Lit Review Friday
I have been meaning to deep dive into the SIBO literature since I started this Learn Something Series. In preparation for the annual fall GastroANP conference, I tackled it by drawing from four prominent papers that approached SIBO from four directions in 2026 and the naturopathic GI lens I learned from.
Lit Review Friday · SIBO: What the 2026 Research Can Tell Us · 2026 · 21 minute read
SIBO sits near the center of naturopathic and integrative gastroenterology. I learned the framework in school, I have watched colleagues build careful practices around it, and I have seen it help people who had been told for years that nothing was wrong. I have also watched the research argue with itself for most of that time.
This year I wanted to read it together. Four papers published in 2026 approach SIBO from different sides: a large breath-gas study, a critical review from some of the field's most careful skeptics, a look at gene expression in the gut lining, and a review of hydrogen sulfide biology. I want to read them the way my community uses this work, where testing, diet and clinical judgment meet real patients every day.
February. Pimentel and colleagues, Journal of Clinical Gastroenterology. 3,004 people took an at-home three-gas breath test and answered a symptom questionnaire. Hydrogen tracked with diarrhea, methane with constipation, and hydrogen sulfide with diarrhea, urgency and abdominal pain. Bloating, the most common reason people got tested, did not correlate with any single gas level. 1
May. Shah, Holtmann and Gibson, JGH Open. A critical review that places the SIBO controversy in the limits of culture and breath testing, and proposes a broader frame called small intestinal dysbiosis: which microbes are there, where they live and what they do. 2
June. de Freitas Germano and colleagues, mSystems. Small bowel biopsies from people with sulfide overproduction showed broad changes in genes for cellular energy and redox balance, with fewer changes in bacterial or methane overgrowth. Exploratory work that needs confirmation. 3
June. Kumar and Banerjee, Gut Microbes. A review of hydrogen sulfide as a normal signal in the gut, and of what happens when sulfide production outpaces the host's capacity to handle it. 4
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Where we are in defining a healthy gut
I like to think about this conversation starting one step before SIBO. Researchers have no validated, quantitative definition of a healthy gut microbiome: no single number, species list or diversity score separates a thriving gut ecosystem from a struggling one in every person. "Dysbiosis" describes a microbial community that has shifted away from what supports its host, and the field has not agreed on how to measure that shift. IBS still has no biomarker. When Shah, Holtmann and Gibson propose expanding SIBO into small intestinal dysbiosis, they are also describing how early the science is. 2
Every gut test stands on that ground, and imperfect tests still carry information.
In the naturopathic and integrative gastroenterology community I work alongside, clinicians use breath testing for reasons the diagnostic-accuracy studies were not designed to measure.
Validation. A person told for years that every test came back normal gets a result that names what they feel. For many patients, that recognition is where care starts.
A starting point. Clinical care runs on algorithms, and an algorithm needs an entry point a clinician can write down, repeat and teach. A breath test often serves as that entry point, provisional as everyone involved knows it is.
Gas patterns. Hydrogen, methane and hydrogen sulfide track different symptom patterns and real organisms in the small intestine, so the gas profile can shape which approach a clinician tries first. 1,13,14
Something to follow. A repeat test gives the clinician and the patient one more way to discuss whether a plan is working, alongside how the person feels.
After years of normal results and "it's probably stress," many patients arrive exhausted. A name, a mechanism and a plan can change how a person relates to their own body before treatment begins, and that change helps explain why these frameworks spread. A label also carries weight. A diagnosis can open a life back up, and it can become a reason to narrow one.
The healthcare system shapes this too. When no validated test exists, clinicians reach for the most practical imperfect one, and protocols grow from that starting point. I think those protocols can still help people. I also think clinicians and patients should treat that entry point as more provisional than the algorithm built on top of it suggests.
