The small intestinal bacterial overgrowth. Irritable bowel syndrome hypothesis: implications for treatment
Bibliographic record
Abstract
Traditionally, small intestinal bacterial overgrowth (SIBO) has been characterised by symptoms of diarrhoea, bloating and sometimes signs of malabsorption. It has been defined as >105 colony-forming units (cfu)/ml of bacteria in aspirates obtained from the small intestine.1 This condition has typically been diagnosed in patients with readily identifiable alterations in small bowel function which predispose patients to SIBO (eg, resected ileocaecal valve, small intestinal hypomotility and possibly hypochlorhydria). Recently, however, this clinical paradigm has been challenged by new theories about the aetiology of irritable bowel syndrome (IBS) and has led to renewed scrutiny of the tests employed to diagnose this condition and controversy concerning the use of antibiotics to treat IBS for suspected SIBO. The proposal that SIBO accounts for the symptoms of IBS2 3 is a novel and interesting hypothesis, given the rapidly growing evidence that luminal bacteria have previously unrecognised actions on multiple intestinal functions.4 While it has long been recognised that increased numbers of luminal bacteria in the small intestine disrupt digestion and absorption, it is now clear that they have other important actions, such as immune activation4 5 Immune-mediated cytokines could have multiple actions including altered epithelial secretion, exaggerated nociceptive signalling and abnormal motility.4 Together, these changes could lead to symptoms which meet the criteria for IBS. It has also been proposed that this mechanism could account for overlap syndromes, such as fibromyalgia.6 The publication of Pimentel and colleagues in 20007 played a pivotal role in establishing the concept that SIBO is a major pathogenic mechanism underlying IBS. Two major tenets emerged from this study: (1) based on the results of the lactulose hydrogen breath test (LHBT), the large majority of patients with IBS have SIBO, and (2) when SIBO is eradicated with antibiotics based on the findings …
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.002 | 0.007 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.001 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.001 | 0.002 |
| Scholarly communication | 0.002 | 0.004 |
| Open science | 0.001 | 0.002 |
| Research integrity | 0.006 | 0.006 |
| Insufficient payload (model declined to judge) | 0.014 | 0.003 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".