Speaker 1: I decided that I was going to have to drink
Speaker 1: the bacteria myself. I thought I would just be having
Speaker 1: no symptoms for a few years, after which I would
Speaker 1: have an ulcer and then hallelujah, it'd be proven. Actually
Speaker 1: I was very shy about this experiment. I didn't tell anyone,
Speaker 1: not even my wife or Robin until afterwards. I asked
Speaker 1: my boss in gasterentrology, Ian Hyslop, to do an endoscopy
Speaker 1: for me one day. As he put the scope down me,
Speaker 1: he was saying, Berry, I'm not going to ask why
Speaker 1: I'm doing this, and from around the tubing, I gritted out,
Speaker 1: just take the biopsy. So he took some biopsies from
Speaker 1: me and they were all clear, no bacteria. Then I
Speaker 1: infected myself with bacteria that i'd cultured from a patient
Speaker 1: who did not actually have ulcers, just indigestion and gastritis.
Speaker 1: I was able to eradicate his infection with some antibiotics,
Speaker 1: so already I knew that I could, if necessary, take
Speaker 1: a treatment which worked on this bug. I had some
Speaker 1: safety features built in. I thought I drank the bacteria,
Speaker 1: and at first I was okay.
Speaker 2: But instead of.
Speaker 1: Being perfectly well and having a silent infection. After about
Speaker 1: five days, I started having vomiting attacks. Typically at dawn.
Speaker 1: I would wake up, run to the toilet, and vomit.
Speaker 1: And it was a clear liquid, as if you had
Speaker 1: drunk a pint of water and regurgitated it straight back.
Speaker 1: Not only that there was no acid in it. I
Speaker 1: remembered from my medical student days that if you have
Speaker 1: a meal where you drink so much beer that it's
Speaker 1: coming back up straight away, it doesn't have any acid
Speaker 1: in it. I knew there was something unusual about vomiting
Speaker 1: and not having acid, and this is just one experiment
Speaker 1: on yourself, and you say, am I imagining this? Until
Speaker 1: I had another biopsy, I couldn't know for certain that
Speaker 1: I had the bacteria. Finally, after ten days, I had
Speaker 1: the biopsy, had another endoscopy, and the bacteria were everywhere
Speaker 1: in the lining of my stomach. There were absolute millions
Speaker 1: of the white cells that we call pus cells polymorphs.
Speaker 1: There was no acid being produced by my stomach. I
Speaker 1: was very uncomfortable with that endoscopy, gagging and throwing up.
Speaker 1: But I'd proven that the bacteria could infect a healthy
Speaker 1: person and cause gastritis. I'd proven Robin's disease. That's a
Speaker 1: really good one.
Speaker 2: I love that one. The words from the man himself,
Speaker 2: very Marshall. So that was from an interview conducted by
Speaker 2: doctor Norman Swan in two thousand and eight for the
Speaker 2: Australian Academy of Science.
Speaker 1: Sorry I didn't read it in an Australian accent.
Speaker 2: I'm not think that everyone will forgive you.
Speaker 3: I think they'll be thankful for.
Speaker 4: Hi.
Speaker 2: I'm erin Welsh and.
Speaker 3: I'm erin Allman Updyke.
Speaker 2: And this is this podcast will kill you.
Speaker 1: And today we're talking about Helicobacter pylorie.
Speaker 2: Wonderful little bacteria, just such a gem. Okay, So before
Speaker 2: we get into all of the nitty gritty of the
Speaker 2: horrible things that it can do to you, let's get
Speaker 2: into the nitty gritty of what we're drinking. What is
Speaker 2: our quarantine ee?
Speaker 1: Well, of course it's Barry's beaker.
Speaker 2: Barry because Barry Marshall, one of the co discoverers of
Speaker 2: this link between H. Pylori and ulcers and gastritis.
Speaker 1: Et cetera, who we just heard from in our first
Speaker 1: hand account.
Speaker 2: Yeah, and so imagine as you're sipping this quarantini that
Speaker 2: you are Barry Marshall taking that sip of the inoculate
Speaker 2: of hpylory to give yourself gastritis.
Speaker 1: So yum, in the name of science, in the name
Speaker 1: all in the name of science.
Speaker 2: That's what we cheers to today.
Speaker 1: Yes, so what are we cheersing with? What's in this drink?
Speaker 5: Oh?
Speaker 2: Yeah, okay, So it has got coffee because coffee definitely
Speaker 2: exacerbates ulcers. Ulcers. It's got well alcohol in the form
Speaker 2: of rye whiskey mm hm.
Speaker 1: It's got chocolate liqueur and hazelnut syrup. Yes, yum, soups dillish.
Speaker 2: And so we'll post the recipe for that quarantini and
Speaker 2: for our non alcoholic placey Berita on all of our
Speaker 2: social media pages.
Speaker 1: TPWKY on Twitter, and this podcast will Kill You on
Speaker 1: Facebook and Instagram, and we'll also post it on our website,
Speaker 1: This Podcast will Kill You dot Com, where if you
Speaker 1: haven't already you can also find.
Speaker 2: Our merch yep.
Speaker 1: All right, so should we just jump right into the
Speaker 1: podcast today?
Speaker 2: Yeah, I'm really excited about this one. We too.
Speaker 3: We're always excited though, like I know, it's it's good
Speaker 3: after this.
Speaker 1: Quick break, all right, h Pylori The bacterium.
Speaker 2: Dump dump dorm.
Speaker 3: There we go.
Speaker 1: Helicobacter pylori is a gram negative bacterium, and the truth
Speaker 1: is that over eighty percent of people who are infected
Speaker 1: are asymptomatic.
Speaker 2: So that's probably at least one of us.
Speaker 1: Yeah, statistically speaking, it's highly likely. So that's interesting. I
Speaker 1: never thought about getting tested.
Speaker 2: Have you ever had any ulcer symptoms or gastritis?
Speaker 1: No, well, I having some right now, but that's unrelated.
Speaker 2: Another burto for breakfast.
Speaker 1: Well you know, okay, So H. Pylori is shaped a
Speaker 1: little bit like a helix, which is where it gets
Speaker 1: the name helicobacter from. But it's not a spiral keet
Speaker 1: like a spiraled bacteria. It's actually just a curved rod.
Speaker 1: And importantly, it has flagella on it, which it uses
Speaker 1: to move, and it's a very highly motile bacteria. And
Speaker 1: that'll become even more important we talk about the pathophysiology
Speaker 1: of this disease, so the transmission is actually not entirely clear,
Speaker 1: which I think is so interesting.
Speaker 2: Yeah, that is really interesting.
Speaker 1: Yeah, we don't really know how people get infected. The
Speaker 1: thing is, it's estimated that up to fifty percent of
Speaker 1: the world's population is infected with H.
Speaker 3: Pylori.
Speaker 2: Is it vertically transmitted then, like mother to offspring.
Speaker 3: Great question.
Speaker 1: I haven't seen any data that suggests that it's directly
Speaker 1: vertically transmitted. Most of the data that I've seen suggests
Speaker 1: that it's either fecal oral or just through saliva. Okay,
Speaker 1: So it could be that mothers pass it to their
Speaker 1: offspring indirectly, but not directly through what we would normally
Speaker 1: consider vertical transmission.
Speaker 2: Okay, okay, interesting, But yeah, it's.
Speaker 1: Very interesting that it's unclear how this bacteria that is
Speaker 1: so widespread is actually transmitted.