Bloating brought people to the test
Pimentel and colleagues paired at-home measurements of hydrogen, methane and hydrogen sulfide with a symptom questionnaire. Bloating, the symptom that most often sent people to the test, gave the most interesting result. Individual gas levels showed no correlation with bloating severity, and the combined analysis linked bloating to sulfide-related patterns. A fair reading keeps both. 1
Of 6,000 consecutive people asked to complete the questionnaire, 3,004 were included in the analysis. Severe or very severe bloating was reported by 52.9%, compared with 17.8% for diarrhea, 17.1% for constipation, and 17.1% for abdominal pain. 1
That gap between one measurement and a broader pattern runs through the SIBO literature. A test can pick up a biological signal that does not explain a person's symptoms. A study can find an association and never test whether changing it helps. A treatment can improve symptoms while its mechanism stays unclear. 1,2
The recent papers push past breath gases and bacterial counts toward microbial function and the response of the intestinal lining. I think that is a useful direction, as long as each finding carries its limits with it. 1,2,3,4
Where is the literature on SIBO breath tests?
Small intestinal bacterial overgrowth means too many bacteria in the small intestine, with symptoms to match. Clinicians recognize classical SIBO after changes to bowel anatomy or with serious problems in intestinal movement. The controversy sharpens when the same framework stretches across the much larger group of people with IBS and unexplained gut symptoms. 6,7
In 2008, Khoshini, Dai, Lezcano and Pimentel reviewed 71 papers on SIBO diagnosis and concluded there was no validated diagnostic test or gold standard. They described a validation problem inside their own field, one clinicians and researchers still work around today. 5
Small bowel aspirate culture draws fluid from the small intestine and counts the bacteria that grow in the lab. Many studies use it as the reference test. The catheter can pick up contamination on the way down, culture misses organisms that will not grow in those conditions, and sampling methods and thresholds change what gets counted. A reference with those limits cannot referee another test with much authority. 2,5,8
When the comparison test is also uncertain
Cangemi, Lacy and Wise compared lactulose breath testing with duodenal aspirates in the same patients. Low agreement tells you the two methods sort people differently. It cannot tell you which one matches the biology. 8
The study included 106 patients. Evidence of contamination appeared in 19.8% of aspirates. Reported agreement between the tests was 63.5%, with a kappa of -0.02 after accounting for agreement expected by chance. The authors concluded that breath testing may be preferable because it is safer, cheaper, and less likely to yield a contaminated result. 8
Those practical advantages count. A test can be useful without being perfect, and the invasive measurement is not always the more accurate one. The harder question is what a result can support: detecting a signal, supporting a diagnosis in a specific setting, or choosing a treatment. Each use needs its own kind of evidence, and this comparison answers part of it. 5,8
Why glucose and lactulose differ
In a breath test, a person drinks a sugar solution and breathes into a collection bag at intervals. Clinicians read the result from when the gas rises, which stands in for where in the gut the fermentation happened. The bag captures the gas and cannot see where it came from. 2,7,11
The small intestine absorbs glucose quickly, so a glucose test can miss microbes further down. Lactulose is not absorbed and travels on to the colon, where bacteria ferment it too. If lactulose reaches the colon early, colonic gas can look like small intestinal fermentation. A timed rise hints at location without showing it. 7,11
In Losurdo and colleagues' meta-analysis, pooled lactulose-test sensitivity was 42.0% and specificity was 70.6%. For glucose testing, sensitivity was 54.5% and specificity was 83.2%. These estimates use small bowel culture as the reference, with the limitations that reference carries. 9
Sensitivity is how often a test catches people the reference method calls positive. Specificity is how often it clears people the reference calls negative. Neither number gives you your own chance of having SIBO after a result. That depends on your symptoms, your history and how likely SIBO was before you tested. 6,7,9
Massey and Wald draw the sharpest line between the two sugars. They argue that lactulose testing rests on an incorrect premise and should be dropped for diagnosing SIBO, and they keep a role for glucose testing. 11
