If somebody on the street knew who Barry Marshall was, they’d probably tell you he got his share of a 2005 Nobel Prize for drinking some bacteria (Helicobacter pylori) and getting a stomach ulcer from it. They’d be wrong. Marshall in fact did not develop an ulcer. What he got was a case of gastritis – inflammation of the stomach lining – that largely resolved itself in a couple of weeks, according to original 1985 paper.
Maybe it’s partly because gastritis isn’t a common term. And maybe Marshall hammed it up a tiny bit. It’s hard to tell. In his Nobel autobiography, he implies he sought treatment for the gastritis after he had made his point.
Either way, the gastritis was extremely suggestive but not enough to rigorously prove a link between H. pylori and ulcers. It would take until about the mid-90s for researchers to fill in enough pieces of the puzzle to believe the link and endorse prescribing an antibiotic for ulcers as a rule, which was a separate question, according to anesthesiologist Kimball Atwood in this 2004 Skeptical Inquirer article.
Atwood argued an urban legend of sorts has grown up around Marshall’s self-experiment, citing claims that the gradual acceptance of Marshall and Warren’s hypothesis provides evidence of the medical-industrial complex dragging its feet.
Whether anyone dragged their feet in a socially significant way is subjective but you can’t argue with the illness Marshall actually reported, which was not an ulcer. This is interesting because it shows how quickly even a Nobel moment can get lost down the memory hole.
H. pylori is an ongoing public health story. Sci Am published a feature in 2005, the same year Marshall and his buddy Robin Warren won their Nobel, arguing that people in rich countries could be at greater risk of esophageal cancer because the bug actually protects against it. (See also my story on nitrate’s bad rap.)
Seth Roberts goes so far as to say the bacterium is not even the cause of stomach ulcers:
Marshall and Warren did not consider that lifestyle factors might cause immune efficiency to go down, leading to increased growth of the bacterium.
I guess it depends on what you consider normal. Where’s Aristotle when you need him?