Speaker 2: And so it's is it because it could be transmitted
Speaker 2: in an many different ways, it's likely not just one,
Speaker 2: I mean potentially.
Speaker 3: Yeah, I really don't know.
Speaker 2: That's not what I was expecting.
Speaker 3: I know, it's not what I was expecting either.
Speaker 1: Cool, it's yeah, there's not a lot of evidence that
Speaker 1: it necessarily persists in the environment, but the fact that
Speaker 1: it's so widespread suggests that maybe it actually does somehow.
Speaker 1: And the other thing is that it's really easy to
Speaker 1: infect children, but the people who tend to be most
Speaker 1: infected are actually adults and not necessarily children.
Speaker 3: So that's pretty weird too.
Speaker 2: So children clear the infection.
Speaker 1: Maybe, but then do they get reinfected or is it
Speaker 1: just that they actually don't get infected as children, Like,
Speaker 1: if you screen a bunch of children, most of them
Speaker 1: are not going to be infected. If you screen a
Speaker 1: bunch of adults, a lot of them will be infected.
Speaker 1: But children are just as susceptible as adults. And usually
Speaker 1: if you have something that's transmitted fecal oral, you might
Speaker 1: think that children would get it more frequently than adults
Speaker 1: because they're more likely to put poop in their mouths
Speaker 1: and things. Yeah, anyways, we don't know exactly how it's transmitted,
Speaker 1: but we do know the kinds of symptoms that it causes.
Speaker 1: So acutely an acute infection, shortly after you're infected, you
Speaker 1: can get symptoms of acute gastritis, which basically is just
Speaker 1: inflammation and irritation of the gastrointestinal tract. So maybe some
Speaker 1: abdominal pain, maybe some nausea like good old Berry.
Speaker 3: Tended to experience.
Speaker 1: That's like, But often you don't get any of these symptoms.
Speaker 1: What usually happens is that the helicobacter develops into a
Speaker 1: chronic infection. It basically just lives makes a home in
Speaker 1: your stomach mucosa. And this is impressive because your stomach
Speaker 1: is a pretty inhospitable environment. Right, The pH is like two,
Speaker 1: it's between one point five and three point five, which
Speaker 1: is really really acidic. And on top of that, it's
Speaker 1: constantly moving. Your stomach fills up with food and then
Speaker 1: it has to empty out and to keep all of
Speaker 1: the stuff that you eat from going back up and
Speaker 1: out eu esophagus, it's always undergoing peristalsis, which are these
Speaker 1: rhythmic contractions that it does in order to push the
Speaker 1: food out into your duodenum, which is the first part
Speaker 1: of your small intestine. So it's not a static environment.
Speaker 1: It's a super dynamic environment. So how can this measly
Speaker 1: little bacterium survive in such difficult conditions?
Speaker 3: Do you want to know?
Speaker 2: I do want to know why I'm here.
Speaker 1: It has two main mechanisms by which it's able to survive.
Speaker 1: First of all, it has those flagella. So flagella are
Speaker 1: basically protein structures coming off of bacteria that they can
Speaker 1: use to swim. So once the Helicobacter pylori makes it
Speaker 1: into your stomach, it can resist being flushed out of
Speaker 1: your stomach with the rest of your food, because it
Speaker 1: can swim against the current.
Speaker 2: That's a very powerful little flagella, I know, flagellum.
Speaker 3: Yeahagellum.
Speaker 1: They have like four, so you could say flagella.
Speaker 2: Okay, those are some powerful flagella.
Speaker 3: Yeah, they're really powerful.
Speaker 1: And then they can use them not just to swim
Speaker 1: against the current of peristalsis, but to swim down into
Speaker 1: the mucus that lines your stomach. So for a little
Speaker 1: bit of basic stomach anadome. Because your stomach is such
Speaker 1: a harsh acidic environment, your stomach cells produce a ton
Speaker 1: of mucus, and that mucus lines your stomach cells in
Speaker 1: order to protect your own cells from getting eaten roy
Speaker 1: and eroded by that acid. So the mucus forms this
Speaker 1: like protective lining. The helicobacter can use those flagellas to
Speaker 1: kind of burrow their way into that mucus layer. Oh yeah,
Speaker 1: it's pretty cool, and a lot of times they actually
Speaker 1: live in that mucus layer, but if they wanted to,
Speaker 1: they could swim down through that mucus layer and actually
Speaker 1: attach directly to the epithelial cells. They have these special
Speaker 1: proteins called adhesons that adhere to the epithelial cells, and
Speaker 1: that way, it's another mechanism by which they can make
Speaker 1: sure they don't get flushed out. Okay, So they're very
Speaker 1: good at a swimming against the current down into your
Speaker 1: mucus and potentially attaching to your epithelial cells. So that's
Speaker 1: the first way that they're able to survive. The second
Speaker 1: way is that they actually can neutralize their own micro environment.
Speaker 2: Oh cool, right, sort of like their own little pod
Speaker 2: of bubble, like a little the bacteria bubb right exactly.
Speaker 1: So if the pH directly surrounding the bacteria is too
Speaker 1: low or too acidic, they produce urine, which is an
Speaker 1: enzyme that breaks down urea, which is a normal waste
Speaker 1: product that's found throughout your body that when it's broken down,
Speaker 1: breaks down into carbon dioxide and ammonia, and ammonia is
Speaker 1: a base. This base neutralizes the acid immediately surrounding Helicobacter
Speaker 1: bacteria so that they can live happily ever after in
Speaker 1: a slightly less acidic environment.
Speaker 3: Hmmmm, isn't that cool?
Speaker 2: That's really cool.
Speaker 1: So they're good swimmers, they can stick to your cells,
Speaker 1: and they they change their own micro environment to be
Speaker 1: more hospitable for their growth and survival.
Speaker 2: Huh.
Speaker 1: Okay, So the thing about H. Pylori infection is that
Speaker 1: there are two different interrelated long term issues associated with
Speaker 1: chronic H. Pylori infection, because again, this is a bacteria
Speaker 1: that essentially makes its home in your stomach and lives
Speaker 1: there for a very very long time. All Right, these
Speaker 1: two different issues. They're related, but they're also kind of opposite,
Speaker 1: which I think is really interesting and it seems like
Speaker 1: it's not entirely understood yet. But the issue that you
Speaker 1: end up with depends on where in your stomach these
Speaker 1: bacteria colonize.
Speaker 3: Okay, Okay, So if H.
Speaker 1: Pylori colonizes in what's called the antrum of your stomach,
Speaker 1: which is closer to the output end of your stomach,
Speaker 1: then what it tends to do by mechanisms we don't
Speaker 1: fully understand, is it causes hyper secretion of acid, so
Speaker 1: it actually increases your acid output, and if your stomach
Speaker 1: is making too much acid, that acid overflows out of
Speaker 1: your stomach and into your duodenum. This causes chronic irritation
Speaker 1: of your duodenum that leads to what we call gastric metaplasia.
Speaker 1: Means your stomach and metaplasia means your cells are changing
Speaker 1: in shape and type. So it means that your intestinal
Speaker 1: cells start to look more like your stomach cells.
Speaker 2: Ooh, that's really weird.
Speaker 1: It's really weird, and it's not good. This leads to
Speaker 1: duodenal ulcers. Okay, Okay, So you've got acids spilling out
Speaker 1: of your stomach into your duodenum, causing irritation and cell
Speaker 1: changes that lead to ulceration, which are basically holes that
Speaker 1: form in the layers of your small intestine.