Repeatability does not settle meaning
Jiménez-Castillo and colleagues asked a different question: do breath results repeat? Healthy adults took glucose and lactulose tests, came back two weeks later and took them again. The lactulose results repeated closely, even though positives were common in people with no ongoing gut complaints. 10
Among 40 healthy adults tested twice, two weeks apart, lactulose positivity was 60.0% at baseline and 60.0% at retest. The reported intraclass correlation coefficient was 0.88. Glucose positivity was 15.0% initially and 10.0% at retest. 10
Matching percentages on two visits do not show that each person got the same result twice. Stable gas readings and diagnostic meaning are separate questions. The study shows the lactulose test repeats under its protocol, and it makes it hard to assume that crossing the positive line explains someone's symptoms. 10
Reading the 60% figure as a universal false-positive rate would overreach. It belongs to 40 healthy adults, one protocol and one set of criteria. Healthy-volunteer results challenge a broad reading of positive tests and say little about every protocol in every clinic. 9,10
Taken together, this literature calls for humility about what one breath result means for one person. The ACG still suggests breath testing, the authors of the aspirate comparison favored it over culture, and the gases track real organisms. The disagreement concerns how much weight a single result can carry. 6,8,14
What a breath test cannot rule out
A breath test measures fermentation gases. It cannot detect or rule out other causes of gut symptoms, and it does not replace a gastrointestinal workup, including the evaluation that looks for colorectal cancer. That boundary matters more each year, because colorectal cancer is appearing earlier in life.
Incidence in US adults aged 20 to 49 rose about 3% a year from 2013 to 2022, while it fell in adults 65 and older. 16
Mortality in adults younger than 50 has risen about 1% a year since 2004, and colorectal cancer is now the leading cause of cancer death in adults younger than 50. 16
The share of cases diagnosed before age 55 rose from 11% in 1995 to 20% in 2019, and 60% of new cases in 2019 were diagnosed at an advanced stage, up from 52% in the mid-2000s. 17
The symptoms that come before an early-onset diagnosis can look like everyday gut trouble. Fritz and colleagues studied 5,075 people diagnosed with colorectal cancer before age 50. Four signs in the three months to two years before diagnosis carried higher risk: abdominal pain, rectal bleeding, diarrhea and iron deficiency anemia. Each additional sign raised the risk further. Among people whose first sign appeared in that window, the median time to diagnosis was 8.7 months. 18 Abdominal pain and diarrhea also send many people toward an IBS or SIBO label, so a positive breath test should prompt a conversation about these signs.
Rectal bleeding or blood in the stool, iron deficiency anemia, and abdominal pain or diarrhea that persists, worsens or is new for you. These were the red flags associated with early-onset colorectal cancer in the study above, and they warrant a clinician's evaluation at any age. 18
Routine colorectal cancer screening for average-risk adults without symptoms starts at age 45. Symptoms call for evaluation now, whatever a person's age. 19
A thorough IBS workup and a breath test can sit side by side. The 2021 ACG guideline on IBS favors a positive diagnosis over a long diagnosis of exclusion, with targeted tests such as celiac serology and, in people with diarrhea, fecal calprotectin to look for inflammatory bowel disease. 20 A breath test adds information to that workup and cannot stand in for it.
Health care in the United States is a privilege many people do not have. A colonoscopy can require insurance, time off work, transportation, a prep day at home and someone to drive you afterward. Some people find their way to integrative and naturopathic care because conventional care was hard to reach or had already dismissed them. National data show the size of the gap: in 2016, 26% of eligible adults had never been screened for colorectal cancer, and in 2018, 31% were not up to date. 19
Limited access makes the conversation more important. Whatever resources a person has, the red flags and the question of what evaluation is possible belong in the plan, and the clinicians I respect most in naturopathic gastroenterology refer out when they see those signs. A breath result can add to the picture. A person with warning signs still needs a clinician to look further.
Why do ACG and ESNM/ANMS disagree?
