Your Gut Is Not A Mystery. It Is A Sorting Problem.

Carvacrol has broad antimicrobial activity, and one trial found herbal antimicrobials non-inferior to rifaximin in SIBO. Non-selective, so it hits commensals too.

How it works: A potent antimicrobial essential oil (carvacrol/thymol) used short-term for gut-flora balance and immune defense.

The mechanistic case: Broad-spectrum antimicrobial — best used in short courses, not indefinitely.

Antimicrobial as well as metabolic — a component of most herbal SIBO protocols.

How it works: A plant alkaloid that activates AMPK — the same energy-sensing pathway as exercise and metformin — with powerful effects on glucose and lipid metabolism.

The mechanistic case: Gut-microbiome remodeling and 'nature's Ozempic/metformin' longevity framing are popular and plausible but outrun the human outcome data.

Stabilized allicin has particular activity against methane-producing archaea, which is the hardest SIBO subtype to treat.

How it works: The sulfur compound responsible for most of garlic's biological activity — and it is chemically unstable, which is the entire practical problem with this category.

The mechanistic case: Widely used for SIBO and gut dysbiosis, particularly methane-predominant, on the basis of the in-vitro antimicrobial data. In-vitro activity is not the same as activity in a gut lumen after digestion, and the human trial evidence for that use is thin.

Antifungal fatty acid with better mucosal persistence than caprylic acid.

How it works: A long-standing fatty-acid formula traditionally used to support healthy gut flora balance and manage yeast/candida overgrowth.

The mechanistic case: The 'candida' framework is popular in functional medicine; internal-overgrowth diagnosis is debated.

Human trials exist and they disagree: a randomized pilot found an effect on H. pylori, and a separate in-vivo study found no effect on bacterial load at all (PMID 12888582). The steadier signal is symptomatic relief in dyspepsia. Supportive, not an eradication therapy.

How it works: Tree resin from the Greek island of Chios with a small but real evidence base in upper-GI symptoms.

The mechanistic case: Proposed mucosal protection and antibacterial activity in the stomach specifically.

Competitively excludes pathogens and is unaffected by antibacterials, so it can run throughout.

How it works: A beneficial probiotic YEAST (not a bacterium) that is uniquely resistant to antibiotics — making it ideal support during and after antibiotic courses.

The mechanistic case: Anti-inflammatory and pathogen-crowding mechanisms are well-characterized for this strain.

Produces reuterin, an antimicrobial that suppresses gram-negative organisms without stripping the commensals — which is the argument for running it alongside an eradication protocol rather than instead of one. The H. pylori data is the strongest part of that case, and it is adjunct data, not monotherapy.

How it works: A specific probiotic species with genuinely strain-specific effects. Worth separating from general probiotics because in this field the strain is the drug — two products both saying 'L. reuteri' can behave completely differently.

The mechanistic case: Rodent work links L. reuteri to oxytocin signaling via the vagus, with downstream effects reported on social behavior, wound healing and testicular size. This is the basis of the 'reuteri yoghurt' trend and it has NOT been demonstrated in humans.

Biofilm disruption and antimicrobial activity; a standard component of H. pylori regimens.

How it works: The pink stuff. An old drug with genuinely good evidence for two specific jobs — and a couple of properties nobody warns you about.

The mechanistic case: Sometimes used for bile acid diarrhea and for sulfur-producing gut overgrowth on the basis of bismuth binding hydrogen sulfide — plausible, thinly evidenced.

Binds E. coli fimbriae so bacteria are flushed rather than killed — genuinely elegant, and it has trial evidence for recurrent UTI without driving resistance.

How it works: A sugar that is absorbed and then excreted almost unchanged into urine, where E. coli binds it instead of binding to the bladder wall.

The mechanistic case: E. coli FimH adhesins bind mannose residues; saturating urine with mannose is a coherent competitive-inhibition mechanism. The mechanism being sound is not the same as the intervention working.

Proanthocyanidins prevent E. coli adhesion to the urothelium. Meta-analysis supports prevention of recurrent UTI — prevention specifically, not treatment of an active one.

How it works: The original UTI supplement. The evidence went from positive to negative to positive again, and where it landed depends entirely on the dose of one specific molecule.

The mechanistic case: Type-A proanthocyanidins block E. coli P-fimbriae adhesion to the urothelium. It prevents attachment; it does not treat an established infection.

Traditional antimicrobial used in the same protocols.

How it works: A traditional Ayurvedic antimicrobial used for gut, skin and oral health. Included with a clear safety section because this one has real toxicity concerns that the wellness framing tends to skip.

The mechanistic case: Broad in-vitro antimicrobial, antifungal and antiparasitic activity underpins its use in gut protocols. That activity has not been demonstrated to translate to human gut outcomes.

Disrupts fungal cell membranes; used for Candida overgrowth.