Speaker 2: Okay, So I have a question. So you said that
Speaker 2: if the bacteria are in the output end of your stomach,
Speaker 2: then stomach acid production increases, but doesn't make Doesn't that
Speaker 2: make the environment more inhospitable? So is it? Is it
Speaker 2: your body's reaction. It's not the bacteria that are producing
Speaker 2: the acid, it's your body being like, wait, there's your
Speaker 2: neutralizing too much.
Speaker 1: That's a really great question. It's not entirely clear. It
Speaker 1: suggested that maybe they damage certain cells that would decrease
Speaker 1: acid production, so then they end up overproducing acid because
Speaker 1: those like inhibitory cells are damaged. It's totally unclear, and
Speaker 1: it's about to get even weirder because that's not the
Speaker 1: weird good great, yeah, okay, so that's how you end
Speaker 1: up getting duadenal ulcers.
Speaker 2: If you have an H.
Speaker 1: Pylori infection, that's not the only thing you can end
Speaker 1: up with.
Speaker 2: If H.
Speaker 1: Pylori colonizes higher up in what's called the body of
Speaker 1: your stomach, closer to the input end of your stomach.
Speaker 2: That's like the big section, the big fleshy lump party.
Speaker 1: Not so tubular, not so tubular exactly. If it infects there,
Speaker 1: it actually decreases acid production.
Speaker 2: Okay, now I'm confused, I know, right.
Speaker 5: So H.
Speaker 1: Pylori, if it infects higher up in the body of
Speaker 1: your stomach, it actually tends to lead to acid hypo secretion,
Speaker 1: less acid secretion, which increases inflammation because the cells are
Speaker 1: invading in that portion of your stomach and they're directly
Speaker 1: causing inflammation. So it's not the acid itself that's causing
Speaker 1: an ulcer like it is in the duodenum. It's the
Speaker 1: bacteria itself causing ulcers in the stomach from the inflammation. Interesting, okay,
Speaker 1: And on top of that, your stomach cells undergo what's
Speaker 1: called intestinal metaplasia, So now your stomach cells look less
Speaker 1: like stomach cells more like intestine cells. They can't handle
Speaker 1: the acid that is there, so that further leads to
Speaker 1: gastric ulcers, and gastric ulcers can lead to gastric cancer.
Speaker 2: Okay, hold on a second, so let me just get
Speaker 2: this straight. Depending on where these bacteria colonize in your stomach,
Speaker 2: it can either make your stomach look more like your
Speaker 2: intestine or your small intestine look more like your stomach. Yes,
Speaker 2: that's bizarre.
Speaker 1: I love it bizarre. It's it is fascinating, and it's
Speaker 1: it's completely different mechanisms, right Like, in one, you're ending
Speaker 1: up with hyper secretion of acid. In one, you're ending
Speaker 1: up with hyposeecretion of acid. In both you end up
Speaker 1: with ulcers, and in one you end up with cancer.
Speaker 2: And that's with the the gas gastric Yeah, okay, so
Speaker 2: can we just do terminology really quickly because I read
Speaker 2: so many different words in front of ulcer. So there's peptic,
Speaker 2: there's duodenal, there's gastric and is peptic just an umbrella
Speaker 2: term for stomach ulcer I believe?
Speaker 1: So yeah, peptic ulcer is peptic ulcer disease is just
Speaker 1: you've got an ulcer somewhere around your stomach. A duodenal
Speaker 1: ulcer is an ulcer in your duodenum, so that's you're
Speaker 1: the first part of your small intestine. Those ulcers have
Speaker 1: a very very very very low risk of ever developing cancer.
Speaker 1: They basically you basically never get cancer in your small
Speaker 1: intestine for whatever reason.
Speaker 3: It's very rare.
Speaker 1: They can erode all the way through and then cause
Speaker 1: massive bleeding, but you don't tend to get cancer in
Speaker 1: your small intestine. Gastric ulcers are an ulcer in your stomach,
Speaker 1: and those do have a pretty high rate of converting
Speaker 1: into gastric cancer.
Speaker 2: Okay, Okay, I think I've finally got that. The location
Speaker 2: and the umbrella turns down. It's a lot of words.
Speaker 1: Yeah, so that's how they cause disease. It's we we
Speaker 1: know very little comparatively about h pylori, more less than
Speaker 1: I expected, quite honestly.
Speaker 2: Well, it's a pretty recent discovery.
Speaker 3: It's true.
Speaker 2: It's true. Okay, So if you are infected and you
Speaker 2: are showing symptoms, like what what are the symptoms or
Speaker 2: signs that you experience if you have peptic ulcers or
Speaker 2: gastritis or whatever else is there a difference between the
Speaker 2: ulcers and the symptoms.
Speaker 1: Yeah, it's a great question. So you can't tell the
Speaker 1: difference between something like gastric cancer and just peptic ulcer
Speaker 1: disease based on symptoms alone, because the symptoms are actually
Speaker 1: very similar, if not exactly the same.
Speaker 2: Oh my god, great, So you could be like, is
Speaker 2: this an ulcer or cancer? WebMD might be right.
Speaker 1: Don't trust WebMD on this. Let me tell you. But
Speaker 1: the symptoms include things like a burning stomach pain. So
Speaker 1: people of peptic ulcer disease might often say they have
Speaker 1: acid reflux.
Speaker 3: Okay, right, So you might have like a.
Speaker 1: Burning in your sort of substernal region. You might have
Speaker 1: a feeling of fullness or a lot of bloating in
Speaker 1: your stomach. You might have nausea or vomiting, especially if
Speaker 1: you're vomiting something like blood that's suggestive of something like
Speaker 1: peptic ulcer disease. Your face looks a little horrified just
Speaker 1: the concept.
Speaker 2: Yeah, vomiting blood, Nope. Yeah.
Speaker 1: And then the other things that we get really concerned
Speaker 1: about if you have these type of signs are things
Speaker 1: like unexplained weight loss because maybe you're not eating as
Speaker 1: much because you have pain, when you eat so unexplained
Speaker 1: weight loss or appetite changes, and then dark stools, because
Speaker 1: what can actually happen is that those ulcers can cause
Speaker 1: bleeding and if you're not vomiting up the blood, it'll
Speaker 1: travel through your gastrointestinal tract and by the time it
Speaker 1: comes out in the stool, it doesn't look like blood anymore.
Speaker 1: It just looks like very very dark stools. So if
Speaker 1: you've ever had a doctor ask you, are your stools dark,
Speaker 1: that's what they're asking about, is their secret blood.
Speaker 2: Did you eat beats? No?
Speaker 1: Yeah, that's is a little different the episode of Portlandia
Speaker 1: where they're.
Speaker 2: It's beats with Jeff Yes, is it beats? Okay?
Speaker 3: Anyway?
Speaker 2: Yep? Anyway. Yeah.
Speaker 1: So those are the symptoms, and you can't necessarily distinguish,
Speaker 1: especially those more severe symptoms of peptic ulcer disease from
Speaker 1: gastric cancer, just based on symptoms. So we do what's
Speaker 1: called an endoscopy, which is where they put a camera
Speaker 1: down into your stomach and they take a look at
Speaker 1: the ulcer. If they find an ulcer, then they can
Speaker 1: biopsi it and then figure out what's going on.
