A gluten-free diet can provide relief for a variety of gastrointestinal (GI) conditions. However, for patients with small intestinal bacterial overgrowth (SIBO) or irritable bowel syndrome (IBS), determining whether a gluten-free diet is appropriate can be particularly tricky.
Screening for SIBO
SIBO is defined as excessive amounts of pathogenic bacteria in the small bowel. It is characterized by bloating and distension from gas produced by these bacteria. Other symptoms include abdominal discomfort, constipation, diarrhea, floating stools, feelings of incomplete may evacuation, fecal urgency, flatulence, burping, trapped gas, heartburn, and indigestion, though symptoms will be patient-specific [1]. Constipation is more common with methane (CH4) predominant SIBO and there is high overlap between the symptoms of SIBO and gluten-related disorders.
Common medical conditions like diabetes and chronic inflammatory diseases can increase risk for SIBO. GI conditions including inflammatory bowel disease (IBD), chronic constipation, celiac disease, non-celiac gluten-sensitivity, wheat allergy, IBS and chronic use of acid blocking medication or antibiotics can also predispose a patient for development of SIBO. Research has found a high incidence of SIBO in celiac patients who experience ongoing symptoms when following a gluten-free diet [2].
The gold standard for diagnosing and assessing active SIBO is a small bowel aspirate culture, but this procedure is invasive, expensive, and has a high risk for contamination. Instead, a breath hydrogen test is often used. Patients consume a drink of glucose (more common) or lactulose (considered less reliable) and breath samples are collected every 15 minutes for 90 minutes. A rise of >20ppm in hydrogen (H2) or >10ppm in methane above baseline is considered positive for a diagnosis of active SIBO. Hydrogen Sulfide (H2S) and methane compete for hydrogen, so a test for hydrogen sulfide can also help assess for sulfide-producing bacteria, which are associated with diarrhea, fecal urgency and abdominal pain, though this test is less common [1].
The Connection between IBS and SIBO
IBS is a common heterogeneous condition with a highly complex pathogenesis. Patients often experience bloating, cramping, abdominal pain, diarrhea and/or constipation. IBS has a waxing and waning course and no biomarkers exist, so diagnosis of IBS is based on patient symptoms and history. Risk factors for IBS include female sex, psychological factors, such as stress and anxiety, and inflammation or infection. Bacterial gastroenteritis (i.e. food poisoning) can lead to the development of post-infectious IBS (PI-IBS), which can increase risk for SIBO since it disrupts the gut-brain axis and impairs intestinal motility.
Some experts believe that SIBO and IBS could be disorders on the same spectrum, and research suggests that many cases of IBS may be SIBO-related. Up to 50% of people with IBS are estimated to also have SIBO, meaning treatment of SIBO can help resolve IBS symptoms in these patients [3].
Treatment
Treatment for SIBO should address the underlying cause. For example, patients with SIBO due to celiac disease or another gluten-related disorder must follow a strict gluten-free diet. Once the underlying cause of SIBO is addressed, doctors may prescribe antibiotics to eradicate the bacterial overgrowth. Some evidence also points to the effectiveness of probiotic supplementation in symptomatic patients [1]. Other complementary interventions focus on the prevention of bacteria build-up in the intestinal tract. These include the use of motility agents, digestive enzymes, alternative therapy (acupuncture, hypnotherapy, relaxation, and stress techniques), and herbal supplementation.
Dietary interventions for SIBO focus on the reduction of fermentable products that the bacteria would otherwise consume. This usually means avoiding alcohol sugars and other fermentable sweeteners like sucralose. A reduction in processed foods, fiber, and prebiotics (such as inulin) may also be helpful. Still, data on the effectiveness of two common SIBO diets, the low-FODMAP or the gluten-free diet, is limited. A recent meta-analysis noted that there was no good evidence to support gluten-free approaches and “very low quality evidence” for low-FODMAP diets [4].
Still, a low-FODMAP diet may be helpful for patients with IBS and SIBO despite the mixed evidence on its effectiveness for SIBO specifically. ACG clinical guidelines still suggest trialing a low-FODMAP approach for SIBO. A reduction of FODMAPs reduces the amount of carbohydrates available for fermentation by the bacteria in the colon. Some studies have shown that reduced FODMAP intake has been associated with fewer fermentation products and lower hydrogen output [5]. In addition, lower FODMAP intake may reduce the osmotic effect of fermentable carbohydrates, since they increase water delivery to the colon and can alter bowel habits [6].
Research suggests that some patients with IBS (where celiac disease has been excluded) may also find symptom relief when eliminating gluten. A gluten-free diet is often low in FODMAPs, specifically fructans found in wheat, barley and rye [7]. Given what is known about the overlap between SIBO and IBS, this subset of IBS patients who experience a benefit may be those with underlying SIBO. However, the mechanism behind their symptom improvement may be the reduction in FODMAPs. As always, when recommending a gluten-free diet for IBS or SIBO, it is vital to exclude celiac disease prior to the removal of wheat and/or gluten from the diet.
Other less common diets that may be recommended included paleo, the specific carbohydrate diet (SCD), the gut and psychology syndrome (GAPS), candida, and other elemental diets.
A Patient-Centric Approach
From a low-FODMAP diet to the simple reduction of sugar alcohols, the approaches that can be beneficial for IBS and SIBO are diverse and patient-specific. While a gluten-free diet may help many patients, its restrictive nature means only patients who truly benefit should remain on a gluten-free diet long-term.
For patients with SIBO or IBS due to non-gluten-related conditions, other dietary and medical interventions may be equally or more effective. Remember, replacing gluten-containing foods with gluten-free replacements can exacerbate symptoms, as patients may turn to high-FODMAP or highly refined foods to replace their gluten-containing counterparts. In all cases, long-term dietary recommendations for SIBO and IBS include a focus on plant-based whole foods, limited intake of processed foods and sugar, stress reduction, exercise, and good sleep habits.
References
- 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
- Chang MS, Green PH. A review of rifaximin and bacterial overgrowth in poorly responsive celiac disease. Therap Adv Gastroenterol. 2012;5(1):31-36. doi:10.1177/1756283X11422264
- Ghoshal UC, Nehra A, Mathur A, Rai S. A meta-analysis on small intestinal bacterial overgrowth in patients with different subtypes of irritable bowel syndrome. J Gastroenterol Hepatol. 2020;35(6):922-931. doi:10.1111/jgh.14938
- Dionne J, Ford AC, Yuan Y, et al. A systematic review and meta-analysis evaluating the efficacy of a gluten-free diet and a low FODMAPs diet in treating symptoms of irritable bowel syndrome. Am J Gastroenterol 2018;113:1290–300.
- McIntosh K, Reed DE, Schneider T, et al. FODMAPs alter symptoms and the metabolome of patients with IBS: A randomised controlled trial. Gut 2017;66:1241–51.
- Ong DK MS, Barrett JS, Shepherd SJ, Irving PM, Biesiekierski JR, Smith S, Gibson PR, Muir JG,. Manipulation of dietary short chain carbohydrates alters the pattern of gas production and genesis of symptoms in irritable bowel syndrome. Journal of gastroenterology and hepatology. 2010;25(8):1366-73
- Biesiekierski JR, Peters SL, Newnham ED. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology 2013. 145(2):320-8.