How it works: A medium-chain fatty acid used in antifungal and candida protocols. Honest read: the in-vitro data is real and the human evidence is essentially absent.

The mechanistic case: Demonstrated in-vitro antifungal activity against Candida species, likely through membrane disruption. Whether meaningful concentrations reach the colon after absorption in the small intestine is the unanswered question — and it's a big one.

Disrupts lipid-enveloped organisms — viruses and some bacteria.

How it works: A monoglyceride of lauric acid, popular in antiviral and antimicrobial protocols.

The mechanistic case: Demonstrated in-vitro activity against lipid-enveloped viruses and some bacteria, by disrupting the lipid envelope. Whether ingested monolaurin reaches meaningful systemic concentrations is not established — and it is a food additive precisely because it's digestible.

Traditional antiparasitic; thujone content means duration limits matter.

How it works: A traditional antiparasitic bitter, and the plant behind absinthe. Included with a firm safety note.

The mechanistic case: Related Artemisia species produce artemisinin, which is a genuinely important antimalarial — but A. absinthium is not the artemisinin species, and that conflation drives a lot of the marketing.

Traditional antiparasitic, usually combined with wormwood and clove.

How it works: A tannin-rich traditional antiparasitic, usually sold alongside wormwood and clove as a 'parasite cleanse'.

The mechanistic case: High tannin content has an astringent effect on the gut lining, which may explain some symptomatic reports independently of any antiparasitic action.

Broad claims, and a long documented history of products being adulterated with synthetic preservatives that were doing the actual antimicrobial work.

How it works: Sold as a natural broad-spectrum antimicrobial. Multiple independent analyses point to an uncomfortable explanation for why it works in a dish.

The mechanistic case: Repeated published analyses have found that commercial GSE products showing antimicrobial activity contained synthetic preservatives — benzethonium chloride, methylparaben, triclosan — while preparations verified free of those additives showed little to no activity. The straightforward reading is that the antimicrobial effect belongs to the added disinfectant, not the grapefruit.

Oleuropein with broad antimicrobial activity in vitro.

How it works: A polyphenol (oleuropein) extract with antimicrobial, antiviral, immune and cardiovascular benefits.

The mechanistic case: Oleuropein is predicted to lower blood pressure through ACE inhibition and calcium channel modulation, and to have antimicrobial activity — the mechanisms behind both traditional uses. Predicted additivity with antihypertensives, which is the interaction to watch rather than a theoretical benefit.

An endogenous antimicrobial peptide that also disrupts biofilm — the reason resistant overgrowth persists through antibiotics.

How it works: Innate-immune antimicrobial peptide — disrupts microbial membranes and modulates inflammation and wound healing.

The mechanistic case: The only human cathelicidin — an endogenous antimicrobial peptide that disrupts bacterial membranes directly and also modulates immune signaling and promotes angiogenesis. Vitamin D upregulates its expression, which is one of the better-supported links between vitamin D status and infection. Membrane disruption is not selective, which is why high concentrations irritate host tissue too — and the likely explanation for the inverted dose-response in the ulcer trial.

Proposed biofilm disruptor. The rationale is better than the evidence.

How it works: A proteolytic enzyme taken on an empty stomach for systemic anti-inflammatory, mucus-clearing and fibrin-breakdown effects.

The mechanistic case: 'Clot/scar-tissue' claims are popular; the anti-inflammatory/mucolytic data is firmer.

Lapachol and naphthoquinones with antifungal and antibacterial activity in vitro. Traditional use is long; human trials are absent and high doses are toxic.

How it works: A South American bark traditionally used for antifungal (candida), immune and antimicrobial support.

The mechanistic case: Popular in candida/gut-cleanse protocols — mechanistically plausible, clinically under-studied.

A formulated blend for acute gut irritation — demulcents plus anti-inflammatories.

How it works: Thorne GI-Encap, a demulcent formula sold to coat and calm an irritated GI lining. Which soothing botanicals it uses, and how much of each, is not claimed here: no filed Supplement Facts panel has been read for it.

The mechanistic case: Mucosal-healing claims are reasonable but blend-level trial data are limited.

Food-grade amorphous silica marketed as a parasite treatment on a mechanical-abrasion theory that has no human evidence behind it. Inhalation of the powder is a genuine lung hazard.

How it works: Fossilized algae skeletons, marketed for parasites and detox. The mechanism claimed for it does not survive contact with how digestion works.

The mechanistic case: The stated mechanism — microscopic sharp edges physically damaging parasites — is how it works as an agricultural insecticide on exoskeletons in dry conditions. In a wet gut lumen, against organisms with no exoskeleton, that mechanism does not apply.

A zonulin antagonist that directly tightens intercellular junctions — the most rigorously tested barrier drug there is, which is exactly why its record matters. A phase 2b in celiac disease was positive on symptoms at the lowest dose only (PMID 25683116); the phase 3 was stopped early for futility. Tightening the barrier pharmacologically is a real mechanism. Nobody has yet shown it pays off clinically.

