Berberine for Gut Health, Small Intestinal Bacterial Overgrowth (SIBO) & Dysbiosis

Table of Contents

1. The Chedid 2014 Trial — Berberine vs Rifaximin for Small Intestinal Bacterial Overgrowth
2. Small Intestinal Bacterial Overgrowth — The Condition and Why Antibiotic Resistance Is a Problem
3. Berberine's Antimicrobial Spectrum
4. Berberine for Clostridium difficile Infection
5. Berberine for Helicobacter pylori
6. Berberine for Giardia and Other Protozoa
7. Berberine for Candida and Yeast Overgrowth
8. The Dysbiosis Rotation Protocol
9. Berberine's Effect on the Beneficial Microbiome
10. Protocols Practitioners Describe for Small Intestinal Bacterial Overgrowth Eradication
11. Aftercare — Preventing Relapse
12. Key Research Papers
13. Connections
14. Featured Videos

The Chedid 2014 Trial — Berberine vs Rifaximin for Small Intestinal Bacterial Overgrowth

The 2014 Chedid, Dhalla, Clarke, Roland, et al. trial at Johns Hopkins is the foundational modern evidence for using herbal antimicrobials including berberine in small intestinal bacterial overgrowth. The investigators conducted a retrospective chart review of 104 patients with newly diagnosed small intestinal bacterial overgrowth (positive lactulose breath test) who were treated with either:

• Rifaximin 1,200 mg/day (400 mg three times daily) for 4 weeks — the standard prescription antibiotic for small intestinal bacterial overgrowth
• Herbal antimicrobials — two commercial pairs of herbal blends from two different supplement makers, containing berberine-rich plant extracts plus oregano, thyme, sage, and lemon balm components. Two capsules twice daily, for 4 weeks.

The post-treatment results:

• Normalization of lactulose breath test: rifaximin 23 of 67 (34%), herbal antimicrobials 17 of 37 (46%) (P=.24; adjusted odds ratio 1.85, 95% confidence interval 0.77–4.41)
• Adverse events: 6 of 67 in the rifaximin group (1 anaphylaxis, 2 hives, 2 diarrhoea, 1 Clostridium difficile infection) vs 1 of 37 in the herbal group (diarrhoea) (P=.22)
• Cost: the herbal therapy cost no more than $120 for a 30-day supply; a month's supply of rifaximin retailed for $1,247.39

The authors concluded that the herbal therapies were "at least as effective as rifaximin" for breath-test normalization; no formal non-inferiority test was run, and the difference was not statistically significant. Fewer side effects were reported with the herbs, at a much lower cost. The trial limitations are real — retrospective design (not a randomized controlled trial, RCT), patients choosing their own treatment, modest sample size, two different herbal blends (not pure berberine), single center, and symptoms not formally assessed with a standardized questionnaire — but the signal is strong enough to have changed clinical practice in integrative gastroenterology. Herbal antimicrobials, with berberine as the most-validated component, are now a standard first-line or second-line option for small intestinal bacterial overgrowth treatment in many integrative gastrointestinal (GI) clinics.

For the broader small intestinal bacterial overgrowth clinical picture and a deeper treatment discussion, see the small intestinal bacterial overgrowth main page and the small intestinal bacterial overgrowth Treatment Protocols deep-dive.

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Small Intestinal Bacterial Overgrowth — The Condition and Why Antibiotic Resistance Is a Problem

Small intestinal bacterial overgrowth (SIBO) is a condition in which excessive numbers of bacteria colonize the small intestine, where bacterial density should normally be low (the small bowel is designed to be relatively sterile compared to the colon). Diagnostic threshold has historically been >10^5 colony-forming units (CFU)/mL in jejunal aspirate, although the lactulose breath test (LBT) and glucose breath test (GBT) are the practical clinical tools.

Symptoms are nonspecific but consistent: bloating, postprandial abdominal distension, alternating diarrhea and constipation, excessive gas, food intolerances (particularly to foods high in FODMAPs — fermentable oligosaccharides, disaccharides, monosaccharides and polyols — that are fermented by the overgrown bacteria), nutritional deficiencies (B12 from bacterial competition, fat-soluble vitamins from bile acid deconjugation, iron from intestinal inflammation), and weight loss in severe cases. The mechanisms linking small-bowel bacterial overgrowth to symptoms are reasonably well-understood: bacterial fermentation of carbohydrates produces hydrogen and methane gas distending the bowel, bacterial deconjugation of bile acids impairs fat digestion and produces diarrhea, bacterial metabolites including lipopolysaccharide (LPS) contribute to systemic inflammation.

