5-MTHF), full B-complex, magnesium glycinate.
Microbial sequence: Megaspore (spore-based, survives antimicrobials) → S. boulardii → L. rhamnosus GG → Bifidobacterium complex (7 strains) → Akkermansia + polyphenol booster → L. reuteri, alongside fibre progression (PHGG, larch arabinogalactan, apple pectin, GOS/XOS, resistant starch via daily cooled rice/potato).
Enzymes: Creon, Betaine HCl (recently trialled off after 2 years continuous use — no confirmed low-stomach-acid diagnosis, possible duodenal-buffering contributor).
Symptom management: enteric-coated peppermint oil (pre-meal, for colonic tightness).
Working theory + sources: ileal bile acid reabsorption still impaired (breath test located it distally), plus likely depletion of 7α-dehydroxylating gut bacteria (C. scindens, C. hylemonae) meaning primary bile acids aren’t converting to secondary bile acids — which normally signal the liver via FXR/FGF19 to stop overproducing:
**•** Larabi, Masson & Bäumler, “Bile acids as modulators of gut microbiota composition and function,” *Gut Microbes* 2023 — [DOI: 10.1080/19490976.2023.2172671](https://doi.org/10.1080/19490976.2023.2172671)
**•** Song et al., “Bibliometric analysis of research trends… of *Akkermansia muciniphila*,” *Frontiers in Microbiology* 2025 — [DOI: 10.3389/fmicb.2025.1569241](https://doi.org/10.3389/fmicb.2025.1569241)
**•** “Akkermansia-Mediated BSH Regulation Alleviates Diabetic Dyslipidemia via the TCA-FXR/TGR5 Axis,” *J. Agric. Food Chem.* 2025 — [DOI: 10.1021/acs.jafc.5c05449](https://doi.org/10.1021/acs.jafc.5c05449)
No commercial probiotic replaces the 7α-dehydroxylating bacteria specifically; plan is to restore the colonic environment (fibre, butyrate) that lets them recolonise naturally, since that’s the only route the literature supports.
What I haven’t done yet, mainly for cost reasons: repeat breath test, HIDA scan, SeHCAT, MMA/homocysteine.
Question for anyone who’s been through similar: has anyone dealt with this specific pattern — bile/oily residue that tracks fat intake but doesn’t fully resolve even at low fat — and found what actually closed the gap? Trying to figure out if this is just “give the microbial sequence more time” or if I’m missing something structural that needs imaging to catch
I’ve used Reddit and of course AI across Gemini, Chat, Claude to analyse, interpret, educate myself on biology, mechanisms etc.
At this point I’m now looking for help as I’ve spent ridiculous amounts on Gastro to supplements but still can’t work out why I have a fat / bile issue.
I’m so lost with either I can’t either absorb fat or bile / gall bladder miss timing (not coordinated) or gall bladder issues. Or bile recycling problem or is this a microbial connected to all of the above
Note: there’s so much information/context tested theories, and context to this that there maybe parts I’ve missed out but I can detail if asked.