How it works: Zonulin antagonist — tightens intestinal tight junctions to reduce 'leaky gut' permeability; furthest-along gut-barrier drug (celiac trials).

The mechanistic case: An octapeptide zonulin antagonist — zonulin regulates the tight junctions between intestinal epithelial cells, and larazotide is designed to keep them closed. The mechanism is well characterized and the tight-junction effect is demonstrable. What the phase 3 questioned is whether closing tight junctions translates into how someone feels — a gap between mechanism and outcome that recurs constantly in gut-barrier research.

Directly trophic — increases villus height and crypt depth. Approved as teduglutide for short-bowel syndrome, which is proof the mechanism works in humans.

How it works: Intestinal growth factor — drives gut mucosal growth and reduces permeability; the analog teduglutide treats short-bowel syndrome.

The mechanistic case: An intestinotrophic hormone released alongside GLP-1 — it increases villus height, crypt depth and mucosal blood flow, and reduces intestinal permeability. The proliferative mechanism is also the caution. Teduglutide's label carries a colorectal polyp warning and requires colonoscopic surveillance, because a hormone whose job is to grow intestinal mucosa does not distinguish welcome growth from unwelcome.

The enterocyte's preferred fuel. Best evidence in burns, critical illness and post-surgical recovery, where the demand genuinely outstrips supply.

How it works: The most abundant amino acid in the body and a primary fuel for gut and immune cells. Conditionally essential during heavy stress, illness or intense training.

The mechanistic case: Popular for 'leaky gut' repair in healthy people — mechanistically reasonable but under-proven outside clinical populations.

Stabilizes the gastric mucosa and reduces NSAID-induced small-intestinal permeability in controlled trials. The chelate delivers zinc to the damaged site rather than to the bloodstream.

How it works: A zinc-and-carnosine complex that adheres to and heals the stomach and gut lining — excellent for ulcers, gastritis and leaky gut.

The mechanistic case: The zinc-carnosine complex is predicted to work by adhering to ulcerated mucosa and releasing both components locally — so the prediction is a topical gastric effect rather than a systemic zinc effect. The complex is proposed to matter more than either component alone. That predicts it should not be counted toward your zinc intake for correcting a deficiency, which is how it is often misused.

The colonocyte's primary fuel and a direct regulator of tight-junction protein expression. Delivering it directly bypasses the need for a fiber-fermenting microbiome you may not have.

How it works: The primary short-chain fatty acid that fuels colon cells — the postbiotic your gut bacteria normally make from fiber, supplied directly.

The mechanistic case: Metabolic and gut-brain benefits are emerging; tributyrin forms improve delivery.

Increases mucus secretion and mucosal blood flow; the deglycyrrhizinated form removes the blood-pressure problem.

How it works: Licorice with the blood-pressure-raising glycyrrhizin removed — soothes the stomach and supports the mucosal lining for reflux and ulcers.

The mechanistic case: Predicted to work by increasing mucin secretion and mucosal blood flow rather than by suppressing acid — a fundamentally different mechanism from a PPI, and the reason it is proposed as complementary rather than alternative. The deglycyrrhizination is the whole safety argument: removing glycyrrhizin removes the 11β-HSD2 inhibition that raises blood pressure and drops potassium. Predicted to retain the mucosal effect without the mineralocorticoid one, which is plausible but not directly demonstrated.

Inner-leaf gel improved ulcerative colitis scores in a randomized trial. Whole-leaf contains anthraquinone laxatives and is a different product entirely.

How it works: A soothing inner-leaf gel for gut-lining comfort, regularity and (topically) skin — used internally for reflux and IBS.

The mechanistic case: Internal use is best with decolorized (aloin-free) inner-leaf products.

Reduces exercise-induced intestinal permeability in athlete trials — a clean, measurable result.

How it works: The nutrient- and antibody-rich 'first milk,' packed with immunoglobulins, lactoferrin and growth factors for gut-lining and immune support.

The mechanistic case: 'Leaky gut' and recovery benefits are mechanistically supported and increasingly studied.

Binds luminal antigens and toxins, reducing the load on the barrier. Real trial evidence in IBS-D.

How it works: Concentrated bovine immunoglobulins that bind microbial antigens in the gut lumen — a barrier-support product with better evidence than most in this category.

The mechanistic case: Binding lipopolysaccharide and other antigens in the lumen is proposed to reduce immune activation at the mucosal surface.

Required for mucosal epithelial differentiation and secretory IgA production.

How it works: The preformed, ready-to-use form of vitamin A — essential for vision, immune function, skin health and gene expression (where beta-carotene conversion is often poor).

The mechanistic case: Preformed A is more reliable than carotenoids for those who convert poorly.

