Think about it: peptic and duodenal ulcer were fairly common, and so were effective antibiotics, starting in the mid-40s. . Every internist in the world – every surgeon – every GP was accidentally curing ulcers – not just one or twice, but again and again. For decades. Almost none of them noticed it, even though it was happening over and over, right in front of their eyes.
This is unfair. Modern attempts to eradicate h pylori use “triple therapy” of two different antibiotics plus a PPI, taken simultaneously, all for a unusually long period of time (one to two weeks). If you just give a patient a random antibiotic for some other disease, that’s not going to produce astounding results: you need the PPI to alter the transport of the antibiotic and prevent it from getting immediately broken down in the acidic environment of the stomach, and you need both antibiotics in case the bacteria develop resistance to one. Although some doctors probably got lucky and eliminated h pylori by chance, it’s not like every time anyone took an antibiotic it was curing their stomach ulcers and no one noticed.
Why else didn’t people catch onto h pylori’s role in stomach ulcers quicker? Well, at least 80% of people with h pylori don’t have ulcers or any symptoms whatsoever, and 20% of people with ulcers don’t have h pylori, so that’s going to confuse people. Second, h pylori is hard to stain and very hard to culture, so all you have are these Bigfoot-esque rumors of “I saw this bacterium in the stomach...I think...no, I don’t have any to show you.” A bunch of studies looked for bacteria in the stomach and find none, because of previously mentioned staining and culturing problems. And whenever people tried treating ulcers with antibiotics—and they did do the studies—they get equivocal results because they weren’t using the exact right drug combo to hit h pylori and keep it gone. The first person to successfully culture h pylori was the guy who won the Nobel Prize for discovering it.
Now, just from reading this article, you might believe that doctors are lax about looking at possible infective causes for chronic disease. Let’s look at what PubMed has to say about possible infective causes of schizophrenia. There are 195 studies on “schizophrenia + influenza”, 100 on “schizophrenia + herpesvirus”, 84 on “schizophrenia + toxoplasma”, 24 on “schizophrenia + cytomegalovirus”, 17 on “schizophrenia + varicella”, 10 on “schizophrenia + Lyme disease”, 4 on “schizophrenia + neurocysticercosis”, and one on “schizophrenia + trichinosis” (note that some of these studies are counted multiple times). This is not too atypical: after (among other things) the whole h pylori debacle people realized this was low hanging fruit and have been trying to pick it for the past thirty years.
I think that’s generally a useful principle: if you know something is low-hanging fruit, then unless you’re special so does everyone else, which means it’s not low-hanging fruit anymore. And that’s probably why h pylori seems so clear to Cochrane with thirty years of hindsight, while the people who figured it out at the time won the Nobel Prize, which generally isn’t given for pointing out the obvious.
This illustrates an important point: doctors are lousy scientists, lousy researchers. They’re memorizers, not puzzle solvers.
Was this discovery made as soon as was theoretically possible, or are we rationalizing reasons to justify why it was in fact fairly slow? Or to put it another way, it seems like it was fairly slow, could we do better if the process of Science was different?
Like for instance, balancing the cost of putting researchers on the case, trying different combinations of antibiotics (which as experiments go shouldn’t be too much of a health risk, neither too much of a material cost) on people with peptic ulcer, against the bayesian evidence for and against the bacterial hypothesis?
Even if the evidence was low, the cost to implement such a research project probably is lower than what’s invested in bogus medicine like homeopathics or the like, which has more evidence against itself (at least a bacteria is more likely a causal phenomenon for something than magical water memory).
I think that’s generally a useful principle: if you know something is low-hanging fruit, then unless you’re special so does everyone else, which means it’s not low-hanging fruit anymore.
This illustrates an important point: doctors are lousy scientists, lousy researchers. They’re memorizers, not puzzle solvers.
...
Oh, be nice now.
Actually being an accomplished researcher in the field of medicine, having done more science in the field than vast majority doctors in the world, he has good reason to say this.
This is unfair. Modern attempts to eradicate h pylori use “triple therapy” of two different antibiotics plus a PPI, taken simultaneously, all for a unusually long period of time (one to two weeks). If you just give a patient a random antibiotic for some other disease, that’s not going to produce astounding results: you need the PPI to alter the transport of the antibiotic and prevent it from getting immediately broken down in the acidic environment of the stomach, and you need both antibiotics in case the bacteria develop resistance to one. Although some doctors probably got lucky and eliminated h pylori by chance, it’s not like every time anyone took an antibiotic it was curing their stomach ulcers and no one noticed.
Why else didn’t people catch onto h pylori’s role in stomach ulcers quicker? Well, at least 80% of people with h pylori don’t have ulcers or any symptoms whatsoever, and 20% of people with ulcers don’t have h pylori, so that’s going to confuse people. Second, h pylori is hard to stain and very hard to culture, so all you have are these Bigfoot-esque rumors of “I saw this bacterium in the stomach...I think...no, I don’t have any to show you.” A bunch of studies looked for bacteria in the stomach and find none, because of previously mentioned staining and culturing problems. And whenever people tried treating ulcers with antibiotics—and they did do the studies—they get equivocal results because they weren’t using the exact right drug combo to hit h pylori and keep it gone. The first person to successfully culture h pylori was the guy who won the Nobel Prize for discovering it.
Now, just from reading this article, you might believe that doctors are lax about looking at possible infective causes for chronic disease. Let’s look at what PubMed has to say about possible infective causes of schizophrenia. There are 195 studies on “schizophrenia + influenza”, 100 on “schizophrenia + herpesvirus”, 84 on “schizophrenia + toxoplasma”, 24 on “schizophrenia + cytomegalovirus”, 17 on “schizophrenia + varicella”, 10 on “schizophrenia + Lyme disease”, 4 on “schizophrenia + neurocysticercosis”, and one on “schizophrenia + trichinosis” (note that some of these studies are counted multiple times). This is not too atypical: after (among other things) the whole h pylori debacle people realized this was low hanging fruit and have been trying to pick it for the past thirty years.
I think that’s generally a useful principle: if you know something is low-hanging fruit, then unless you’re special so does everyone else, which means it’s not low-hanging fruit anymore. And that’s probably why h pylori seems so clear to Cochrane with thirty years of hindsight, while the people who figured it out at the time won the Nobel Prize, which generally isn’t given for pointing out the obvious.
Oh, be nice now.
Doctors seem more engineers than scientists to me. For some reason they seem to get offended by such assessment.
I’d be offended if I were an engineer.
I don’t have a bad opinion of engineers. Doctors seem to for some reason.
(I have a bad opinion of doctors, relative to degree of education.)
Was this discovery made as soon as was theoretically possible, or are we rationalizing reasons to justify why it was in fact fairly slow? Or to put it another way, it seems like it was fairly slow, could we do better if the process of Science was different?
Like for instance, balancing the cost of putting researchers on the case, trying different combinations of antibiotics (which as experiments go shouldn’t be too much of a health risk, neither too much of a material cost) on people with peptic ulcer, against the bayesian evidence for and against the bacterial hypothesis?
Even if the evidence was low, the cost to implement such a research project probably is lower than what’s invested in bogus medicine like homeopathics or the like, which has more evidence against itself (at least a bacteria is more likely a causal phenomenon for something than magical water memory).
The efficient research hypothesis?
...
Actually being an accomplished researcher in the field of medicine, having done more science in the field than vast majority doctors in the world, he has good reason to say this.
It is Cochran, without an e. I agree with those who enjoy West Hunter. It is a new blog, and among the best—highly informative.