Speaker 2: Okay. Is that usually the first step is an endoscopy
Speaker 2: if you have symptoms, or do they do the breath
Speaker 2: test or what so.
Speaker 1: The urease breath test is a test to check for H.
Speaker 1: Pylori infection, and yes, you can absolutely do that. So
Speaker 1: if you go to a doctor with symptoms of peptic
Speaker 1: ulcer disease, it's very likely that they'll do a uiase
Speaker 1: breath test.
Speaker 3: The other thing you can.
Speaker 2: Do is treat the H.
Speaker 1: Pylori so it is treatable. It's a little difficult to treat.
Speaker 1: There's three different medications that you give. First as a
Speaker 1: proton pump inhibitor, which decreases acid production. Second is two
Speaker 1: different antibiotics and you take these for quite a long time.
Speaker 1: I think it's at least a few weeks of antibiotic
Speaker 1: treatment to clear that H. Pylori infection. And if your
Speaker 1: symptoms go away, then it was all from the H.
Speaker 1: Pylori And if they don't, then they'll probably do follow
Speaker 1: up treatment.
Speaker 3: So yeah, that's that's H. Pylori infection.
Speaker 2: How interesting?
Speaker 3: Yeah, wow, fun little bug.
Speaker 2: I think it's definitely got a lot of tricks of
Speaker 2: its sleeve.
Speaker 1: It's got a lot of tricks and we there's so
Speaker 1: many that we don't know yet, which I think is
Speaker 1: so fun and interesting. Yeah, so, Aaron, how'd we get here?
Speaker 1: Where'd this thing come from?
Speaker 2: Oh? I can't wait to tell you good But first
Speaker 2: a little break. I feel like there's this notion of
Speaker 2: ulcers and gastritis as being this modern disease brought on
Speaker 2: by this modern stressful work environment, acidic foods, lack of sleep,
Speaker 2: et cetera. But guess what what it's not. It's old.
Speaker 2: It's really old.
Speaker 3: We've always had ulcers.
Speaker 2: Actually kind of. So humans in H. Pylori have been
Speaker 2: together for thousands of years, so since before humans left
Speaker 2: East Africa over fifty thousand to seventy thousand years ago.
Speaker 2: Holy cow. Yeah, so, which explains why there's such a
Speaker 2: huge proportion of the population that's infected. It's really just
Speaker 2: been with us. So researchers can actually see the traces
Speaker 2: of different waves of human migration in the genetic diversity
Speaker 2: of these H. Pylori strains. Stop it.
Speaker 1: Yes, I love it when we get to talk about
Speaker 1: human migration because of disease.
Speaker 2: I know, it's really cool. So basically, as a general
Speaker 2: rule with this, the most genetically diverse H. Pylori strains
Speaker 2: are associated with the oldest migrations and the source population
Speaker 2: in East Africa when humans migrated out, and then the
Speaker 2: genetic diversity decreases with each migration, and then distance and
Speaker 2: so on. So yeah, isn't that cool?
Speaker 4: Yeah?
Speaker 3: I love it all right.
Speaker 2: So we've got this evolutionary evidence of early human and h.
Speaker 2: Pylori association, and we've also got ancient writings about ulcers
Speaker 2: and gastritis. So gastric symptoms have been recorded for millennia,
Speaker 2: dating back, of course to Hippocrates. Where would we be
Speaker 2: without Hippocrates?
Speaker 3: Nowhere?
Speaker 2: And on an episode of this podcast, will kill You Nope.
Speaker 2: So yeah, So Hippocrates describe epigastric burning like indigestion and
Speaker 2: air swallowing, both of which are symptoms of gastritis.
Speaker 3: I think air swallowing just burping.
Speaker 2: Air swallowing is what was written. Weird, Maybe it's just burping,
Speaker 2: I don't know. And around the same time as Hippocrates,
Speaker 2: there is an inscription carved on a pillar at the
Speaker 2: temple of Asclepius at Epidaurus that might be describing how
Speaker 2: to perform surgery on a gastric ulcer. Ooh, quote a
Speaker 2: man with an ulcer in his stomach. He incubated and
Speaker 2: saw a vision. The gods seemed to order his followers
Speaker 2: to seize and hold him that he might insize his stomach.
Speaker 2: So he fled, but they caught and tied him to
Speaker 2: the door knocker. Then Asclepius opened his stomach, cut out
Speaker 2: the ulcer, sewed him up again, and loosed his bonds.
Speaker 2: He went away whole, but the chamber was covered with
Speaker 2: his blood on Earth one star. That's just inscribe.
Speaker 1: We've done a pillar at a temple. Yeah, it does
Speaker 1: a story of we're gonna do surgery on this guy
Speaker 1: against his will.
Speaker 2: I don't know, but we should add that to our
Speaker 2: like take a picture of this and also our personal
Speaker 2: vacation list. Oh yes, yeah, so we also in addition
Speaker 2: to this pillar, we also have a mummy dating from
Speaker 2: a little bit after this, around one hundred and sixty
Speaker 2: seven BCE from the Western Han dynasty that appears to
Speaker 2: have a peptic ulcer. We don't know if it was
Speaker 2: caused by H. Pylori, but yeah, definitely seems possible in
Speaker 2: a mummy. Cool.
Speaker 1: That's so cool that mummies are preserved so well that
Speaker 1: you could see something like that in the tissue.
Speaker 2: I know, huh. So about a thousand years after that
Speaker 2: we get a bit more specific when even Senna Avicenna
Speaker 2: wrote about how some of these painful or uncomfortable symptoms
Speaker 2: appear after you eat. He even went as far to
Speaker 2: suggest that they pay heartburn and thirst felt by some
Speaker 2: people were all caused by a gastric ulcer. Okay, then
Speaker 2: in the late fifteen hundreds, so about five hundred years
Speaker 2: after Avicenna described this, the first gastric ulcer was definitely
Speaker 2: described by the Italian physician Marcelo Donatti. During this time,
Speaker 2: anatomical descriptions from dissections of human cadavers were getting super popular,
Speaker 2: and so people were starting to take a note of
Speaker 2: the inflammation and ulceration of the mucosa in their cadavers.
Speaker 2: I didn't see anything about numbers through the ages in
Speaker 2: regards to the prevalence of gastric ulcers. I think that
Speaker 2: would be a really hard thing to estimate, and especially
Speaker 2: since it's been with humans for since humans have been humans. Basically, yeah,
Speaker 2: it was probably pretty prevalent at least, and also we
Speaker 2: can guess that it was pretty prevalent based on how
Speaker 2: many descriptions there were of it and how much people
Speaker 2: started to pay attention to it as cadaver dissection was
Speaker 2: a lot more popular, and then came the sixteen hundreds.
Speaker 2: Microscopy was developed and popularized by a couple of big names,
Speaker 2: but probably the biggest name is Anthony van Lewin Hook
Speaker 2: Layman Hook. The impact of his technology and also how
Speaker 2: far it has come today really should get an episode
Speaker 2: of its own. Wouldn't that be fun? Yeah? For sure,
Speaker 2: I love the history of microscopy. But the important thing
Speaker 2: is that microscopes allowed people to see this whole new
Speaker 2: world which had been invisible to them up to this point. Essentially,
Speaker 2: this led to the field of microbiology and molecular biology
Speaker 2: because people could finally start understanding how the pieces that
Speaker 2: made up living organisms fit together. Bacteria were described and
Speaker 2: started being blamed rightfully so for some in some cases,
Speaker 2: for many diseases, and people started sticking everything they could
Speaker 2: find under these new lenses, and stomach tissue or stomach
Speaker 2: contents was no exception. And because bacteria live on basically
Speaker 2: every surface ever, of course, stomach contents look to be
Speaker 2: chock full of bacteria. Some of these microscope lookers became
Speaker 2: convinced that the bacteria were the cause of gastric inflammation
Speaker 2: and disease, and a couple of these people had identified
Speaker 2: bacterial colonies in gastric ulcers and in the surrounding mucosa
Speaker 2: and went so far as to say that these bacteria
Speaker 2: were the cause of ulcers. That was in eighteen seventy five. Whoa, yeah,
Speaker 2: they were like, oh, there's bacteria here. It seems to
Speaker 2: be in aligning, it seems to be associated with inflammation.