The gut is where its preclinical evidence is strongest — protective against NSAID and alcohol damage, and accelerates healing of experimental colitis, fistulae and anastomoses in rodents. Oral dosing is mechanistically defensible here specifically, since it was isolated from gastric juice.

How it works: Cytoprotective peptide from gastric juice — upregulates VEGFR2/angiogenesis, nitric-oxide and growth-factor pathways to accelerate tendon, gut, muscle and nerve repair.

The mechanistic case: The animal literature is unusually broad and unusually consistent — accelerated tendon-to-bone healing, protection against NSAID-induced gut damage, and effects on the nitric-oxide system across many rodent models from largely one research group. The proposed mechanism is upregulation of VEGF-driven angiogenesis and growth-factor receptor expression at the injury site. That same angiogenic mechanism is the reason for the one caution that actually matters here: anything that reliably grows new blood vessels is a question mark in the presence of an undiagnosed tumor, and nobody has studied that in humans.

BPC-157 supplied as an arginate salt. The gut argument is BPC-157's argument — it was isolated from gastric juice, and mucosal repair is the best-replicated part of its animal literature. The salt form is a shelf-stability claim, not a second mechanism, and no human study has compared the two.

How it works: The BPC-157 pentadecapeptide supplied as an arginate salt rather than the usual acetate. The sequence, and therefore the mechanism, is the same: VEGFR2 and nitric-oxide signaling driving angiogenesis, with the growth-factor upregulation behind the tendon, gut, muscle and nerve repair BPC-157 is known for. What the arginate counter-ion changes is the physical chemistry of the salt, and vendors market it as the more stable of the two. That is a formulation claim, not a potency claim: nobody has published a head-to-head of arginate against acetate in a living system.

The mechanistic case: Identical to BPC-157 by definition: VEGFR2 and nitric-oxide signaling driving angiogenesis, with growth-factor upregulation behind tendon, gut, muscle and nerve repair. A counter-ion changes the salt's physical chemistry, not the peptide's sequence or its receptor interactions. The mechanistic argument FOR the arginate is pharmacokinetic — a more stable salt could mean more intact peptide surviving to the point of action. Plausible, unmeasured, and worth treating as a hypothesis rather than a feature.

Anti-inflammatory at the mucosa and stable enough orally to reach the colon.

How it works: Anti-inflammatory tripeptide from α-MSH — calms NF-κB signaling systemically and in the gut.

The mechanistic case: The tripeptide carries alpha-MSH's anti-inflammatory action without its melanocortin receptor binding — so it is predicted to calm inflammation without the pigmentation, flushing or erectile effects the full hormone causes. That separation is the entire reason to use the fragment. Rodent colitis models show reduced inflammatory markers with oral dosing, and the mechanism (NF-κB inhibition in gut epithelium) is why oral delivery makes sense here when it would not for most peptides.

A gastric-mucosa peptide fraction, proposed under the Khavinson tissue-specificity model to act on the stomach lining it was extracted from. That would put it in the same territory as Zinc-Carnosine and DGL above; unlike those, nothing outside the originating Russian program has looked at it.

How it works: Gastric-mucosa-derived peptide fraction. Khavinson-school organ peptide extracts. The claim is tissue specificity: a short peptide fraction from one organ is proposed to act on that same organ, restoring its protein synthesis toward a younger pattern by binding regulatory DNA sequences. The mechanism is coherent and the human evidence for it is thin outside the group that proposed it.

The mechanistic case: The proposal is tissue specificity: a short peptide fraction taken from one organ acts preferentially on that same organ, binding regulatory DNA sequences and shifting protein synthesis toward a younger pattern. It is a coherent mechanism and it is why these are dosed as short courses rather than continuously. Oral delivery is the open question, not the mechanism. Peptides are poorly absorbed intact from the gut, which is why the oral capsules run 10-20x the injectable milligram dose. Whether enough survives to reach the target tissue has not been shown in a way anyone outside the manufacturer can check.

A demulcent that forms a mucilage layer over irritated mucosa. Mechanically sensible and symptomatic — there is no evidence it changes the underlying barrier, and traditional use is the bulk of the case.

How it works: A demulcent bark that forms a soothing gel to coat and calm an irritated digestive tract — classic support for reflux, IBS and sore throat.

The mechanistic case: The mucilage is predicted to act as a physical demulcent — coating and protecting mucosa — rather than through any absorbed compound. That predicts it can only work where it physically touches, which is the throat and upper gut, and not systemically. The same mechanism predicts delayed absorption of anything taken with it.

Same demulcent mechanism, traditionally paired with slippery elm.

How it works: A demulcent — its mucilage forms a slippery gel that physically coats irritated mucous membranes. Simple, cheap, mechanically sensible.

The mechanistic case: The mucilage coating mechanism is straightforward physical chemistry and doesn't require systemic absorption to be plausible.

A formulated blend across the same targets.