The standard pharmacologic treatment is the non-absorbable antibiotic rifaximin 550 mg three times daily for 14 days. The advantage of rifaximin is that it stays in the gut lumen, achieving high local concentrations without systemic absorption. The disadvantages are:

• Cost — the 2014 Chedid paper reported that a month's supply of rifaximin retailed for $1,247.39, with a 2014 Medicare Part D copay of $638.09 at a preferred pharmacy
• Insurance prior-authorization burden — the U.S. Food and Drug Administration label for rifaximin lists travelers' diarrhea caused by noninvasive E. coli (age 12 and older), reducing the risk of overt hepatic encephalopathy coming back, and irritable bowel syndrome (IBS) with diarrhea, but not small intestinal bacterial overgrowth, so insurance coverage is variable
• Relapse rate — in one study of 80 patients cleared with rifaximin, the breath test turned positive again in 12.6% at 3 months, 27.5% at 6 months and 43.7% at 9 months, often leading to repeated treatment
• Emerging resistance — while rifaximin's non-absorption keeps systemic resistance pressure low, gut-flora resistance can develop with repeated courses
• Methane-dominant small intestinal bacterial overgrowth — methane producers (formally now reclassified as "intestinal methanogen overgrowth" or IMO) respond poorly to rifaximin monotherapy and typically require combination with neomycin or metronidazole, which adds cost and side effects

This is the niche that practitioners describe for berberine. As a botanical antimicrobial with a different mechanism than rifaximin, berberine is described in use as primary therapy, as second-line after rifaximin failure, as a rotating agent between rifaximin courses to slow resistance development, or in patients without insurance coverage for whom rifaximin is unaffordable.

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Berberine's Antimicrobial Spectrum

Berberine has a notably broad antimicrobial spectrum compared to most natural products:

• Gram-positive bacteria — effective against Staphylococcus aureus (including some methicillin-resistant Staphylococcus aureus (MRSA) strains in vitro), Streptococcus species, Enterococcus species, Clostridium difficile
• Gram-negative bacteria — effective against Escherichia coli (including some enterotoxigenic and enteropathogenic strains), Salmonella species, Shigella species, Vibrio cholerae, Campylobacter jejuni, Helicobacter pylori, Klebsiella pneumoniae
• Yeasts and fungi — effective against Candida albicans, Candida glabrata, Cryptococcus neoformans
• Protozoa — effective against Giardia lamblia, Entamoeba histolytica, Trichomonas vaginalis, Leishmania species
• Viruses — some in vitro activity against influenza, herpes simplex virus (HSV), and others, but the in vivo evidence is limited

The molecular mechanisms underlying this broad-spectrum activity:

1. DNA intercalation — berberine inserts between adjacent DNA base pairs, interfering with DNA replication and transcription. This is similar in concept to how some antibiotics (quinolones target DNA gyrase) and chemotherapy agents (doxorubicin intercalates DNA) work.
2. FtsZ inhibition — berberine inhibits bacterial FtsZ, the bacterial tubulin homolog that forms the constriction ring during bacterial cell division. Without functional FtsZ, bacteria cannot complete cytokinesis and stop dividing. This mechanism is bactericidal at high concentrations.
3. Cell membrane disruption — berberine inserts into bacterial cell membranes, particularly Gram-positive membranes, disrupting membrane integrity and proton motive force.
4. Efflux pump inhibition — berberine inhibits bacterial multi-drug efflux pumps (NorA in S. aureus, AcrAB in E. coli), which can resensitize bacteria that have become resistant to conventional antibiotics. This is a particularly interesting property given the antibiotic resistance crisis.
5. Quorum sensing disruption — berberine interferes with bacterial cell-to-cell signaling (autoinducers such as autoinducer-2, AI-2), reducing biofilm formation and virulence factor expression.

The multi-mechanism antimicrobial profile is one reason berberine resistance has been slow to develop — bacterial single-step resistance mutations cannot easily overcome five different molecular targets simultaneously.

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Berberine for Clostridium difficile Infection

Clostridium difficile (C. diff) infection is one of the most challenging hospital-acquired infections in modern medicine. The standard treatment paradigm has shifted away from metronidazole toward oral vancomycin and fidaxomicin, but recurrence rates remain 20-30% after a first episode and rise to 40-60% after a second. The principal driver of recurrence is the destruction of the protective commensal microbiome by the very antibiotics used to treat the infection — a vicious cycle of dysbiosis-driven C. diff overgrowth.