Speaker 2: This is what causes the ulcers. So then what happened?
Speaker 1: Why did it take us another one hundred plus years
Speaker 1: to figure it out?
Speaker 2: Okay, well I'll get to that, but yeah, it did
Speaker 2: kind of. The link didn't necessarily become forgotten, but it
Speaker 2: definitely was not as popular as some of the other
Speaker 2: leading hypotheses. Interesting, and so the late eighteen hundreds did
Speaker 2: see some other progress guarding bacteria and peptic ulcers and gastritis.
Speaker 2: For instance, the pathologist Arnold C. Klebs, who was son
Speaker 2: of the Clubs for whom Clubciella was named, Yes, he
Speaker 2: spotted a bacillis in the gastric glands, which he noted
Speaker 2: were inflamed. And so this could be actually the first
Speaker 2: sighting of H. Pylori infectious gastritis in humans. And then
Speaker 2: there was an Italian anatomus named Bizo zero who reported
Speaker 2: his findings of a Spirokeet like organism in the stomach
Speaker 2: lining of several dogs that he studied, which was probably
Speaker 2: a Helicobacter species. And remember those two guys who I
Speaker 2: just mentioned that first declared this link between gastric ulcers
Speaker 2: and bacterial infections. So even though mostly everyone else had
Speaker 2: dropped that concept, they were still convinced. And so by
Speaker 2: eighteen eighty eight a ton of progress had been made
Speaker 2: in identifying different bacterial species and the diseases they caused
Speaker 2: just in general. So these guys started picking candidate microbs
Speaker 2: such as Staphoreus and Strep to see if they caused
Speaker 2: ulcers when injected into the stomach of various lab animals,
Speaker 2: and no surprise, they did. But that was sort of
Speaker 2: a problem, right, because if all of these different species
Speaker 2: could cause gastric ulcers, how do you distinguish between the
Speaker 2: types of ulcers and between whether this bacteria causes an
Speaker 2: ulcer or whether they're just general ulcer causing bacteria. After
Speaker 2: Latoul was able to induce ulcers, in his guinea pigs.
Speaker 2: Other people started to get interested and found that a
Speaker 2: whole bunch of bacterial species could lead to gastri duodenal ulcers.
Speaker 2: But there was still so much to be figured out,
Speaker 2: and gastric ulcers were a tricky business because, like I said,
Speaker 2: you can get ulceration with many different diseases, and you
Speaker 2: could induce it with many different bacterial species. So how
Speaker 2: do you pinpoint exactly which species causes ulcers for sure,
Speaker 2: rather than just these opportunistic infections.
Speaker 1: Right, which does it in real life versus just if
Speaker 1: you injected in the lab exactly?
Speaker 3: Yeah?
Speaker 2: And so really what became more popular in terms of
Speaker 2: why gastritis and peptic ulcers exist was that excess acid
Speaker 2: that was it, and that could be triggered by the
Speaker 2: ingestion of foods or drinks high in acidity, stress, et cetera.
Speaker 2: And this explanation resolved a few things that were maybe
Speaker 2: a bit more difficult to align with the bacteria hypothesis.
Speaker 2: So often people who experienced ulcers didn't have symptoms all
Speaker 2: of the time. They had flare ups, and then they
Speaker 2: would resolve after cutting back on certain foods or taking
Speaker 2: lots of anti acids, and so during this time, it
Speaker 2: was basically conventional wisdom that bacteria couldn't survive in the
Speaker 2: high acidity environment of the stomach, so if bacteria were
Speaker 2: found in the lesions, they were probably from ingested food
Speaker 2: or the stomach was weakened enough to allow for these
Speaker 2: opportunistic invaders. So it was like they were second and dairy.
Speaker 1: The ulcers were the primary rather than yeah interesting.
Speaker 2: Yeah, And it wasn't so much that people weren't finding
Speaker 2: h pylorian stomach tissue. A camplobacter like or curved rod
Speaker 2: bacteria had been reported as part of the gastric flora
Speaker 2: for decades, but no one had had much luck in
Speaker 2: investigating them. In the nineteen fifties, someone named Edie Palmer
Speaker 2: decided to take a closer look, and he concluded that
Speaker 2: they were just normal commensals of the mouth. These curved
Speaker 2: rod bacteria were basically cast aside as unimportant, which really
Speaker 2: kind of held back the field, probably for a few decades.
Speaker 2: All right, let's take stock of where and when we are.
Speaker 2: It's the early nineteen eighties, and the excess acid hypothesis
Speaker 2: was the prevailing one, despite some reports in the late
Speaker 2: seventies of epidemic gastritis with hypocorhydria, so low acid acido
Speaker 2: and findings of Gram negative bacteria in association with acute gastritis.
Speaker 1: Oh my gosh, I'm getting really excited.
Speaker 2: So the bacteria hypothesis is still hanging in there, and
Speaker 2: one of its proponents is an Australian pathologist named Robin
Speaker 2: Warren who was working at the Royal Perth Hospital in
Speaker 2: Western Australia. Warren had a hunch that the gastric ulcers
Speaker 2: he had seen in patients over the years had bacterial origins.
Speaker 2: In nineteen eighty one, he had written a letter to
Speaker 2: another doctor asking whether there were any gastra entrologists that
Speaker 2: wanted to work on uncovering this mystery with him, And
Speaker 2: this doctor just happened to show this letter to a
Speaker 2: young physician named Barry Marshall Berry who had just started
Speaker 2: his gaster entrology fellowship term where he would have to
Speaker 2: come up with a research project to do.
Speaker 3: Oh my gosh, can.
Speaker 1: Even imagine be Yeah, that's my first year of fellowship
Speaker 1: by nine a project.
Speaker 2: Oh this sounds great. And then it's h by Laurie.
Speaker 4: Oh yeah, gosh, it's it would be incredible, And I
Speaker 4: mean I think it was like so from all of
Speaker 4: the different things that I read, their personalities were perfectly
Speaker 4: suited to one another and to solving this problem.
Speaker 2: Because you have Robin Warren, who seemed from what I
Speaker 2: read to be very methodical, very detail oriented, very sort
Speaker 2: of like step one, step two, step three. And then
Speaker 2: on the flip side of that, you have this young,
Speaker 2: like sort of energetic, impatient guy, Bary Marshall. And so
Speaker 2: they balanced each other out really well, and they were
Speaker 2: both I think most importantly iconoclastic. They wanted to fight
Speaker 2: for this hypothesis because I think I quote or something, well,
Speaker 2: I'm not going to quote actually, because I think that
Speaker 2: for Robin Warren, he was most fascinated by the fact
Speaker 2: that these bacteria were somewhere they shouldn't be. Yeah, and
Speaker 2: Barry Marshall wanted to wanted this opportunity to prove everyone
Speaker 2: else wrong. Of course, So it was just the perfect
Speaker 2: combination of things.