How it works: Thorne EnteroMend. The glutamine is the largest thing in the scoop by a wide margin, and it is the ingredient the gut-lining argument actually rests on.

The mechanistic case: 'Leaky gut' repair is a popular framing; mechanistically reasonable but under-proven as a discrete condition.

Broad-spectrum enzyme support. Genuinely necessary in pancreatic insufficiency; more variable in ordinary bloating.

How it works: Thorne Bio-Gest. That lipase figure is a fraction of a therapeutic enzyme dose, which is the number that decides whether this product is the right one.

The mechanistic case: Routine use in healthy people is popular but less evidence-backed than use in genuine insufficiency.

Diamine oxidase is the enzyme that clears histamine in the gut lumen, so supplementing it before meals is a replacement strategy rather than a botanical one. It only makes sense where a low-histamine trial has already produced a response, and it does nothing at all about histamine released by mast cells inside you.

How it works: The enzyme that breaks down histamine in the gut lumen. Taken before meals by people with histamine intolerance — a group the Vault already had content for without listing the thing they actually buy.

The mechanistic case: Supplemental DAO acts entirely in the gut lumen — it is not absorbed and does not lower systemic histamine. So it can only help with histamine arriving in food, not with histamine your own mast cells release.

Higher-potency lipase, protease and amylase — the clinical-grade version.

How it works: Thorne Dipan-9. One active, at strength: pancreatin 1 g per two-capsule serving, declaring amylase 112,500 USP units, protease 115,000 USP units and lipase 17,500 USP units. There is no ox bile and no betaine HCl in it, which is the difference between this and Bio-Gest.

The mechanistic case: Routine use in healthy people is less evidence-backed than in true insufficiency.

Essential after gallbladder removal, where bile delivery is no longer concentrated or timed to meals. Also relevant in fat malabsorption and pale stools.

How it works: Supplemental bile salts for people who cannot make or release enough of their own — most relevantly after gallbladder removal.

The mechanistic case: Emulsifies dietary fat and enables absorption of fat-soluble vitamins A, D, E and K. Post-cholecystectomy, bile drips continuously rather than releasing in a bolus with meals, which is a coherent reason fatty meals become difficult.

Choleretic — increases bile production. Trial evidence for functional dyspepsia and for cholesterol.

How it works: A choleretic bitter — it increases bile flow. One of the better-evidenced botanicals for functional dyspepsia, and a genuinely underrated one.

The mechanistic case: Bile flow is the proposed mechanism for both the digestive and the lipid effects — more bile means better fat handling and more cholesterol excreted rather than recycled.

A hydrophilic bile acid that protects hepatocytes from the toxicity of hydrophobic bile acids, and reduces ER stress. Used in cholestasis with real clinical rationale.

How it works: A bile acid that supports liver and bile flow, reduces ER (endoplasmic-reticulum) stress, and is popular for liver protection — especially alongside oral compounds that stress the liver.

The mechanistic case: Neuroprotective and metabolic roles are promising in early research.

Proteolytic; with food it aids protein digestion, away from food it acts systemically. Two different uses of one supplement.

How it works: A pineapple-derived proteolytic enzyme for protein digestion (with food) and anti-inflammatory/recovery support (empty stomach).

The mechanistic case: Dual role: digestion WITH meals, anti-inflammatory BETWEEN meals.

Accelerates gastric emptying and has strong meta-analysis support for nausea. The best-evidenced botanical for functional dyspepsia.

How it works: A root with strong evidence for nausea (motion sickness, pregnancy, chemo) plus digestion and anti-inflammatory support.

The mechanistic case: Gingerols and shogaols act on 5-HT3 receptors and accelerate gastric emptying, which predicts anti-nausea effects through a route distinct from prokinetics — and specifically predicts it should work for motion sickness and pregnancy nausea, where it does. Predicted interaction: mild antiplatelet activity through thromboxane inhibition. Theoretically additive with anticoagulants, though the effect size at culinary and supplemental doses appears small.

Carminative — reduces gas and spasm. Component of the gripe-water tradition with modern trial support in infant colic.

How it works: A carminative — it relaxes intestinal smooth muscle and helps trapped gas move. One of the few traditional gut herbs with decent pediatric trial data.

The mechanistic case: Antispasmodic activity via anethole; also mildly phytoestrogenic, which matters for a small number of people.

Supplemental acid where hypochlorhydria is the issue. Contraindicated with active ulcer or ongoing NSAID use, and the self-titration protocols circulating online deserve more caution than they get.

How it works: Supplemental stomach acid (with the enzyme pepsin) for people with low gastric acid, which impairs protein and mineral absorption.

The mechanistic case: Proposed to reduce SIBO/dysbiosis by restoring the stomach's acid barrier — plausible but not firmly proven.

A traditional choleretic — proposed to increase bile flow, which is both a digestive aid and the physical exit route for everything the liver conjugates.