The 2020 American College of Gastroenterology guideline, with Pimentel as first author, conditionally suggests glucose or lactulose hydrogen breath testing for SIBO in people with IBS. The authors rate the evidence behind that suggestion as very low quality and say so. 6
Kashyap and colleagues, in a 2024 clinical practice update endorsed by the European Society of Neurogastroenterology and Motility and the American Neurogastroenterology and Motility Society, take a different position. They argue that the SIBO-IBS hypothesis remains unproven and that reliance on poorly validated breath tests has encouraged inappropriate antibiotic use. They call for rejecting the hypothesis and its reliance on breath testing. 7
The same update recognizes classical SIBO, including after surgical changes to the bowel or with scleroderma. Its critique targets the stretch from classical SIBO to IBS. Calling it a rejection of SIBO erases that distinction, and pinning the rejection on the ACG gets the ACG's position backwards. 6,7
Classical SIBO: recognized in appropriate anatomical and motility-related settings. 6,7
The broad SIBO-IBS hypothesis: challenged by ESNM/ANMS as unproven and inadequate to justify current reliance on breath testing. 7
Microbial disturbance in some people with IBS: remains a legitimate research question involving composition and function as well as abundance. 2,7
Whether a particular breath result explains a person's symptoms: depends on the instrument and clinical context. Evidence for a condition, evidence against one diagnostic reading, and a test that cannot tell possibilities apart are three different states of knowledge. 5,7,9
The ACG guideline discloses Pimentel's equity in Gemelli Biotech, and three authors of the nationwide study list Gemelli Biotech affiliations. Readers deserve that context. Whether a result holds up depends on its methods and the strength of its inference, and a disclosed conflict is a reason to read those closely. 1,6
What did the four 2026 papers add?
Each paper asks a different question. Pimentel and colleagues compare breath gases with reported symptoms. Shah, Holtmann and Gibson review the diagnostic framework. De Freitas Germano and colleagues look at gene expression in the intestinal lining. Kumar and Banerjee review how sulfide interacts with host metabolism. Read together, they reach different parts of the same biological problem. 1,2,3,4
Gas patterns and symptoms
The nationwide study links particular gases to particular symptoms in people who took the test. It did not change anyone's gas production or assign a treatment, so it cannot show that lowering a gas would ease a symptom. 1
Higher hydrogen correlated with more severe diarrhea, with P=0.031. Methane correlated with constipation, with P=0.002. Higher hydrogen sulfide correlated with diarrhea, with P<0.0001; urgency, with P=0.003; and abdominal pain, with P=0.01. 1
SIBO positivity was 27% with lactulose and 7.3% with glucose. These are observed positivity rates and say nothing on their own about either sugar's accuracy. 1
The paper reports p-values without correlation coefficients, effect sizes or confidence intervals, so a reader cannot tell how strong these relationships are. With 3,004 people, even a small association reaches significance. A p-value alone cannot tell a clinician how much a gas level means for one patient. 1
Bloating shows why that matters. You cannot read bloating severity off a single gas level, and the combined analysis still ties bloating to sulfide-related patterns. Quoting only the first finding undersells the study. Quoting only the second oversells what it can predict for one person. 1
The gases also track real organisms. In the REIMAGINE study, Villanueva-Millan and colleagues compared breath results with fluid sampled from the duodenum. Breath hydrogen sulfide rose with small intestinal sulfide producers, and breath methane rose with methanogens. Any skeptical account needs to keep that connection. 14
Several steps remain open. Organisms that track with a gas may or may not cause a person's symptoms, and a microbial association does not validate every diagnostic cutoff or point to the right treatment. The finding strengthens what the signal means biologically and leaves its clinical use to further testing. 1,14
A broader definition of small intestinal disturbance
Shah, Holtmann and Gibson place much of the controversy in the instruments. Culture captures part of the microbial community, and breath testing cannot pinpoint where gas forms. They propose small intestinal dysbiosis as a broader frame, with molecular and functional study of the microbes living along the intestinal lining. 2
