Whether Small Intestinal Bacterial Overgrowth (SIBO) can cause or contribute to Gastritis is a common question, reflecting the complex nature of the digestive system. While these two conditions affect different parts of the gastrointestinal tract, a growing body of evidence suggests a significant physiological overlap. This overlap links the bacterial imbalance of SIBO to inflammation in the stomach lining, often revolving around shared risk factors and the systemic immune response triggered by bacterial overgrowth.
Understanding SIBO and Gastritis Separately
Small Intestinal Bacterial Overgrowth (SIBO) is characterized by an excessive number of bacteria in the small intestine, which should normally maintain a low bacterial count. This overgrowth leads to the fermentation of undigested carbohydrates, resulting in symptoms like bloating, gas, abdominal pain, and sometimes diarrhea or constipation. SIBO is fundamentally a disorder of the small bowel, the long tube responsible for most nutrient absorption.
Gastritis is defined as the inflammation of the stomach lining, known as the gastric mucosa. The stomach is located far upstream from the small intestine, and its inflammation typically results in upper abdominal pain, nausea, vomiting, or a burning sensation. Common independent causes of Gastritis include infection with the bacterium Helicobacter pylori, regular use of nonsteroidal anti-inflammatory drugs (NSAIDs), or excessive alcohol consumption. Although this stomach-focused inflammation is distinct from small intestine overgrowth, the two conditions can share common predisposing factors.
The Physiological Link Between SIBO and Gastritis
The primary mechanism linking SIBO to Gastritis involves the retrograde flow of bacterial byproducts and the initiation of a systemic inflammatory response. When excessive bacteria colonize the small intestine, they feast on nutrients and produce large amounts of metabolic waste. These waste products and gases can travel proximally up the digestive tract toward the stomach.
One of the most potent of these byproducts is Lipopolysaccharide (LPS), an endotoxin released from the cell walls of Gram-negative bacteria that are often overgrown in SIBO. LPS is known to increase the permeability of the intestinal barrier, allowing it to leak into the bloodstream, a state sometimes referred to as endotoxemia. This leakage triggers a systemic immune reaction, prompting the release of pro-inflammatory signaling molecules called cytokines throughout the body.
This chronic, low-grade systemic inflammation can compromise the integrity of the protective mucus layer in the stomach. The gastric mucosa, already vulnerable to factors like stomach acid, becomes more susceptible to injury when the body’s inflammatory markers are elevated. Therefore, SIBO does not cause Gastritis directly through infection but rather creates a hostile internal environment that promotes or worsens the inflammation of the gastric lining.
Furthermore, a shared root cause can often explain the co-occurrence of both conditions. A reduction in stomach acid, known as hypochlorhydria, is a risk factor for both SIBO and Gastritis. Low stomach acid fails to kill incoming bacteria, allowing them to colonize the small intestine, which causes SIBO. Separately, low stomach acid is also a feature of certain types of chronic Gastritis, such as autoimmune atrophic Gastritis, creating an environment where both digestive issues can develop simultaneously.
Clinical Assessment and Differentiation
Diagnosing SIBO and Gastritis often requires specialized tests, particularly when a causal link is suspected. Gastritis is definitively diagnosed through an upper endoscopy, where a gastroenterologist visually inspects the stomach lining. During this procedure, a biopsy is typically taken to check for inflammation and to test for the presence of the H. pylori bacterium, a major, independent cause of Gastritis.
SIBO is most commonly identified using a non-invasive breath test, usually with a substrate like lactulose or glucose. After consuming the sugar solution, the test measures the hydrogen and methane gases produced by the bacteria in the small intestine. A significant, early rise in these gas levels confirms the bacterial overgrowth.
When a patient presents with both conditions, clinicians must differentiate whether the Gastritis is a primary condition (e.g., from NSAID use) or a secondary consequence of SIBO-driven inflammation. It is important to confirm SIBO and rule out other independent Gastritis causes before attributing the stomach inflammation to bacterial overgrowth. This careful distinction directs the therapeutic plan toward the most appropriate target.
Targeted Therapeutic Strategies
Treating both SIBO and Gastritis requires a strategic approach, as therapies for one condition can inadvertently worsen the other. For instance, standard Gastritis treatment involves proton pump inhibitors (PPIs) to reduce stomach acid, helping the inflamed mucosa heal. However, decreasing stomach acid eliminates a natural defense against bacteria, which can exacerbate or trigger SIBO recurrence.
When SIBO is suspected as the driving factor, the treatment hierarchy prioritizes eradicating the bacterial overgrowth first. This is typically achieved using targeted antibiotics, such as Rifaximin, or an elemental diet designed to “starve” the overgrown bacteria. Reducing the bacterial load decreases the production of inflammatory metabolites and endotoxins like LPS, which lessens the systemic inflammation affecting the stomach.
Once SIBO is controlled and the source of chronic inflammation is removed, Gastritis symptoms often improve naturally. If stomach inflammation persists, treatment can focus on healing the gastric mucosa using protective agents or addressing any remaining local causes. This methodical approach ensures the underlying cause is addressed first, minimizing the risk of symptom recurrence.