Speaker 3: I love it.
Speaker 2: Yeah, Okay, Marshall decides to join this project, and neither
Speaker 2: of them had strict backgrounds in microbiology, so they decided to,
Speaker 2: you know, say, who cares, We're just going to try
Speaker 2: to do this. Anyway, we're going to isolate and culture
Speaker 2: this Camplo bacter like bacterium that Warren had found in
Speaker 2: so many of his patients. I also wonder a bit
Speaker 2: about whether not having that microbiology or gastroentrology specific background
Speaker 2: probably helped them a bit too, sort of not having
Speaker 2: those preconceived notions or the dogma that are so pounded
Speaker 2: into you during particularly research training.
Speaker 1: Yeah, you haven't already been sort of indoctrinated or ingrained
Speaker 1: on any one specific belief, so you have this option
Speaker 1: to just explore or all these different possibilities.
Speaker 2: Yeah. H thinking outside the box is much easier when
Speaker 2: you don't know the shape of the box that you're in. Totally. Yeah.
Speaker 2: In any case, they started their microbe hunt not necessarily
Speaker 2: starting out saying that these bacteria caused ulcers, but more, hey,
Speaker 2: look what we found. It's a new bacterial species that
Speaker 2: can survive in the gut, and maybe it has some
Speaker 2: links to gastritis and inflammation. But saying you're going to
Speaker 2: isolate and culture and undescribed bacterium is quite different than
Speaker 2: actually doing it. As they both learned, culturing something new
Speaker 2: can be a bit of a tricky game. You have
Speaker 2: to figure out the or know the right culture formula
Speaker 2: to use and the right settings for optimal growth. And
Speaker 2: when something is as extreme as something that can live
Speaker 2: in your stomach's acidic environment, it's a difficult place to start. Yeah, So,
Speaker 2: after months of trying to culture isolates from gastritis patients
Speaker 2: and not getting anything, they may have started to lose
Speaker 2: a little hope. But then a fortunate accident occurred, as
Speaker 2: these things do, seemed to happen. It turns out that
Speaker 2: the lab tech who was responsible for culturing the isolates
Speaker 2: and checking on those cultures was throwing away the plates
Speaker 2: or broth after two days. This was happening at a hospital.
Speaker 2: Hospital is busy place. It tends to be chaotic. There's
Speaker 2: a lot of other epidemics and things going through the lab,
Speaker 2: so there really wasn't room for dozens of stomach bacterial
Speaker 2: culture plates to just hang around. But on a particularly
Speaker 2: busy weekend, Easter weekend in fact, the tech didn't have
Speaker 2: enough time to look at the plates after the usual
Speaker 2: two days, so he left them over the weekend until Tuesday,
Speaker 2: five days after the biopsy, and when he went back
Speaker 2: to check on the cultures, boom colonies were present, they
Speaker 2: were just slow. They were just slow.
Speaker 3: They're like, give me some time.
Speaker 2: Yeah, I'm growing here. So these bacteria had probably been
Speaker 2: in all, or at least the vast majority of those samples,
Speaker 2: but they just needed a little bit longer to incubate.
Speaker 2: Oh So, now that Marshall and Warren could culture these bacteria,
Speaker 2: they could do so many things that could find out
Speaker 2: what antibiotics could be used against it, try to develop
Speaker 2: an animal model of infection, try to find out what
Speaker 2: these bacteria were related to, and most importantly, try to
Speaker 2: find out what these bacteria did in the stomach. So
Speaker 2: they decided to test one hundred patients to see if
Speaker 2: the bacterium was present and to look for patterns of
Speaker 2: infection or any sort of disease state, and they found
Speaker 2: that all patients with duodenal ulcers had the bacterium. Not conclusive,
Speaker 2: but definitely suggestive. Marshall and Warren then started to develop
Speaker 2: a hypothesis these bacteria cause gastritis, and then gastritis leads
Speaker 2: to ulcers. People could have recurrent ulcers because their immune
Speaker 2: system would be stronger at various points or whatever, but
Speaker 2: the bacteria would always be there, so it never went
Speaker 2: away completely, and this also explained why earlier trials of
Speaker 2: physicians treating their gastrite as patients with antibiotics saw a
Speaker 2: reduction in acid and symptoms. They tried to publish some
Speaker 2: of their findings in The Lancet, in a letter and
Speaker 2: as an abstract at an annual meeting of the gastra
Speaker 2: Entroological Society of Australia, but faced difficulty and rejection. Yeah,
Speaker 2: the Lancet couldn't get reviewers to agree on whether their
Speaker 2: findings were important or whether their conclusions were true, and
Speaker 2: the gastor Interrological Society of Australia just flatly completely rejected
Speaker 2: their abstract. They were like, we received sixty seven submissions
Speaker 2: and we could only accept fifty six this year. We're sorry,
Speaker 2: we couldn't get your those are the numbers. Why did
Speaker 2: they have I have to point out how many there
Speaker 2: were and why fifty six? I think it just seems
Speaker 2: unnecessarily hard not just put up a couple extra boards
Speaker 2: to tack your poster on.
Speaker 3: I mean goodness, I.
Speaker 2: Know, right, it seems seems rude. So the bacteria hypothesis
Speaker 2: seemed to fit with so much of what was known
Speaker 2: about ulcers but this concept met with a ton of
Speaker 2: resistance among doctors, many of whom would dismiss the bacteria
Speaker 2: as being opportunistic, only able to establish after the stomach
Speaker 2: was already weakened, and they would argue that if this
Speaker 2: bacterium actually caused disease, the link would have been made
Speaker 2: a long time ago. It's really silly, yeah, I mean,
Speaker 2: after all, it had been observed in the stomach for ages,
Speaker 2: so it should have been known by now. Things weren't
Speaker 2: always civil, and there was a lot of rude or
Speaker 2: dismissive comments made behind Marshall and Warren's backs, and many
Speaker 2: did not take them seriously as not having official microbiology
Speaker 2: or gastentrology credentials. Then, the ulcer drug business, which was
Speaker 2: one of the biggest in the nineteen eighties, wasn't exactly
Speaker 2: in support of this notion. Something I never thought of
Speaker 2: before reading this article. People with gastritis or ulcers were
Speaker 2: spending a little bit of money every day on the drugs,
Speaker 2: and they were often long term, if not lifetime customers.
Speaker 2: So if you could cure those conditions with the course
Speaker 2: of antibiotics, boom, the industry would be devastated. Yeah, so
Speaker 2: they spent a bunch of money doing research trying to
Speaker 2: prove that ulcers were not caused by bacteria. Shocking right.
Speaker 2: Even though the research was sound, Marshall and Warren had
Speaker 2: to demonstrate the cause and effect of the bacteria and ulcer.