Berberine is mechanistically attractive in C. diff for several reasons:

• Direct in vitro activity against C. difficile at clinically achievable luminal concentrations
• Less destructive to commensal anaerobes (Lactobacillus, Bifidobacterium, Akkermansia) than vancomycin or fidaxomicin, preserving the microbiome scaffold needed for recovery
• Direct inhibition of toxin A and toxin B activity at the intestinal epithelium (the virulence factors that produce the colitis)
• Affordable for long-duration adjunct or maintenance therapy

Integrative practitioners describe using berberine 500 mg three times daily as an adjunct to vancomycin or fidaxomicin during the initial treatment course, then continuing it alone for 4-8 weeks after the prescription antibiotic is stopped, with the aim of suppressing C. diff regrowth while the microbiome recovers. This approach has not been tested in randomized controlled trials. The standard-of-care antibiotics (vancomycin, fidaxomicin) are the first-line treatment for an acute C. diff infection, and practitioners describe berberine at most as an adjunct.

For more on C. diff and antibiotic-associated diarrhea, see the C. difficile page, or the Probiotics page for microbiome-restoration approaches.

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Berberine for Helicobacter pylori

Helicobacter pylori is the bacterial cause of most peptic ulcer disease, chronic gastritis, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma, and is a class I carcinogen for gastric adenocarcinoma. Standard eradication therapy is bismuth quadruple therapy (proton pump inhibitor (PPI) + bismuth subsalicylate + metronidazole + tetracycline) or clarithromycin-based triple therapy (proton pump inhibitor + clarithromycin + amoxicillin), each for 10-14 days. Eradication rates have declined over the past two decades as antimicrobial resistance (particularly clarithromycin resistance) has spread, dropping from >90% to 70-80% in many regions.

Berberine has been tested as both adjunct and substitute in H. pylori eradication regimens. Multiple trials in Chinese populations have shown that:

• A 2019 meta-analysis of 13 randomized trials in China found that adding berberine to standard triple therapy raised the eradication rate (relative risk 1.22, 95% confidence interval 1.16–1.27) and lowered adverse events (relative risk 0.65) compared with triple therapy alone
• Berberine + dual therapy (proton pump inhibitor + amoxicillin) approaches the eradication rate of full triple therapy in some trials
• Berberine appears to be active against clarithromycin-resistant H. pylori strains in vitro
• Berberine reduces gastric inflammation and may accelerate symptom resolution

The mechanism is the broad antimicrobial activity discussed above, plus specific effects on the H. pylori urease enzyme (which neutralizes gastric acid to allow H. pylori colonization) and on the CagA virulence factor expression. The use case is most attractive in patients with prior treatment failure, in regions with high clarithromycin resistance, or as adjunct to maximize eradication rates in first-line treatment.

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Berberine for Giardia and Other Protozoa

The historical Ayurvedic use of berberine-containing herbs for "amoebic" diarrhea has been validated mechanistically. Berberine has demonstrated activity against:

• Giardia lamblia — the most common protozoal cause of traveler's diarrhea worldwide; berberine produces in vitro killing at concentrations achievable in the gut lumen
• Entamoeba histolytica — the causative agent of amoebic dysentery; berberine has been used clinically in this indication in regions where standard treatment (metronidazole + paromomycin) is unavailable
• Trichomonas vaginalis — topical and oral berberine has been studied
• Leishmania species — in vitro and limited clinical evidence

The clinical positioning is that berberine is generally an adjunct to or alternative for standard antiprotozoal drugs (metronidazole, tinidazole, nitazoxanide, paromomycin) rather than first-line monotherapy in developed-world settings. In resource-limited settings, practitioners cite the cost advantage and the historical experience in describing berberine as a first-line option for symptomatic protozoal diarrhea.

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Berberine for Candida and Yeast Overgrowth

Candida overgrowth (intestinal and systemic) is a contested concept in mainstream medicine but a real clinical entity in many integrative practices, where patients present with bloating, brain fog, sugar cravings, recurrent vaginal yeast infections, and intolerance to fermented foods. The diagnostic certainty is lower than for small intestinal bacterial overgrowth (no breath test equivalent), and the diagnosis often relies on a constellation of symptoms plus stool culture or organic acid testing.

