Updated: Aug 22
IBS is a common condition characterised by abdominal pain or discomfort, bloating and altered stool form (such as diarrhoea or constipation) and passage. Worldwide, the prevalence of IBS varies from 4% to 30%. In Australia, up to 1 in 5 people suffer from IBS.
What is SIBO?
In brief, SIBO is a condition in which there is an overgrowth of bacteria in your small intestine.
Clinically, it is defined as having an excess of 105 bacterial colony forming units (CFU) per millilitre on culture, after an upper small intestinal aspirate.
Frequency of SIBO varies from 4% to 78% among patients with IBS.
SIBO seems to be more pronounced in those with gastro anatomical abnormalities such as ileo-tranverse anastomosis, stricture, fistula, slow motility and reduced gut defence.
Classic SIBO symptoms
abdominal pain or discomfort
Due to symptom cross-over, it is possible that many people are misdiagnosed with IBS, when SIBO is the actual cause. It is also more common in patients with diarrhoea-predominant IBS. Hence, those with IBS-D should be evaluated for SIBO. It is also important to note that those with SIBO also commonly have dysbiosis.
Testing for SIBO
ASPIRATE: Upper gastrointestinal tract (Jejunal) aspirate – With a result of bacteria in excess of 105 CFUs per mm on culture. This is the gold standard test, however invasive, expensive and rarely conducted.
BREATH TEST: Lactulose and glucose hydrogen breath tests – With an elevated hydrogen response. This is the most commonly used test as it is non-invasive.
Normally, dietary carbohydrates, unabsorbed in the small intestine, produce hydrogen in the large intestine by bacterial fermentation.
In patients with SIBO, the excess bacteria in the small intestine ferment the consumed dietary carbohydrates, and in turn produce hydrogen. This then gets absorbed and is exhaled in the breath.
Glucose Hydrogen breath test - involves giving patients a load of carbohydrate (glucose) and measuring expired hydrogen concentrations over a period of time.
Normally glucose is absorbed, however in patients with SIBO, bacteria will ferment the glucose, produce hydrogen which then will be exhaled via the breath.
Limitation – those with rapid intestinal transit may produce a false positive.
Sensitivity of this test is around 44%.
Lactulose Hydrogen breath test - involves giving patients a load of carbohydrate (lactulose) and measuring expired hydrogen concentrations over a period of time.
Lactulose is a non-absorbable disaccharide which will produce an early peak (raise in expired Hydrogen) due to fermentation in the small intestine (typically within 90mins) or a double peak (first due to small intestine fermentation and second from the large intestine), if SIBO is present.
Bloating is a very common symptom of IBS. The pathogenesis of bloating is often caused by an increased amount of gas in the gut, its abnormal distribution and increased visceral perception in response to distension of the gut (known as visceral hypersensitivity). Excess gas and bloating is also a common characteristic of SIBO. Studies have shown that when IBS patients have been treated with probiotics and antibiotics, their abdominal bloating has been relieved via a reduction in gas production.
Mechanism behind IBS symptoms
Excessive numbers of bacteria in the small intestine (SIBO):
Disrupts digestion and absorption
May alter immune activation - Immune mediated cytokines could have multiple actions including:
- altered epithelial secretion
- exaggerated nociceptive signalling
- abnormal motility
= Together these changes may lead to IBS like symptoms
In patients with SIBO, bacteria ferment ingested carbohydrates in the small intestine causing increased gas production. Accumulation of this gas in the intestine results in:
abdominal pain or discomfort
diarrhoea or constipation (*methanogens)
Intestinal wall damage & diarrhoea
Bacteria in the intestine may produce toxic by-products after fermentation, which may damage the inner lining of the small intestine and colon. For example, thinning of the mucosa and crypts and increased intra-epithelial lymphocytes. This may cause osmotic load in the intestine resulting in diarrhoea.
Bacteria also de-conjugates bile salts present in the intestine. These de-conjugated bile salts can stimulate colonic water secretion causing diarrhoea. They can also cause mucosal inflammation and release pro-inflammatory cytokines. SIBO is known to be associated with increased IL-8 levels (pro-inflammatory cytokine).
Methanogens & constipation
Fifteen percent (15%) of people may have methanogenic flora in the gut. Between 8.5% to 26% of IBS patients exhale methane in their breath. Excessive methane production is associated with constipation. Hence methane estimation in SIBO breath tests is particularly important in patients with constipation-predominant IBS. Therefore, ensure the breath testing apparatus that is used also evaluated expired methane (not just hydrogen).
Step 1: Test don't guess - it is super important to work with a practitioner who conducts credible and reliable SIBO testing before jumping into SIBO diagnosis and treatment.
Step 2: Dietary management - A low FODMAP diet. Discuss this with your dietitian.
Dietary manipulation can be beneficial for relieving symptoms of SIBO including bloating, abdominal pain, flatulence, and altered bowel habits. In patients with SIBO, gut bacteria ferment carbohydrates, such as fructose, oligosaccharides, disaccharides (lactose), polyols, and monosaccharides (fructose), resulting in gas formation and the above symptoms. The low FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) diet is very likely the best-known diet for SIBO.
Step 3: Consider the benefits verse the risks before treating with antibiotics. Antibiotics do not discriminate between good and bad gut microbes. Up to 1/3 of your good gut microbes can be wiped out each time you take a course of antibiotics. Discuss treatment options with your practitioner. These can include.
Step 4. Re-test for SIBO and work towards a diverse, fibre and prebiotic rich, plant-based diet.
World J Gastroenterol 2014 March 14; 20(10): 2482-2491