The new frame adds questions about which organisms are present, where they live and what they do, and it keeps microbial abundance in the picture. Renaming the condition leaves the measurement problem in place. The proposal sets a research direction. 2
Shah's earlier prevalence meta-analysis shows why that direction matters. It found an association between IBS and SIBO, and its estimates moved with the diagnostic method. The test partly decided who counted as having SIBO. 12
Across 25 studies including 3,192 people with IBS and 3,320 controls, breath-test-defined SIBO prevalence was 35.5% in IBS and 29.7% in controls. Culture-defined prevalence was 13.9% and 5.0%, respectively. The authors named the tests' limited sensitivity and specificity as a constraint. 12
Those numbers support looking for microbial differences in IBS, and they warn against treating a positive breath test as a clean line between people with symptoms and healthy controls. The association and the measurement problem both hold. 12
Gandhi and colleagues' methane meta-analysis adds another layer. Methane positivity was not more common in IBS overall, and it was more common in constipation-predominant IBS than in diarrhea-predominant IBS. A signal can match one symptom pattern without separating the whole diagnosis from controls, which argues for more specific biological questions. 13
Gene expression in the intestinal lining
De Freitas Germano and colleagues, with Pimentel as senior author, studied small bowel biopsies alongside breath measurements and bacterial cultures. They compared host gene expression across intestinal sulfide overproduction, bacterial overgrowth and methanogen overgrowth, and added a rat experiment using sulfide-producing bacteria. 3
The sulfide group showed broad differences in genes linked to the electron transport chain and redox balance. These systems run cellular energy production and oxidation-reduction chemistry. The SIBO and methane groups showed fewer significant gene-expression differences. Rat findings also implicated mitochondrial respiration, water balance, immune responses, and gut motility. 3
Gene expression gives clues about what cells are gearing up to do. It does not measure how much energy a cell makes. The authors call the work exploratory and say it needs confirmation, and fewer significant findings in the other groups leave open whether those conditions affect the host. 3
The authors read their results as distinct biological states that may need individualized treatment. That fits with the February gas-symptom study, since the two measure different things. My reading is that measuring the host response adds an important layer to the microbial picture. 1,3
Sulfide production and the capacity to handle it
Kumar and Banerjee describe hydrogen sulfide as a molecule with normal signaling and metabolic jobs. The cells lining the colon oxidize it, and the review follows how that chemistry interacts with oxygen and with the microbes living beside the lining. 4
In their model, sulfide oxidation helps keep the colon low in oxygen, where obligate anaerobes thrive and hand back metabolites like butyrate. Trouble starts when sulfide production outpaces the host's capacity to handle it. The model puts the focus on the balance between exposure and processing. 4
I would treat the strongest version of the oxygen argument with caution. A key experimental link in the review rests on mouse work listed as submitted for publication when the review appeared, so I treat that part of the chain as provisional. Most of the underlying biology is colonic and experimental, and it does not transfer cleanly to a small bowel breath-test result in a person. 4
A positive sulfide breath test does not show that a person's sulfide handling has failed, and the model offers no matching host explanation for methane or hydrogen. Holding those boundaries makes the sulfide biology more useful. It gives researchers a mechanism to test, with the clinical inference still ahead of them. 3,4
Common ground without settling the argument
I see common ground in the move toward microbial function and host response. The critical review asks for a fuller picture of the small intestinal ecosystem, and the biopsy study looks at the cells living beside it. These approaches can inform each other while their authors keep disagreeing about diagnosis and treatment. 2,3
An ecological reading still has to earn its clinical conclusions. Microbes making a substance, breath levels tracking organisms and host genes shifting do not add up to a full causal chain in one person. Each link needs its own evidence. The broader frame helps by making the next questions sharper. 2,3,4,14
“Helping someone doesn't require getting the entire mechanism story right. But improvement alone can't tell us which part of the care helped.”
From the episode
Why can treatment help when diagnosis is uncertain?
