Why do ulcers happen

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Last updated: April 8, 2026

Quick Answer: Ulcers occur when the protective lining of the stomach or duodenum is eroded by stomach acid and digestive enzymes, often due to Helicobacter pylori infection or NSAID use. Approximately 10% of people worldwide develop peptic ulcers during their lifetime, with H. pylori causing about 80% of gastric ulcers and 90% of duodenal ulcers. The discovery of H. pylori's role in ulcers by Barry Marshall and Robin Warren in 1982 revolutionized treatment, shifting from acid suppression to antibiotic therapy. Ulcers can lead to serious complications like bleeding, perforation, or obstruction if left untreated.

Key Facts

Approximately 10% of people worldwide develop peptic ulcers during their lifetime
Helicobacter pylori causes about 80% of gastric ulcers and 90% of duodenal ulcers
Discovery of H. pylori's role in ulcers by Barry Marshall and Robin Warren in 1982
NSAID use accounts for about 20-25% of peptic ulcer cases
Peptic ulcers affect about 4 million Americans annually

Overview

Peptic ulcers are open sores that develop on the inner lining of the stomach (gastric ulcers) or the upper portion of the small intestine (duodenal ulcers). Historically, ulcers were believed to be caused primarily by stress and spicy foods, leading to treatments focused on diet modification and acid suppression. This understanding changed dramatically in 1982 when Australian researchers Barry Marshall and Robin Warren discovered Helicobacter pylori bacteria in ulcer patients, demonstrating that most ulcers had an infectious cause. Their groundbreaking work earned them the 2005 Nobel Prize in Physiology or Medicine. Before this discovery, ulcer treatment typically involved long-term acid-reducing medications and sometimes surgery, with high recurrence rates. Today, peptic ulcers remain a significant global health concern, affecting millions worldwide and representing a major cause of gastrointestinal bleeding and hospitalization.

How It Works

Ulcers develop when the protective mechanisms of the gastrointestinal lining are compromised, allowing stomach acid and digestive enzymes to damage the underlying tissue. The stomach normally produces hydrochloric acid and pepsin to digest food, but it's protected by a mucus-bicarbonate barrier. Two primary factors disrupt this balance: Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs). H. pylori bacteria colonize the stomach lining, producing enzymes and toxins that weaken the protective mucus layer and cause inflammation. This allows acid to reach the epithelial cells, leading to erosion and ulcer formation. NSAIDs like ibuprofen and aspirin inhibit prostaglandin production, which are crucial for maintaining mucosal blood flow and mucus secretion. Other contributing factors include smoking, excessive alcohol consumption, severe physiological stress (such as from critical illness), and rarely, conditions like Zollinger-Ellison syndrome that cause excessive acid production.

Why It Matters

Understanding ulcer causes has transformed medical practice, shifting treatment from symptom management to curative antibiotic therapy for H. pylori infections. This has significantly reduced ulcer recurrence rates from over 80% to under 10% with proper treatment. Ulcers remain clinically important because they can lead to serious complications: bleeding occurs in about 15-20% of cases, perforation in 2-5%, and gastric outlet obstruction in 1-2%. These complications require emergency medical intervention and can be life-threatening. Proper diagnosis and treatment prevent long-term disability and reduce healthcare costs associated with hospitalizations and surgeries. Additionally, recognizing NSAID-related ulcers has led to safer prescribing practices and the development of protective medications for high-risk patients.