Berberine has documented in vitro activity against Candida albicans, Candida glabrata, and several other yeast species, with mechanisms including direct membrane disruption and inhibition of fungal cell wall synthesis. The clinical evidence in human Candida overgrowth is limited (this is true of essentially all interventions for this entity), but the in vitro evidence and clinical experience in integrative gastrointestinal practice are the basis on which integrative practitioners use berberine as a component of multi-agent antifungal protocols.

The herbal blends used in the Chedid 2014 small intestinal bacterial overgrowth trial (two commercial berberine-containing blends) were originally formulated for combined bacterial and fungal overgrowth, reflecting the clinical reality that the two often coexist. Berberine plus caprylic acid, oregano oil, and saccharomyces boulardii is a common combination protocol for Candida-and-bacterial dysbiosis in integrative practice.

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The Dysbiosis Rotation Protocol

A framework integrative practitioners describe for chronic dysbiosis management is the "rotation" concept — cycling between multiple antimicrobial agents with different mechanisms to (a) avoid the resistance development that occurs with repeated use of any single agent, (b) achieve broader-spectrum coverage by addressing the different microbial populations that respond to different agents, and (c) reduce the risk of complete commensal collapse that occurs with prolonged single-agent suppression.

A rotation protocol practitioners describe for chronic small intestinal bacterial overgrowth or chronic dysbiosis includes:

• Round 1 (4 weeks) — rifaximin 550 mg three times daily, plus a low-FODMAP or biphasic diet
• 2-week washout with prokinetic and digestive support
• Round 2 (4 weeks) — berberine 500 mg three times daily plus oregano oil or thyme essential oil capsules
• 2-week washout
• Round 3 (4 weeks) — allicin-based garlic extract plus neem leaf extract, or a different commercial herbal antimicrobial blend
• Maintenance phase — biofilm disruptors (N-acetylcysteine (NAC), lactoferrin), prokinetic agents (low-dose naltrexone, prucalopride, ginger), probiotic re-seeding (multi-strain probiotic plus saccharomyces boulardii)

The rationale practitioners give for rotation is mechanistic: berberine and rifaximin have entirely different mechanisms (DNA intercalation + FtsZ inhibition + efflux pump inhibition vs RNA polymerase inhibition), so a bacterial population that survives one is unlikely to survive the other. Repeated single-agent treatment selects for resistant subpopulations; rotation prevents this selection pressure from building.

Berberine's role in the rotation is as a broad-spectrum component that covers both bacteria and yeast, and as a low-cost option compared with repeated rifaximin courses. Practitioners combine it with a complementary herbal agent (oregano oil, allicin) to widen the spectrum.

For more on dysbiosis and integrative gut management, see the Gut Healing page.

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Berberine's Effect on the Beneficial Microbiome

A key question with any antimicrobial used long-term is the collateral damage to beneficial commensals. The available evidence suggests berberine has a more favorable profile than broad-spectrum systemic antibiotics:

• Akkermansia muciniphila — this beneficial mucin-degrading bacterium, considered a marker of healthy gut barrier function, has been shown to increase with berberine treatment in both rodent models and human studies. This is one of the most distinctive microbiome signatures of berberine.
• Bifidobacterium and Lactobacillus — effects are mixed; some studies show no change, some show modest decreases that recover with co-administration of probiotics
• Short-chain fatty acid producers — Faecalibacterium prausnitzii, Roseburia, and other butyrate producers generally show stable-to-increased abundance on berberine, in contrast to the suppression seen with broad-spectrum systemic antibiotics
• Lipopolysaccharide-producing Gram-negatives — decreased, which contributes to the reduced metabolic endotoxemia that drives some of berberine's systemic metabolic benefits
• Overall alpha diversity — generally preserved or modestly reduced; the dramatic loss of diversity that follows fluoroquinolone or amoxicillin-clavulanate courses is not seen with berberine

The mechanism for this relatively benign profile appears to be that berberine's antimicrobial activity is most potent against pathobionts and overgrowth-associated organisms while sparing the dominant commensals. Whether this reflects intrinsic species-level differences in berberine sensitivity, ecological dynamics (overgrowth organisms are more metabolically active and therefore more susceptible to FtsZ inhibition), or both, is not fully resolved.

Practitioners take this to mean that berberine is more compatible with concurrent probiotic use than systemic antibiotics are; some take the probiotic and the berberine at the same time of day, and others separate them by 2 hours as a conservative approach.