How it works: A traditional bitter used for bile flow and as a mild diuretic. Popular in 'liver detox' products, which is where the honest version diverges from the marketing.

The mechanistic case: Bitter compounds stimulate bile flow, which is a plausible route to easier fat digestion. The diuretic effect is real enough to matter for potassium in theory, though dandelion is unusually potassium-rich itself.

TMG, distinct from betaine HCl — a methyl donor rather than an acid source. The names cause endless confusion.

How it works: A methyl donor (trimethylglycine) that acts as a cellular osmolyte for power/strength output and lowers homocysteine for cardiovascular support.

The mechanistic case: Performance benefits are reasonably supported; mechanisms (osmolyte + methylation) are well-characterized.

Effects are strain-specific and not transferable between products. Real trial evidence exists for particular strains in particular conditions; 'a probiotic' as a category claim does not.

How it works: Clinically-studied, shelf-stable bacterial strains that support a balanced gut microbiome and digestion.

The mechanistic case: Gut-brain-axis mood benefits ('psychobiotics') are an active, promising area but strain- and person-specific and not yet broadly proven.

Multi-strain, high-CFU coverage. Most useful after antibiotics or acute disruption.

How it works: A high-CFU, multi-strain probiotic for broader microbiome and digestive support when a stronger dose is warranted.

The mechanistic case: More CFU isn't automatically better — strain match to goal still matters most.

A yeast, so antibiotics don't kill it — which makes it uniquely useful concurrently with a course, and it has strong meta-analysis support for antibiotic-associated and C. difficile diarrhea.

How it works: A beneficial probiotic YEAST (not a bacterium) that is uniquely resistant to antibiotics — making it ideal support during and after antibiotic courses.

The mechanistic case: Anti-inflammatory and pathogen-crowding mechanisms are well-characterized for this strain.

A spore-former that survives stomach acid and shelf storage. Trial evidence in IBS.

How it works: A hardy, spore-forming probiotic that survives stomach acid intact to reach the gut — well-studied for digestion and immune support.

The mechanistic case: Immune and protein-absorption benefits are emerging but promising.

One of the few species where the strain genuinely is the drug: DSM 17938 and ATCC PTA 6475 behave differently from each other and from anything else labeled L. reuteri. The trial support is strongest for infant colic and as an adjunct during H. pylori eradication, so buy the strain rather than the species.

How it works: A specific probiotic species with genuinely strain-specific effects. Worth separating from general probiotics because in this field the strain is the drug — two products both saying 'L. reuteri' can behave completely differently.

The mechanistic case: Rodent work links L. reuteri to oxytocin signaling via the vagus, with downstream effects reported on social behavior, wound healing and testicular size. This is the basis of the 'reuteri yoghurt' trend and it has NOT been demonstrated in humans.

Lives in the mucus layer and stimulates its production. Abundance correlates inversely with obesity and metabolic disease, and a human pilot with the pasteurized form showed metabolic improvement — one of the most mechanistically specific probiotics available.

How it works: A mucin-degrading gut bacterium that is depleted in obesity and metabolic disease. The counter-intuitive part is that the PASTEURIZED (dead) form outperformed the live one in trial.

The mechanistic case: The membrane protein Amuc_1100 signals through TLR2 and improves gut barrier integrity, which survives pasteurization and is the leading explanation for why heat-killed worked better.

Chicory prebiotic that selectively feeds bifidobacteria. Also the most likely thing here to cause severe bloating if you have overgrowth.

How it works: A fermentable prebiotic fiber that feeds bifidobacteria. Distinct from psyllium, which is a bulking fiber and barely fermented — they do different jobs and are not interchangeable.

The mechanistic case: Fermentation produces short-chain fatty acids including butyrate, which is the proposed route to most of the wider claims.

Prebiotic with the best trial evidence for bifidobacterial increase, and generally better tolerated than inulin.

How it works: A prebiotic fiber that feeds bifidobacteria specifically, rather than feeding the whole gut indiscriminately the way inulin does. That selectivity is the reason it is often tolerated by people who cannot take inulin.

The mechanistic case: Bifidogenic fermentation raises short-chain fatty acid production, which is the proposed route to the barrier and immune effects.

Uniquely low-fermentation prebiotic — the one that is usually tolerated in IBS and even used alongside SIBO treatment.

How it works: A soluble, non-gelling, low-FODMAP fiber. The unusual part is that it improves both constipation and diarrhea, which most fibers cannot claim.

The mechanistic case: Fermented slowly and along the length of the colon rather than rapidly at the start, which is the plausible reason it produces less gas than inulin.

Reaches the colon undigested and is the most potent butyrate-producing substrate available.

How it works: Starch that escapes digestion in the small intestine and is fermented in the colon, where it is unusually good at producing butyrate specifically.

