Stomach ulcers are caused by stress and spicy food.

In 1982, a young pathologist named Robin Warren had already spent several years trying to persuade his colleagues at Royal Perth Hospital in Western Australia that he was seeing something real: curved bacteria colonizing the inflamed stomach lining of patients with gastritis and peptic ulcers. His colleagues were not persuaded. The idea was medically incoherent. Everyone knew that the stomach's highly acidic environment, pH as low as 1 or 2, made it effectively sterile. Nothing could live there.

The prevailing theory of peptic ulcers had been built on thirty years of sound reasoning. Under conditions of sustained psychological stress, the body releases cortisol and other stress hormones, which stimulate excess production of gastric acid. Excess acid erodes the protective mucous lining of the stomach and duodenum, producing painful lesions. The connection seemed obvious and clinical: patients in stressful jobs, high-pressure relationships, or traumatic circumstances showed up with ulcers. The treatments followed accordingly, bland diets, antacids, rest, psychotherapy, and in severe cases, surgery to sever the vagus nerve and reduce acid output. The notion that emotional strain was the engine of ulcer disease had been reinforced by a generation of gastroenterologists and taught in medical schools across the world.

Warren began working with a clinical fellow named Barry Marshall in 1981. Marshall set out to culture the bacteria from patient biopsies. For months the cultures failed, standard incubation periods of 24 to 48 hours were too short. Then, over an Easter holiday in 1982, a set of petri dishes was accidentally left in the incubator for five days. When the technicians returned, they found colonies growing. The organism was eventually identified as a previously unknown bacterium, later named Helicobacter pylori.

When Marshall and Warren published their findings in The Lancet in 1984, the response was largely dismissive. Gastroenterologists who had built careers on the acid-stress model had strong reasons to be skeptical, and the evidence required overturning assumptions so deeply embedded that questioning them felt eccentric. Senior clinicians suggested the bacteria were post-mortem contaminants or incidental findings in already-damaged tissue. The idea that a bacterium caused ulcers was described in some circles as charming but implausible.

Marshall decided to settle the question by the most direct means available. In July 1984, he drank a solution of H. pylori cultured from a patient's stomach. Within ten days he had developed acute gastritis, stomach inflammation, nausea, vomiting, and endoscopy confirmed bacterial colonization. He treated himself with antibiotics and bismuth, and the infection cleared. He had fulfilled Koch's postulates by infecting himself. The experiment was later published, but it did not immediately transform clinical practice.

What changed practice was the clinical evidence that began accumulating through the late 1980s. Antibiotic regimens that eradicated H. pylori were achieving something that decades of acid-suppression therapy had never managed: permanent cure. Ulcers treated with antacids alone relapsed in 80 percent of cases within a year. Ulcers treated with antibiotics relapsed in fewer than 5 percent. The numbers were stark enough to force reconsideration even among the most committed skeptics.

The National Institutes of Health issued a consensus statement in 1994 recommending antibiotics for all H. pylori-positive ulcer patients. Clinical practice did not change overnight. Antacids remained the default prescription through the 1990s in many hospitals and general practices, partly because the acid-suppression model was so thoroughly embedded in clinical training, and partly because the pharmaceutical industry had considerable financial interest in maintaining it.

Marshall and Warren received the Nobel Prize in Physiology or Medicine in 2005. The Nobel Committee noted that their discovery had fundamentally altered the management of peptic ulcer disease, a disease that had cost some patients their stomachs. Stress did not disappear from the picture entirely; psychological strain can exacerbate symptoms and may promote conditions that favor bacterial colonization. But it was not the cause. The stomach, it turned out, was not sterile. And the organism that lived there could be killed.