Shah, Holtmann and Gibson acknowledge that antibiotics can improve symptoms and normalize breath results. They also say it remains uncertain whether those effects come from action on the small intestinal microbiota. Their critique leaves room for benefit and questions the explanation attached to it. 2
That matters for reading treatment studies. Symptom improvement, a changed breath result and proof of a mechanism are three different outcomes, and seeing the first tells you little about the other two. Uncertainty about the mechanism also leaves a person's improvement intact. 2
I think the useful research question is which measured changes explain meaningful benefit, for whom and under what conditions. The evidence supports continued study of how microbes contribute to symptoms, with tighter links between diagnostic labels, treatment decisions and the outcomes people live with. 2,6,7
Metabolites, host conditions, and the postbiotic hypothesis
Rivera-Chávez and colleagues offer an experimental example of microbial metabolites shaping the environment microbes live in. In mice, the antibiotic streptomycin depleted butyrate-producing Clostridia, butyrate fell, oxygen at the gut lining rose, and Salmonella bloomed. Tributyrin, a source of butyrate, restored the low-oxygen state and held Salmonella back. 15
The experiment traces a chain from microbial metabolism to host conditions to microbial expansion, and supplying a metabolite changed that chain. It was mouse, colonic biology. It says nothing about treating human small intestinal symptoms, and it did not test a commercial postbiotic. 15
I run Thaena, which makes ThaenaBiotic®, a dietary supplement made from screened human donor material. Our hypothesis is that supplying microbial signals could help when a depleted ecosystem stops producing them. I see that as a question worth testing, and ThaenaBiotic as one possible tool in the toolbox. It is meant to complement a whole-system approach to care, not replace medical care, and it is not a treatment for SIBO or any other condition.
Our observational cohort has no control group and no blinding. It can show that people changed and cannot show why. It has not tested the sulfide mechanism, and we have not run the controlled trial that would test our hypothesis. Finding weaknesses in an antimicrobial model does not prove a restorative approach works.
The honest limitations
The diagnostic studies inherit the weaknesses of their reference methods, and pooling leaves culture's sampling and contamination problems in place. Healthy-volunteer results belong to one population and one protocol. The nationwide gas study describes associations in people who took the test and says nothing about population prevalence, causation or treatment effect. 1,5,8,9,10
The mechanistic papers answer narrower questions than a treatment decision needs. Transcriptomics measures gene expression. The sulfide review leans on a provisional experimental link and on colonic biology. The tributyrin experiment was in mice. Small intestinal dysbiosis is a research framework that still needs useful measurements. 2,3,4,15
My synthesis interprets across those kinds of evidence. It supports asking more of the ecosystem and of the host response. It does not show that the research groups agree, and it does not validate any particular intervention. 1,2,3,4
Frequently asked questions
Is SIBO a recognized condition?
Classical SIBO is recognized, particularly with altered intestinal anatomy or substantial motility problems. The controversy concerns how broadly the diagnosis explains other gut symptoms and how confidently available tests identify it in an individual. 6,7
Does the ACG recommend breath testing?
The ACG guideline conditionally suggests breath testing for SIBO in people with IBS, based on very low quality evidence. The ESNM/ANMS critique comes from different societies and reaches a different conclusion about that use. 6,7
Can a positive breath test explain bloating?
A positive breath test cannot tell you on its own what causes your bloating. The nationwide gas study found no individual-gas correlation with bloating severity, although its combined analysis linked bloating to sulfide-related patterns. 1
Can a SIBO breath test rule out colon cancer?
No. A breath test measures fermentation gases and cannot detect or rule out colorectal cancer. Rectal bleeding, iron deficiency anemia, and abdominal pain or diarrhea that persists or is new warrant a clinician's evaluation at any age, and colorectal cancer is becoming more common in adults under 50. 16,18
What does small intestinal dysbiosis mean?