The mechanistic case: Butyrate is the primary fuel for colonocytes; supplying it locally by fermentation is mechanistically different from swallowing a butyrate capsule.

Slowly fermented, so less gas per gram. A gentle entry point.

How it works: A slowly fermented soluble prebiotic fiber — the gentle option when inulin causes too much gas.

The mechanistic case: Slow, distal fermentation is the proposed reason for the gentler symptom profile — less gas produced quickly in the proximal colon.

A blended prebiotic formulation spanning several fermentation rates, which spreads short-chain fatty acid production along more of the colon than a single fiber does.

How it works: A low-FODMAP soluble-fiber blend that supports regularity, feeds beneficial gut bacteria and blunts post-meal glucose spikes. The filed panel is led by Sunfiber partially hydrolyzed guar gum, with rice bran, ResistAid, apple pectin and a decaffeinated green tea phytosome behind it.

The mechanistic case: Microbiome-mediated immune and mood benefits of prebiotics are promising but individual.

Bulking and viscous rather than heavily fermented — works for both constipation and diarrhea, which is unusual and useful.

How it works: A soluble/gel-forming fiber that normalizes bowel regularity (both directions), lowers cholesterol and blunts glucose spikes.

The mechanistic case: Viscosity is the whole mechanism: the gel slows gastric emptying, blunts the post-meal glucose curve, and binds bile acids so the liver draws on cholesterol to replace them. That predicts effects on glucose and LDL through entirely mechanical means with no absorption required. The same viscosity predicts the interaction: taken alongside medication it delays absorption, so a two-hour separation is the practical consequence of the mechanism rather than an arbitrary rule.

Polyphenol diversity feeds microbial diversity. Not a vegetable substitute.

How it works: A concentrated blend of greens, polyphenols, adaptogens and prebiotics designed to boost daily phytonutrient and antioxidant intake.

The mechanistic case: Greens powders complement but do not replace real vegetables; whole-food fiber and volume matter.

Bundle spanning barrier, microbiome and enzyme support.

How it works: Thorne's gut bundle -- a box of separate products rather than a single formula, sold at the microbiome, the gut lining and digestion together. What Thorne ships inside is Thorne's to change, so this page does not name what is in it.

The mechanistic case: No bundle has been studied as a unit, so any claim about the combination is extrapolated from the individual components. Where two ingredients share a pathway, additivity is plausible; where they do not, expect independence. Read each component's own page for what is actually predicted of it.

Enteric-coated so it reaches the small intestine, where menthol blocks calcium channels in smooth muscle. Meta-analyses put it among the most effective IBS treatments available, prescription included.

How it works: Enteric-coated peppermint oil that relaxes gut smooth muscle — one of the best-evidenced natural tools for IBS.

The mechanistic case: Menthol blocks calcium channels in intestinal smooth muscle, predicting antispasmodic relief in IBS — a direct and unusually clean mechanistic story for a botanical. The enteric coating is mechanistically essential rather than cosmetic: uncoated peppermint oil relaxes the lower esophageal sphincter by the same mechanism and predictably causes reflux.

A fixed nine-herb liquid (STW-5) with placebo-controlled meta-analysis behind it in functional dyspepsia — early fullness and upper-abdominal pain rather than lower-gut IBS. It appears to act region-specifically on gastric tone, relaxing the fundus while tightening the antrum, which is why it reads as a motility agent rather than a bitter.

How it works: A fixed liquid combination of nine herbal extracts — bitter candytuft, angelica root, milk thistle fruit, celandine, caraway, liquorice, peppermint, lemon balm and chamomile. It is one of the very few botanicals in this catalog with a placebo-controlled meta-analysis behind it rather than tradition alone.

The mechanistic case: The proposed mechanism is region-specific rather than global: relaxing the gastric fundus so the stomach accommodates a meal, while stimulating antral motility so it empties. That would explain why it helps fullness and early satiety specifically, rather than acting as a general antispasmodic. The trial evidence is for functional dyspepsia. Extending it to SIBO or IBS is extrapolation from an overlapping symptom set, not a demonstrated effect.

Improves both constipation- and diarrhea-predominant IBS in trials without the fermentation load of other fibers.

How it works: A soluble, non-gelling, low-FODMAP fiber. The unusual part is that it improves both constipation and diarrhea, which most fibers cannot claim.

The mechanistic case: Fermented slowly and along the length of the colon rather than rapidly at the start, which is the plausible reason it produces less gas than inulin.

Normalizes stool form in both directions — one of very few things with that property.

How it works: A soluble/gel-forming fiber that normalizes bowel regularity (both directions), lowers cholesterol and blunts glucose spikes.

The mechanistic case: Viscosity is the whole mechanism: the gel slows gastric emptying, blunts the post-meal glucose curve, and binds bile acids so the liver draws on cholesterol to replace them. That predicts effects on glucose and LDL through entirely mechanical means with no absorption required. The same viscosity predicts the interaction: taken alongside medication it delays absorption, so a two-hour separation is the practical consequence of the mechanism rather than an arbitrary rule.