Speaker 2: That the bacteria caused gastritis and ulcers, not that the
Speaker 2: ulcers paved the way for the bacteria, but they couldn't
Speaker 2: get the bacteria to infect any animal models. So, like
Speaker 2: you heard in our first hand account at the beginning
Speaker 2: of the episode, Barry Marshall took it upon himself to
Speaker 2: take a swig of the bacterial culture from a sixty
Speaker 2: six year old, non ulcered, dyspeptic man. After first establishing
Speaker 2: Marshall himself had no gastric ulceration or inflammation, within less
Speaker 2: than two weeks all of those symptoms appeared, and the
Speaker 2: final confirmation came in the form of an endoscope. The
Speaker 2: infection seemed to more or less resolve on its own
Speaker 2: for Marshall, but the putrid breath that's characteristic of this
Speaker 2: disease remained. So his wife was like, if you don't
Speaker 2: take antibiotics to get rid of this, you have to
Speaker 2: leave the house. So he took. He took antibiotics and
Speaker 2: got rid of it. But it worked. So it worked,
Speaker 2: and so Marshall's we have an end of two actually,
Speaker 2: or at least of two that I could find. So
Speaker 2: Marshall's self inaculation was followed up by another Australian guy
Speaker 2: named Morris who did the same.
Speaker 1: My only Australians. They're all just just like Steve Irwin.
Speaker 1: They're like, I'm just gonna go.
Speaker 2: For it, and progress has been made. Poor guy was
Speaker 2: not as fortunate as Marshall because it took him five
Speaker 2: years for his gas stritis to resolve, even with treatment.
Speaker 2: So don't try this at home, no, do not. Eventually
Speaker 2: people started coming around to the idea, especially in Australia,
Speaker 2: and doctors started to use antibiotics to treat patients they
Speaker 2: would have otherwise done surgery on to remove part of
Speaker 2: the stomach or the intestine. Yeah, of course they saw
Speaker 2: positive results, but other places were a lot slower to
Speaker 2: try out the treatment. And that's not surprising, Like I
Speaker 2: can't really fault them for that. Giving antibiotics willy nilly
Speaker 2: is not a good idea, even if you have strong
Speaker 2: suspicions they might work. And so the study had to
Speaker 2: be repeated there at all over with the drugs available,
Speaker 2: and ideally using a double blind trial where both those
Speaker 2: administering the drugs and those and those getting the drugs
Speaker 2: didn't know whether they were giving slash, being given treatment
Speaker 2: or placebo. Right, and the results were clear gastritis and
Speaker 2: ulcers could be healed by antibiotics. It became the guideline
Speaker 2: for treatment in many places, and I can imagine it
Speaker 2: must have felt really good to have that sort of vindication,
Speaker 2: even if it came with a several year delay. Barry
Speaker 2: Marshall wasn't done yet though. He helped to develop the
Speaker 2: breath test for h pylori, which was Yeah, and that
Speaker 2: was a really wonderful because that meant that people didn't
Speaker 2: necessarily have to have endoscopies, which were uncomfortable and cost
Speaker 2: a lot of money, particularly if you're in the US
Speaker 2: and you have to pay for most everything. Right.
Speaker 1: Plus, you can do it a lot easier. You don't
Speaker 1: need specialized equipment, you don't need specialists, you can just
Speaker 1: you just breathe.
Speaker 2: Yeah, it's really cool concept. I kind of love it.
Speaker 2: In the two decades or so after their early nineteen
Speaker 2: eighties letters in the Lancet. The world had definitely been
Speaker 2: changed by their discovery. Long term sufferers of gastritis and
Speaker 2: ulcers could find relief, and the risk of developing stomach
Speaker 2: cancer could even be reduced a bit. For their efforts,
Speaker 2: Barry Marshall and Robin Warren were awarded the Nobel Prize
Speaker 2: in Physiology or Medicine in two thousand and five, exactly
Speaker 2: one hundred years after Robert Koch was given the Nobel
Speaker 2: for his discovery of the tuberculosis bacterium.
Speaker 3: Wow.
Speaker 2: And I read that Robin Warren's wife, Wynn predicted them
Speaker 2: getting the prize all the way back in like nineteen
Speaker 2: eighty four after their first lance at pub was accepted.
Speaker 3: Really.
Speaker 2: Yeah, they went out to dinner and she was like,
Speaker 2: this is going to get you the Nobel Prize.
Speaker 1: That's adorable on so many levels.
Speaker 2: Yeah, isn't that? I really love it? Okay, all right,
Speaker 2: So with that, I'll hand it off to you. Aaron,
Speaker 2: tell me about the eppie of Helicobacter pylauri today.
Speaker 1: Oh, I can't wait too. Today, it's estimated that right
Speaker 1: around half of the world's population is infected with age pylori.
Speaker 2: That's a lot of people.
Speaker 3: It's a lot of people.
Speaker 1: So I found a recent paper that I will definitely
Speaker 1: post a link to because it has some nice maps.
Speaker 1: It's a meta analysis trying to really look at prevalence
Speaker 1: across different countries, and in developing countries the rate seems
Speaker 1: to be about fifty percent, in developed countries about thirty
Speaker 1: four percent, and overall global prevalence at least according to
Speaker 1: this study, was about forty five percent. So maybe it's
Speaker 1: going down a little bit from the numbers that we
Speaker 1: see cited most often. Okay, but obviously not every person
Speaker 1: infected with H. Pylori is going to get gastric cancer
Speaker 1: or even peptic ulcer disease. And there's a lot of
Speaker 1: research that's being done into the mechanisms of how H.
Speaker 1: Pylori causes disease. And one of the big thoughts is
Speaker 1: that it's virulence of the strain of H.
Speaker 3: Pylori.
Speaker 1: So there's a lot Like you said, there's a lot
Speaker 1: of diversity across H.
Speaker 3: Pylori.
Speaker 1: There's a lot of different strains, and some of them
Speaker 1: are more virulent than others, some produce more inflammation, and
Speaker 1: it tends to be that those that produce more inflammation
Speaker 1: are associated with higher risks of cancer, and it also
Speaker 1: could just be individual genetics. So if you are a
Speaker 1: person who's genetically predisposed to cancer and you happen to
Speaker 1: get an H. Pylori infection, then your risk of cancer
Speaker 1: might be additionally increased.
Speaker 2: Okay, but that's those.
Speaker 1: Are small studies in their infancy. We don't really know
Speaker 1: who is going to get cancer if they have an H.
Speaker 1: Pylori infection and who isn't at this point, right, So yeah,
Speaker 1: I found some a really interesting in one little paper
Speaker 1: that I'll link to where they talked about hookworms. Oh,
Speaker 1: they talked about helmets, and people are saying maybe infection
Speaker 1: with helmets, which we know can modulate the immune system,
Speaker 1: can reduce gastric inflammation and reduce the risk of cancer.
Speaker 1: So if you're coinfected with H. Pylori and helmets, maybe
Speaker 1: your risk is less of getting gastric cancer.
Speaker 2: Hold on, but that's first of all, that's bizarre. The
Speaker 2: second of all, doesn't didn't we learn that having chronic
Speaker 2: infection with helmets creates an inflammatory state which is often
Speaker 2: leads to an increased risk of cancer generally speaking, totally does?
Speaker 3: Yeah, so I don't understand it's not.
Speaker 1: There is not evidence that this is true in humans.
Speaker 1: It does seem to work in animal models. Okay, who
Speaker 1: knows it decreases your risk of gastric cancer but increases
Speaker 1: your risk of colorectal cancer.
Speaker 3: I don't know.
Speaker 2: I mean, you lose if you do, you lose if
Speaker 2: you don't.
Speaker 3: Right, we'd never win. Yeah, the bacteria always win.
Speaker 2: That is that's going to be on the gravestone of humanity.
Speaker 1: Yeah, So, in terms of gastric cancer, I thought people
Speaker 1: might be interested in some gastric cancer stats since that's
Speaker 1: kind of the most serious outcome of H.
