For most of the twentieth century, stomach ulcers were attributed to stress and stomach acid, and treated with antacids and dietary restriction rather than cured. Australian pathologist Robin Warren began finding spiral-shaped bacteria in stomach biopsy samples in 1981, and working with physician Barry Marshall from that year, the pair showed by 1982 that the organism, a bacterium later named Helicobacter pylori, was present in 77 percent of their ulcer patients and 55 percent of their gastritis patients. Gastroenterologists rejected the finding: a 1983 conference organizer ranked their paper submission one of the worst of the year, and Marshall later recalled being told the research was a bit shameful to present. Unable to produce the disease in an animal model, Marshall drank a culture of the bacterium himself in 1984 and developed confirmed gastritis within ten days, publishing the result in the Medical Journal of Australia. Acceptance came slowly: a 1994 National Institutes of Health conference formally endorsed antibacterial treatment for ulcer disease, and Marshall and Warren shared the 2005 Nobel Prize in Physiology or Medicine for the discovery.
Facts
Discovery Year DiscovererBarry Marshall and Robin Warren, Royal Perth Hospital, Australia. 1 Learn More
The Doctor Who Drank the Bacteria
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By 1984, Barry Marshall had a hypothesis that almost nobody in medicine believed: that a spiral-shaped bacterium he and pathologist Robin Warren had been finding in stomach biopsies was not a harmless passenger but the actual cause of peptic ulcer disease, a condition every textbook attributed to stress and stomach acid. Marshall could not prove it in an animal model, so he decided to prove it in the only model he had certain access to: himself.
He drank a culture of the bacterium, later named Helicobacter pylori, in July 1984, having been free of the bacterium before he drank it. Within days his wife and mother noticed his breath had turned foul, and he developed bloating and daily vomiting. Ten days after he drank the culture, a second endoscopy confirmed what he had gambled on: the bacterium had colonized his stomach lining, with the tissue damage of a genuine infection to show for it. It was not a controlled trial and it would not have survived an ethics committee's review by today's standards, but it was the kind of stark, self-directed evidence that a skeptical field could not simply wave away.
A Bit Shameful to Produce Research Like This
This article records tradition as it has been passed down and reported. Its sources are not yet part of the atlas's verified catalogue.
Robin Warren's own account of the moment his and Barry Marshall's work reached the wider medical community is not a story of quick acceptance. In 1983, when the pair submitted their findings to a major gastroenterology conference, the organizers rejected the paper and, according to Marshall's later recollection, told him the committee would be quite happy if he did not attend, because it was a bit shameful to produce research like that. Gastroenterologists had a reasonable-sounding objection: the bacterium turned out to be common in the general population, present in over 80 percent of some surveyed groups, and by some estimates only around 10 percent of carriers ever go on to develop an ulcer.
It took a decade for the field to change its mind through its own machinery rather than through one dramatic self-experiment. In 1994, a National Institutes of Health consensus conference formally endorsed antibacterial treatment for ulcer disease, effectively ending the stress-and-acid explanation as the field's default answer. Marshall and Warren shared the 2005 Nobel Prize in Physiology or Medicine for the discovery, twenty-three years after the biopsies that started it and eleven years after the field they had challenged came around.
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