Small intestinal dysbiosis is a proposed framework for studying microbial composition, location, abundance, and function together. It widens what researchers study and leaves the limits of current diagnostic tools in place. 2
Can treatment help without proving the diagnosis?
Yes. Antibiotics can improve symptoms while the reason they help remains uncertain. Feeling better after treatment does not show that the proposed small intestinal mechanism caused the symptoms. 2
What the evidence supports
What is small intestinal dysbiosis? Small intestinal dysbiosis is a framework Shah, Holtmann and Gibson proposed in 2026. It asks which microbes live in the small intestine, where they live, how many there are and what they do. It widens the research question and does not yet come with a validated test. 2
How accurate are SIBO breath tests? Glucose and lactulose breath tests have documented limits, and so does the culture test researchers use to judge them. Accuracy shifts with the sugar used and the people tested. 5,8,9
Are SIBO breath tests still useful if they are imperfect? They can be. The 2020 ACG guideline conditionally suggests breath testing in people with IBS, and breath hydrogen sulfide and methane track sulfide-producing bacteria and methanogens sampled from the small intestine. The live question is how much a single result can explain about one person's symptoms. 6,14
Can a SIBO breath test rule out colon cancer? No. A breath test measures fermentation gases and cannot detect colorectal cancer, which is rising in US adults aged 20 to 49 and is now the leading cause of cancer death in adults younger than 50. Rectal bleeding, iron deficiency anemia, and abdominal pain or diarrhea that persists or is new warrant a clinician's evaluation at any age. 16,18
Do guidelines recommend SIBO breath testing? The ACG guideline conditionally suggests breath testing in people with IBS, with very low quality evidence. The later ESNM/ANMS update rejects the broader SIBO-IBS hypothesis and its reliance on breath testing, while recognizing classical SIBO. 6,7
Does a breath test explain bloating? In a nationwide study, individual gas levels did not correlate with bloating severity, although a combined analysis linked bloating to sulfide-related patterns. A gas reading on its own cannot tell you what caused a person's bloating. 1
Breath gases carry real information about microbes and symptoms, and researchers still disagree about what a result means for diagnosis. The recent work adds microbial function and host response to the picture, with hydrogen sulfide as a specific mechanistic lead. I see common ground in that direction, and a lot of unfinished work on measurement and treatment. 1,2,3,4,6,7,14
References
- Pimentel M, Leite G, Joo L, et al. Real-world study of three-gas breath testing nationwide and the association with symptoms. J Clin Gastroenterol. 2026;60(5):406-417. doi:10.1097/MCG.0000000000002326. · FREE FULL TEXT
- Shah A, Holtmann G, Gibson PR. Critical review: the past, present, and future of small intestinal bacterial overgrowth (SIBO). JGH Open. 2026;10(5):e70419. doi:10.1002/jgh3.70419. · FREE FULL TEXT
- de Freitas Germano J, Leite G, Villanueva-Millan MJ, et al. Transcriptomics profiles in intestinal sulfide overproduction, small intestinal bacterial overgrowth, and intestinal methanogen overgrowth. mSystems. 2026;11(7):e0045826. doi:10.1128/msystems.00458-26. · FREE FULL TEXT
- Kumar R, Banerjee R. Sulfide dynamics at the gut-microbiota interface: diet, oxygen and redox interplay. Gut Microbes. 2026;18(1):2681720. doi:10.1080/19490976.2026.2681720. · FREE FULL TEXT
- Khoshini R, Dai SC, Lezcano S, Pimentel M. A systematic review of diagnostic tests for small intestinal bacterial overgrowth. Dig Dis Sci. 2008;53(6):1443-1454. doi:10.1007/s10620-007-0065-1.
- Pimentel M, Saad RJ, Long MD, Rao SSC. ACG clinical guideline: small intestinal bacterial overgrowth. Am J Gastroenterol. 2020;115(2):165-178. doi:10.14309/ajg.0000000000000501.