Specific strains reduce IBS symptom severity; strain selection is the entire question.

How it works: Clinically-studied, shelf-stable bacterial strains that support a balanced gut microbiome and digestion.

The mechanistic case: Gut-brain-axis mood benefits ('psychobiotics') are an active, promising area but strain- and person-specific and not yet broadly proven.

Reduces the sympathetic tone that drives gut hypersensitivity.

How it works: A calming amino acid from green tea that promotes relaxed focus by raising alpha brain waves — without sedation.

The mechanistic case: Proposed GABA/glutamate modulation underlies the anxiolytic-without-sedation profile.

Osmotic laxative effect in the citrate and oxide forms; muscle-relaxant contribution in all forms.

How it works: An essential mineral and cofactor for 300+ enzymatic reactions. Thorne uses the bisglycinate chelate — magnesium bound to glycine — which absorbs better and is far gentler on the gut than cheap magnesium oxide.

The mechanistic case: Proposed to buffer the stress response via NMDA-receptor and HPA-axis modulation — a plausible mechanism behind the 'calming' effect, though direct trial evidence is thin.

Traditional Ayurvedic bowel regulator with trial evidence for constipation, and it does not cause the dependence senna does.

How it works: A three-fruit Ayurvedic combination used as a gentle bowel regulator — traditionally positioned as a tonic rather than a laxative.

The mechanistic case: Tannin and polyphenol content is proposed to support the mucosal barrier and act as a mild prebiotic.

A stimulant laxative acting on the myenteric plexus. Effective and habit-forming with chronic use — for rescue, not for management.

How it works: A stimulant laxative that directly triggers colonic contraction. It works, reliably, and that reliability is exactly why it gets misused.

The mechanistic case: Sennosides are activated by colonic bacteria into compounds that stimulate the myenteric plexus directly — a pharmacological push, not a change in the underlying problem.

Antisecretory and antimicrobial. Also used in H. pylori quadruple therapy.

How it works: The pink stuff. An old drug with genuinely good evidence for two specific jobs — and a couple of properties nobody warns you about.

The mechanistic case: Sometimes used for bile acid diarrhea and for sulfur-producing gut overgrowth on the basis of bismuth binding hydrogen sulfide — plausible, thinly evidenced.

5-HT3 antagonism slows transit and has real randomized evidence in diarrhea-predominant IBS.

How it works: 5-HT3 receptor antagonist — blocks serotonin signaling at the vagal afferents and the chemoreceptor trigger zone, which is the pathway GLP-1 nausea travels down.

The mechanistic case: A 5-HT3 receptor antagonist. Chemotherapy and gastric irritation cause enterochromaffin cells in the gut to release serotonin, which activates 5-HT3 receptors on vagal afferents and triggers the vomiting reflex in the area postrema. Blocking the trigger rather than sedating the patient is why it replaced older antiemetics — no dopamine blockade means no extrapyramidal effects and no sedation. It blocks the signal, not the cause. Used against GLP-1 nausea it suppresses a symptom arising from delayed gastric emptying, and the delayed emptying continues.

Antispasmodic and anxiolytic — both ends of the axis at once.

How it works: The most-drunk sleep herb in the world, and one of the few with an actual randomized trial behind it rather than just tradition.

The mechanistic case: Apigenin binds benzodiazepine sites on the GABA-A receptor with low affinity — the same site as diazepam, at a vastly lower potency.

Traditional carminative with modern anxiolytic data.

How it works: A gentle calming herb with more trial support than its mildness suggests.

The mechanistic case: GABA transaminase inhibition is proposed, which would increase GABA availability.

Adsorbs gas and toxins non-selectively — including your medications, which is the interaction people forget.

How it works: A genuine medical treatment for acute poisoning that has been repackaged as a wellness product, where it does almost nothing useful and one clearly harmful thing.

The mechanistic case: The 'detox' framing has no supporting outcome evidence — it binds indiscriminately in the gut lumen and does not remove anything from your tissues or bloodstream.

Small trials in Crohn's show mucosal healing; the microglial and enteric anti-inflammatory argument.

How it works: Its mechanism is dose-dependent — the Vault page explains why, with the figures.

The mechanistic case: Two proposed mechanisms, and they are different. First, transient opioid receptor blockade causes rebound upregulation of endogenous endorphins and receptors — which is why the timing of the dose matters and why the dose has to be low enough to wear off. Second, and probably more important for the inflammatory conditions: naltrexone antagonizes Toll-like receptor 4 on microglia, damping neuroinflammation. This mechanism is not opioid-mediated at all — it works with the non-opioid stereoisomer — which is why it can plausibly help conditions that have nothing to do with endorphins.