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Protocols Practitioners Describe for Small Intestinal Bacterial Overgrowth Eradication

A berberine-based small intestinal bacterial overgrowth eradication protocol as integrative practitioners describe it (the doses are those used in practice):

1. Diagnostic confirmation — lactulose breath test (LBT) or glucose breath test (GBT) to confirm small intestinal bacterial overgrowth and distinguish hydrogen-dominant, methane-dominant (IMO), or mixed
2. Pre-treatment preparation (1 week) — a low-FODMAP or biphasic diet to reduce substrate for the overgrown bacteria; a digestive enzyme + ox bile combination with each meal; a prokinetic (gut-movement agent) at bedtime (ginger 1,000 mg, low-dose naltrexone 2.5-4.5 mg, or 5-hydroxytryptophan (5-HTP) 50-100 mg)
3. Antimicrobial phase (4 weeks) —
   • Berberine 500 mg three times daily with meals
   • Plus oregano oil capsule (containing approximately 200 mg standardized to 60%+ carvacrol) twice daily with meals, OR
   • Plus a commercial berberine-containing herbal antimicrobial blend, such as the blends used in the Chedid 2014 study
   • For methane-dominant small intestinal bacterial overgrowth, practitioners add an allicin extract (enteric-coated garlic extract) 450 mg twice daily, on the reasoning that methanogens are particularly resistant to most antimicrobials and allicin has unique activity against archaea
4. Biofilm disruption (concurrent) — N-acetylcysteine 600 mg twice daily, plus a biofilm-disrupting enzyme product 30 minutes before each antimicrobial dose. The rationale is that bacteria in biofilms are 100-1,000× more resistant to antimicrobials than planktonic bacteria, and disrupting biofilms exposes them to berberine.
5. Post-antimicrobial reseeding (2 weeks) — multi-strain probiotic with at least 25 billion CFU/day plus Saccharomyces boulardii 5-10 billion CFU/day, taken at least 2 hours apart from any remaining antimicrobial doses
6. Maintenance phase (3-6 months) — continued prokinetic (low dose naltrexone (LDN) or ginger nightly), continued low-FODMAP or modified-Mediterranean diet, periodic re-treatment with berberine 500 mg twice daily for 7-10 days at first sign of symptom recurrence
7. Re-test at 6 weeks post-antimicrobial — repeat LBT to confirm eradication. If still positive, practitioners describe a second round with a different rotation (rifaximin if not yet used, or a different herbal blend).

Safety facts. In a randomized crossover study in healthy men, berberine 300 mg three times daily for 2 weeks lowered the activity of three liver enzymes that break down many common medicines (CYP3A4, CYP2D6 and CYP2C9); blood levels of the test drug midazolam rose about 40%, and the authors concluded that drug interactions need to be considered when berberine is taken. In laboratory tests berberine pushed bilirubin off its carrier protein (albumin) about ten times more strongly than the drug phenylbutazone, and the berberine-rich Chinese herb huanglian (Coptis chinensis) has been reported to pose some risk of kernicterus (brain damage from bilirubin) in jaundiced newborns; that paper concluded that herbs high in berberine are "best avoided in jaundiced neonates and pregnant women."

For deeper protocol details, see the small intestinal bacterial overgrowth main page and the relevant sub-articles in the small intestinal bacterial overgrowth deep-dive hub.

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Aftercare — Preventing Relapse

The single most important fact about small intestinal bacterial overgrowth is the high relapse rate. In one study of 80 patients cleared with rifaximin, the breath test turned positive again in 27.5% by 6 months and 43.7% by 9 months. Berberine's role in relapse prevention:

• Periodic short-course retreatment — rather than waiting for full symptom recurrence and a full breath-test relapse, practitioners describe a 7-10 day course of berberine 500 mg twice daily at the first sign of recurring bloating or distention. This "punctuated maintenance" approach is described as extending the time between full treatment rounds.
• Continuous low-dose maintenance — some clinicians use berberine 500 mg once daily continuously as part of long-term maintenance in patients with frequent relapse. The safety data out to 24 months are reassuring, although longer-term continuous use has not been formally studied.
• Combination with prokinetic — the underlying driver of small intestinal bacterial overgrowth relapse is usually impaired migrating motor complex (MMC) function in the small intestine. Berberine does not directly fix the MMC; prokinetic agents (low dose naltrexone, prucalopride, ginger, mosapride, 5-HTP) do. Practitioners describe periodic berberine retreatment plus a continuous prokinetic as their preferred combination.

