Nobel-Prize Cluelessness (stomach ulcers)

Wherein the Nobel Prize is given for discoveries that are misleading. From a New Scientist article about medical self-experimentation:

Junior doctor Barry Marshall was sure the medical establishment was wrong about the cause of stomach ulcers. The received wisdom was that they were caused primarily by lifestyle factors, but Marshall and pathologist Robin Warren were sure that the bacterium Helicobacter pylori was to blame.

It turned out that Helicobacter pylori was present in half the stomachs in the world — only a tiny fraction of which developed ulcers. So much for causation. Marshall and Warren did not consider that lifestyle factors might cause immune efficiency to go down, leading to increased growth of the bacterium. In a famous example of self-experimentation, Marshall ingested a giant amount of the supposedly dangerous bacterium — but, uh-oh, didn’t get an ulcer.

Thanks to JR Minkel.

14 thoughts on “Nobel-Prize Cluelessness (stomach ulcers)

  1. The article said that he was infected and got “gastritis, which can eventually lead to ulcers.” Also, stomach ulcers are treated with antibiotics. It’s like saying that S. aureus doesn’t cause infections because it resides on lots of people’s skin and nasal tracts. Doesn’t follow. Few bacteria cause outright illness with no other factors involved.

  2. Dennis, I’m afraid I don’t understand your point. If ulcers are in fact a sign of an immune system working poorly, they would be better treated with treatments that boost the immune system.

  3. Seth, originally I had trouble understanding your own point. I understand you to be saying that the real cause of ulcers is a poorly functioning immune system. What I’m trying to say is that it is perfectly reasonable to state that H. pylori causes ulcers, just as it is reasonable to state that rhinoviruses cause colds, even though perhaps only people with run-down immune systems get either one.

  4. I believe Robert Sapolsky discusses this in his book Why Zebras Don’t get Ulcers. I believe the conclusion is that Heliobacter is a necessary but not sufficient condition to get ulcers. And that Marshall deserved some credit for changing some minds.

    On a related point, Stephan at Wholehealthsource and Peter at Hyperlipid have each recently discussed the fact that Heliobacter and other bacteria in the body may feast and grow on hydrogen – a bacterial byproduct of poor digestion in the gut. For example, see https://wholehealthsource.blogspot.com/2009/02/sugar-hydrogen-bacteria-and.html

  5. Dennis, thanks for explaining that. You are right, that is how causation talk often goes. But it is misleading. If 100% of people were infected with Heliocopter pylori, would it still make sense to say the bacterium causes ulcers? Well, no.

  6. Seth, I hate to belabor this point, but probably the great majority of infectious illnesses have at least something to do with a compromised immune system. For example, zinc supplementation has been shown to dramatically decrease incidence of the flu, because zinc strengthens immunity. But one would not want to say therefore that the influenza virus does not cause the flu. An immune system at 100% functioning might be able to stop almost any infection, but that doesn’t mean that microbes aren’t the cause of illnesses. Likewise, only 20% of lifelong smokers develop lung cancer, probably because their immune systems don’t eliminate cancerous cells. Therefore cigarettes don’t cause lung cancer?

    Likewise, many people are carriers of Staphylococcus aureus, which causes boils among other things, just as many carry H. pylori. No matter how many people don’t get boils, S. aureus still causes them, just as H. pylori causes ulcers.

    Does anyone besides yourself believe that the Nobel Prize was given to these men by mistake?

  7. It sounds like this debate turns on what we mean by “infection.” I think when we use that term it generally means the out of control growth of some microorganism. Same with cancer. We may have pre-cancerous cells sprinkled here and there in our bodies but until they start growing into potentially life-threatening tumors we wouldn’t diagnose it as cancer.

  8. Dennis, I have never heard anyone else make this point, no. If I simply posted what everyone already knew — or at least agreed with — it wouldn’t be a very interesting blog.

  9. It seems worth noting here that the Spanish Flu that killed millions early in the last century (and which incidentally, started in the midwest U.S., and spread by U.S. military deployment), hit hardest those with the strongest immune systems.

  10. Seth:

    I dont understand your last point, you can watch thieves in every area and that doesnt mean that everyone that works in that area is a thief. For your information the presence of a pathogen is not directly related to the physiological expression of a disease, but if a pathogen is the cause of a disease its absolutely necessary their presence in the body (known as infection), other factors that affect the development of the disease are the pathogenicity (in the H.pylori case the presence or absence of virulent factors that allows the bacteria to be more aggressive with the host, such as CagA, VacA, flagellin, etc) that will depend on the genotype or specific strain that is infecting the host (Helicobacter is known for modify its genome sequence very often), and the multiplicity of infection, that means that a sudden rise of the number of bacteria could provoke the symptoms of the disease, but if this amount remains low you could live infected for ever without notice their presence.

    The most important finding of Warren and Marshall was that Helicobacter is the cause of a acute gastritis with a decrease of the gastric pH (that is not normal for a gastritis) and that bacteria could survive in the gastric environment (until that moment was assumed that acid was responsible for destroying every ingested bacteria).

    I have to say that the host immune status is also very relevant in th development of the gastric ulcers, but even if your immune system is reduced the therapy with antibiotics could erase the symptoms and this could happen only by killing the bacteria, so, ulcers must have a bacterial origin. Unfortunately, with the extensive use of antibiotics and the constant modification of Helicobacter pylori genome, the bacteria has become more resistant to the traditional antibiotics, making necessary to use new antibiotics or look for new strategies to attack the bacteria.

    Sorry if i my message was too long, but i considered necessary to clarify some points that are very important to understand the H. pylori infection and their consequences to the host.

    Greetings

    Seb

  11. Seb, thank you for your comment. I believe that ulcers are due to a poorly-functioning immune system and that it will be much safer and cost-effective to improve immune function (by eating fermented foods) than to search for new drugs that kill h. pylori or new strategies that focus on it. The big correlation is ulcers/bad immune function; the small correlation is ulcers/h. pylori infection.

  12. Seth, in patients with compromised immune system (AIDS for example) H.pylori has bever been a major pathogen, this has rised the hypothesis that a robust immunity could be necessary for the conversion between an asymptomatic and an ulcer phenotype. In some models the presence of anibodies could even result in a enhanced colonization. Try to read “Helicobacter pylori in the 21st century” by Sutton and Mitchell. This bacteria is definitely different from the rest, and thats the main reason why they have been living inside us during so many years.

    Greetings

  13. The 1949 Nobel Prize awarded for the use of lobotomies to treat mental illness (despite no real evidence). So the H. pylori theory isn’t the first bit of junk science to win a Nobel.

    I had a stomach ulcer without the presence of H. pylori.

    Ulcers are unknown in populations that don’t eat refined carbohydrates. They also heal very rapidly on very low carbohydrate diets (<20g/day) regardless of the presence of H. pylori.

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