- Kashyap P, Moayyedi P, Quigley EMM, Simren M, Vanner S. Critical appraisal of the SIBO hypothesis and breath testing (ESNM/ANMS clinical practice update). Neurogastroenterol Motil. 2024;36(6):e14817. doi:10.1111/nmo.14817. · FREE FULL TEXT
- Cangemi DJ, Lacy BE, Wise J. Diagnosing small intestinal bacterial overgrowth: a comparison of lactulose breath tests to small bowel aspirates. Dig Dis Sci. 2021;66(6):2042-2050. doi:10.1007/s10620-020-06484-z.
- Losurdo G, Leandro G, Ierardi E, et al. Breath tests for the non-invasive diagnosis of small intestinal bacterial overgrowth: a systematic review with meta-analysis. J Neurogastroenterol Motil. 2020;26(1):16-28. doi:10.5056/jnm19113. · FREE FULL TEXT
- Jiménez-Castillo RA, Félix-Téllez FA, Vargas-Basurto JL, et al. Diagnostic reliability of glucose and lactulose breath tests: insights from a test-retest study in healthy adults. Neurogastroenterol Motil. 2025;37(12):e70089. doi:10.1111/nmo.70089.
- Massey BT, Wald A. Small intestinal bacterial overgrowth syndrome: a guide for the appropriate use of breath testing. Dig Dis Sci. 2021;66(2):338-347. doi:10.1007/s10620-020-06623-6.
- Shah A, Talley NJ, Jones M, et al. Small intestinal bacterial overgrowth in irritable bowel syndrome: a systematic review and meta-analysis of case-control studies. Am J Gastroenterol. 2020;115(2):190-201. doi:10.14309/ajg.0000000000000504.
- Gandhi A, Shah A, Jones MP, et al. Methane positive small intestinal bacterial overgrowth in inflammatory bowel disease and irritable bowel syndrome: a systematic review and meta-analysis. Gut Microbes. 2021;13(1):1933313. doi:10.1080/19490976.2021.1933313. · FREE FULL TEXT
- Villanueva-Millan MJ, Leite G, Mathur R, et al. Hydrogen sulfide and methane on breath test correlate with human small intestinal hydrogen sulfide producers and methanogens. Dig Dis Sci. 2025;70(11):3846-3856. doi:10.1007/s10620-025-09156-y. · FREE FULL TEXT
- Rivera-Chávez F, Zhang LF, Faber F, et al. Depletion of butyrate-producing Clostridia from the gut microbiota drives an aerobic luminal expansion of Salmonella. Cell Host Microbe. 2016;19(4):443-454. doi:10.1016/j.chom.2016.03.004. · FREE FULL TEXT
- Siegel RL, Wagle NS, Star J, Kratzer TB, Smith RA, Jemal A. Colorectal cancer statistics, 2026. CA Cancer J Clin. 2026;76(2):e70067. doi:10.3322/caac.70067. · FREE FULL TEXT
- Siegel RL, Wagle NS, Cercek A, Smith RA, Jemal A. Colorectal cancer statistics, 2023. CA Cancer J Clin. 2023;73(3):233-254. doi:10.3322/caac.21772.
- Fritz CDL, Otegbeye EE, Zong X, et al. Red-flag signs and symptoms for earlier diagnosis of early-onset colorectal cancer. J Natl Cancer Inst. 2023;115(8):909-916. doi:10.1093/jnci/djad068. · FREE FULL TEXT
- US Preventive Services Task Force; Davidson KW, Barry MJ, Mangione CM, et al. Screening for colorectal cancer: US Preventive Services Task Force recommendation statement. JAMA. 2021;325(19):1965-1977. doi:10.1001/jama.2021.6238.
- Lacy BE, Pimentel M, Brenner DM, et al. ACG clinical guideline: management of irritable bowel syndrome. Am J Gastroenterol. 2021;116(1):17-44. doi:10.14309/ajg.0000000000001036.
This post accompanies the Lit Review Friday episode of Learn Something with Thaena.