For the small intestinal bacterial overgrowth relapse-prevention discussion in detail, see the small intestinal bacterial overgrowth Prokinetics and Relapse Prevention deep-dive.

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Key Research Papers

1. Chedid V, Dhalla S, Clarke JO, et al. (2014). Herbal therapy is equivalent to rifaximin for the treatment of small intestinal bacterial overgrowth. Global Advances in Health and Medicine 3(3):16-24. — PubMed PMID: 24891990
2. Rabbani GH, Butler T, Knight J, et al. (1987). Randomized controlled trial of berberine sulfate therapy for diarrhea due to enterotoxigenic Escherichia coli and Vibrio cholerae. Journal of Infectious Diseases. — PubMed PMID: 3549923
3. Sun D, Courtney HS, Beachey EH (1988). Berberine sulfate blocks adherence of Streptococcus pyogenes to epithelial cells, fibronectin, and hexadecane. Antimicrobial Agents and Chemotherapy. — PubMed PMID: 3058020
4. Domadia PN, Bhunia A, Sivaraman J, et al. (2008). Berberine targets assembly of Escherichia coli cell division protein FtsZ. Biochemistry. — PubMed PMID: 18275156
5. Stermitz FR, Lorenz P, Tawara JN, et al. (2000). Synergy in a medicinal plant: antimicrobial action of berberine potentiated by 5'-methoxyhydnocarpin, a multidrug pump inhibitor. PNAS. — PubMed PMID: 10677479
6. Bandyopadhyay S, Patra PH, Mahanti A, et al. (2013). Potential antibacterial activity of berberine against multi drug resistant enterovirulent Escherichia coli isolated from yaks. Asian Pacific Journal of Tropical Medicine. — PubMed PMID: 23608335
7. Sack RB, Froehlich JL (1982). Berberine inhibits intestinal secretory response of Vibrio cholerae and Escherichia coli enterotoxins. Infection and Immunity. — PubMed PMID: 7035365
8. Hu Q, Peng Z, Li L, et al. (2019). The efficacy of berberine-containing quadruple therapy on Helicobacter pylori eradication in China: a systematic review and meta-analysis of randomized clinical trials. Frontiers in Pharmacology 10:1694. — PubMed PMID: 32116685
9. Zhang X, Zhao Y, Zhang M, et al. (2012). Structural changes of gut microbiota during berberine-mediated prevention of obesity and insulin resistance in high-fat diet-fed rats. PLoS One. — PubMed PMID: 22880019
10. Wang Y, Tong Q, Shou JW, et al. (2017). Gut microbiota-mediated personalized treatment of hyperlipidemia using berberine. Theranostics. — PubMed PMID: 28744326
11. Sun R, Yang N, Kong B, et al. (2017). Orally administered berberine modulates hepatic lipid metabolism by altering microbial bile acid metabolism and the intestinal FXR signaling pathway. Molecular Pharmacology. — PubMed PMID: 27932556
12. Guo Y, Chen Y, Tan ZR, Klaassen CD, Zhou HH (2012). Repeated administration of berberine inhibits cytochromes P450 in humans. European Journal of Clinical Pharmacology 68(2):213-217. — PubMed PMID: 21870106
13. Chan E (1993). Displacement of bilirubin from albumin by berberine. Biology of the Neonate 63(4):201-208. — PubMed PMID: 8513024
14. Lauritano EC, Gabrielli M, Scarpellini E, et al. (2008). Small intestinal bacterial overgrowth recurrence after antibiotic therapy. American Journal of Gastroenterology 103(8):2031-2035. — PubMed PMID: 18802998

PubMed Topic Searches

1. PubMed: Berberine and SIBO
2. PubMed: Berberine and C. difficile
3. PubMed: Berberine and H. pylori
4. PubMed: Berberine and microbiome
5. PubMed: Berberine antimicrobial spectrum
6. PubMed: Berberine and Candida

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Connections

• All Herbs
• Berberine Overview
• Berberine Benefits Hub
• Berberine for Blood Sugar
• Berberine for Cholesterol
• Berberine, AMP-Activated Protein Kinase & Metabolic Syndrome
• Small Intestinal Bacterial Overgrowth (Main Page)
• Gastroenterology Conditions
• Gut Healing
• Probiotics
• Oregano Oil
• Garlic / Allicin
• Goldenseal (Berberine Source)
• Barberry (Berberine Source)
• Elimination Diet / Low-FODMAP
• Ginger (Prokinetic)
• History

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