Gastritis is inflammation of the stomach lining, and it has several distinct causes ranging from bacterial infection to medication use to autoimmune disease. Globally, over 38 million people were living with gastritis in 2021, with about 27 million new cases diagnosed that year alone. Understanding the specific cause matters because treatment depends entirely on what triggered the inflammation in the first place.
H. pylori: The Most Common Cause Worldwide
A spiral-shaped bacterium called Helicobacter pylori is responsible for the majority of chronic gastritis cases globally. This bacterium has a unique ability to survive in the highly acidic environment of the stomach, where it attaches specifically to gastric cells and begins disrupting the lining’s natural defenses.
Once attached, H. pylori depletes glutathione, a molecule your stomach cells rely on to protect themselves from damage and regulate immune responses. The bacterium also produces toxins that attract inflammatory cells to the stomach wall, creating a cycle of ongoing irritation. It disrupts the balance of acid production by stimulating cells that increase stomach acid while suppressing cells that would normally keep acid levels in check. Over time, this combination of weakened defenses and excess acid leads to chronic inflammation, and in some cases, the immune system begins producing antibodies that attack the stomach’s own acid-producing cells, worsening the damage further.
Most people with H. pylori pick it up in childhood, often through contaminated water or close household contact. Many carry it for years without symptoms. When it does cause gastritis, eradication with a combination of antibiotics and acid-suppressing medication typically resolves the inflammation.
Pain Relievers and Other Medications
Nonsteroidal anti-inflammatory drugs, commonly known as NSAIDs, are the second leading cause of gastritis. This group includes ibuprofen, aspirin, and naproxen. These medications work by blocking enzymes that produce prostaglandins, which are chemicals involved in pain and inflammation. The problem is that those same prostaglandins also maintain the protective mucus layer in your stomach. When that layer thins, stomach acid comes into direct contact with the lining, causing irritation and erosion.
The risk increases significantly with long-term or frequent use, higher doses, and taking NSAIDs on an empty stomach. Even with protective medications taken alongside them, up to three-quarters of long-term NSAID users still develop some degree of damage to their digestive tract. Occasional use for a headache is unlikely to cause lasting harm, but daily use over weeks or months is a well-established path to gastritis and even ulcers.
Alcohol and Direct Chemical Irritation
Alcohol at high concentrations acts as a direct chemical irritant to the stomach lining. Rather than working through an indirect mechanism like NSAIDs, concentrated ethanol erodes the tissue on contact. Animal studies show that high-concentration alcohol causes blood vessel blockage in the stomach wall, disrupted blood flow, cell death, and visible bleeding in the lining. The glandular structure of the tissue breaks down, with surface cells dying and sloughing off.
This type of gastritis is most common after binge drinking or heavy sustained alcohol use. It can develop acutely, meaning symptoms appear within hours of heavy consumption, and it can range from mild irritation to visible hemorrhaging. Chronic heavy drinking leads to repeated injury that prevents the lining from fully healing between episodes.
Autoimmune Gastritis
In autoimmune gastritis, the immune system mistakenly targets the stomach’s acid-producing parietal cells. This is an inherited condition, meaning it runs in families. The antibodies produced attack not only the parietal cells themselves but also intrinsic factor, a protein those cells produce that your body needs to absorb vitamin B12 from food.
The result is a slow, progressive loss of stomach acid production and a growing inability to absorb B12. Over years, this leads to a condition called pernicious anemia, marked by fatigue, neurological symptoms like tingling in the hands and feet, and cognitive difficulties. Autoimmune gastritis also increases the risk of certain types of stomach growths over the long term. Diagnosis involves blood tests for antibodies against parietal cells and intrinsic factor, combined with biopsies showing characteristic patterns of tissue change in the upper part of the stomach.
Bile Reflux
Bile, a digestive fluid made by the liver, normally flows downward from the gallbladder into the small intestine. Sometimes it flows backward into the stomach instead, where its alkaline chemistry irritates the acid-adapted stomach lining. This backward flow is called bile reflux, and it causes a specific pattern of inflammation known as bile reflux gastritis.
The most common trigger is previous surgery. Gastric bypass, partial stomach removal, and other stomach procedures can alter the anatomy enough that the valve between the stomach and small intestine no longer closes properly. Gallbladder removal also significantly increases bile reflux compared to people who still have their gallbladder. Unlike acid reflux, bile reflux doesn’t respond to standard acid-reducing medications, since the irritant is bile rather than acid.
Stress-Related Gastritis in Critical Illness
Physiological stress from severe illness, major surgery, burns, or organ failure can trigger a specific form called stress-related mucosal disease. This is not the same as everyday psychological stress. It occurs in critically ill patients and results from reduced blood flow to the stomach lining. When the body diverts blood to vital organs during a health crisis, the stomach’s mucosal defenses weaken. Acid that would normally be neutralized by the protective barrier then damages the exposed tissue.
The severity of this damage tracks closely with the pH inside the stomach wall. Lower pH (more acidic conditions) correlates directly with a higher probability of significant bleeding. This type of gastritis is managed in hospital settings and resolves as the underlying critical illness improves.
Infections Beyond H. pylori
In people with weakened immune systems, other organisms can infect the stomach lining. Cytomegalovirus (CMV) is one of the more common viral causes, particularly in organ transplant recipients and people with cancer. The stomach is the most frequent site of CMV infection in these groups. Adenovirus can also involve the stomach, though it more commonly causes intestinal symptoms.
Fungal gastritis is rarer but occurs in severely immunocompromised individuals. Candida is the most frequent fungal culprit, typically colonizing pre-existing ulcers or damaged tissue rather than infecting healthy stomach lining. People undergoing chemotherapy for blood cancers face additional risk from aspergillus and mucormycosis infections, while those with HIV are more susceptible to histoplasmosis and cryptococcosis in the digestive tract.
What About Spicy Food?
Spicy food is widely blamed for causing gastritis, but the clinical picture is more nuanced. Capsaicin, the active compound in chili peppers, actually has a dose-dependent relationship with stomach health. At normal dietary amounts, capsaicin is generally protective. Research has shown that low doses of capsaicin can prevent stomach mucosal injury caused by alcohol and aspirin. At very high doses, however, capsaicin worsens damage from those same irritants.
In practical terms, spicy food does not cause gastritis in a healthy stomach. But if you already have inflammation from another cause, such as H. pylori or NSAID use, spicy food can aggravate your symptoms and potentially worsen existing damage. The distinction between causing and worsening gastritis is important for knowing what to address first.
Who Gets Gastritis Most Often
Gastritis is not evenly distributed around the world. East Asia has the highest prevalence, with roughly 722 cases per 100,000 people, followed closely by Andean Latin America at 705 per 100,000 and southern Sub-Saharan Africa at 604 per 100,000. Lower-income regions carry a disproportionately heavy burden, with death rates from gastritis more than three times higher in low-income areas compared to high-income regions. The global number of people living with gastritis is projected to reach approximately 51 million by 2050.
These regional differences reflect varying rates of H. pylori infection (which is more common where sanitation infrastructure is limited), differences in NSAID use patterns, alcohol consumption habits, and access to treatment. Age also plays a role: the stomach lining naturally thins with age, making older adults more vulnerable to all forms of gastritis.