Speaker 3: Pylori infection.
Speaker 1: I'm definitely Yeah, depending on what source you read, gastric
Speaker 1: cancer is either the second or third leading cause of
Speaker 1: cancer death.
Speaker 2: Really yes, wow.
Speaker 5: I know.
Speaker 1: I didn't realize that it was so high either. So
Speaker 1: the first is lung dizzy lung cancer. Okay, that's the
Speaker 1: number one cancer diagnosis and the leading cause of cancer death.
Speaker 1: And then the most recent stats that I saw actually
Speaker 1: had colorectal cancer causing more deaths than gastric cancer at
Speaker 1: least in this last year.
Speaker 2: Okay, and this is this is globally.
Speaker 3: This is globally, yeah, worldwide.
Speaker 2: And what numbers are we talking about?
Speaker 3: Great question.
Speaker 1: According to WHO, there were one point zero three million
Speaker 1: new cases of gastric cancer diagnosed in twenty eighteen, one
Speaker 1: million new.
Speaker 2: Cases, million new cases and in one year.
Speaker 1: In one year, and that's estimated, right, and seven hundred
Speaker 1: and eighty three thousand deaths.
Speaker 2: Oh my goodness, I know it's really high.
Speaker 1: For comparison lung cancer, which is number one, two point
Speaker 1: zero nine million cases, one point seven six million deaths.
Speaker 2: Okay, so similar. That's very interesting. Of the new cases
Speaker 2: and the death ratio is very similar with those.
Speaker 1: Yeah, we are, despite so much, not good at treating
Speaker 1: most cancers.
Speaker 2: Yeah, it seems like we have a long way to go.
Speaker 1: Yeah, the death rates for cancers like gastric cancer and
Speaker 1: lung cancer really have not decreased over recent decades. It's
Speaker 1: very very interesting. Actually it's alarming. Yeah, but the overall
Speaker 1: rates of diagnosis of gastric cancer do seem to be decreasing,
Speaker 1: and it's thought that this is due to a number
Speaker 1: of different things.
Speaker 3: But treatment of H.
Speaker 1: Pylori is really high on the list of things that
Speaker 1: we think have helped to decrease the incidence of gastric cancer.
Speaker 3: So that's really cool.
Speaker 2: Well, so thanks again to Marshall and Warren. Marsh mar
Speaker 2: By the way, can I put in a quick plug
Speaker 2: for the Nobel Museum in Stockholm? Yes, tell us all
Speaker 2: about it.
Speaker 3: You just visited.
Speaker 2: I was just there and it was First of all,
Speaker 2: Stockholm is amazing and the museums are incredible and everything
Speaker 2: about it is a wonderful place.
Speaker 1: And I like number one Abba Museum, number two Nobel Museum,
Speaker 1: is that.
Speaker 2: Right, Yeah, probably in that order. And yeah, so they
Speaker 2: have some cool little exhibits on these two, on Marshall
Speaker 2: and Warren, and they have the tube from which Marshall
Speaker 2: drank the inoculate to infect himself. Oh my gosh.
Speaker 1: I get so excited by things like that, like.
Speaker 2: Oh it was throng. I just stood there and I
Speaker 2: was like, I don't care if I'm blocking people. I
Speaker 2: need to see this. So I took a picture. Yeah,
Speaker 2: I'll definitely post it on social media.
Speaker 3: Excellent. Oh I can't wait.
Speaker 2: Yeah.
Speaker 1: Oh I love those kind of museums. They're so fun.
Speaker 2: They are so fun. Okay, sorry I totally interrupted you.
Speaker 2: So tell me. So what's going on with research or
Speaker 2: more preventative things for gastric cancer and peptic ulcers in general.
Speaker 1: Yeah, So there's a vaccine that's awesome. It's awesome, it's
Speaker 1: super exciting. It's undergone at least phase three clinical trials,
Speaker 1: which is usually sort of the last phase before things
Speaker 1: get licensed in China. It's an oral vaccine, but I
Speaker 1: know that I found studies earlier studies on injectable vaccines
Speaker 1: as well, but I think in this case, an oral
Speaker 1: vaccine makes so much sense because it's, first of all,
Speaker 1: it's a GI bacteria, So giving something orally means that
Speaker 1: the vaccine is producing immunity in the cells that are
Speaker 1: actually going to be exposed to the bacteria, right, So
Speaker 1: it's a great idea. But oral vaccines are also a
Speaker 1: lot easier to administer. You don't have to have specialized
Speaker 1: medical personnel. So I love that it's an oral vaccine.
Speaker 1: And the efficacy that they found so far is about
Speaker 1: seventy percent effective in preventing infection with H. Pylori, which
Speaker 1: is super exciting.
Speaker 2: Yeah.
Speaker 1: So I'll post a link both to the there's the
Speaker 1: phase three trial paper and then there's also a really
Speaker 1: cheeky paper.
Speaker 5: I want to read you the title of it. So
Speaker 5: it's called at last vaccine induced protection against Helicobacter pylori
Speaker 5: at last.
Speaker 1: So I'll post both of those on our website as
Speaker 1: well so that you can read more about it. But yeah,
Speaker 1: there is a vaccine which is very exciting. I'm not
Speaker 1: sure how much longer it will take to get to
Speaker 1: market in China, where you have higher prevalence of H.
Speaker 1: Pylori than you do in the States, and how long
Speaker 1: it might take to get it in the States, but
Speaker 1: it's pretty huge and very exciting.
Speaker 2: Yeah, I want that vaccine just in case. Well, I
Speaker 2: feel like, do you feel every time you get a
Speaker 2: vaccine a bit more like a superhuman? Like a superhero.
Speaker 1: We've talked about this. Yeah, I could totally see that.
Speaker 2: Yeah.
Speaker 3: Yeah.
Speaker 1: I also think this is so exciting because we are
Speaker 1: learning more and more about the associations with infectious disease
Speaker 1: and cancer.
Speaker 2: Yes, and other chronic diseases.
Speaker 1: Yes, And being able to produce a vaccine that literally
Speaker 1: pro events cancer.
Speaker 3: Are you kidding me? That's amazing.
Speaker 2: It's incredible. And I think that the number of unexplored
Speaker 2: links keeps growing, and those that are being explored also
Speaker 2: keeps growing, and I think that's just going to be
Speaker 2: one of the big futures of medicine is finding these
Speaker 2: links between infectious disease and chronic disease.
Speaker 3: Absolutely.
Speaker 1: I agree we're biased because we love infectious disease.
Speaker 2: But yeah, but no, it's it's huge and also really
Speaker 2: important if we can lessen some of the burden of
Speaker 2: disease around the world.
Speaker 3: Absolutely.
Speaker 2: Yeah.
Speaker 1: Oh so, yeah, that's h pylori.
Speaker 2: Wow. I really liked this one too.
Speaker 3: It was really fun today, had a great.
Speaker 2: Time researching it and talking about it. It's fun and
Speaker 2: learning about it. Yeah. Okay, all right, so should we
Speaker 2: do sources? Let's do it? Okay. So I have a
Speaker 2: bunch of different articles that I read and we'll post.
Speaker 2: I'll post all of these, but two I want to
Speaker 2: shout out. So one was called a century of Helicobacter
Speaker 2: pylori and that was by kid and Maudlin. And also
Speaker 2: I leaned very heavily on this incredibly thorough and long
Speaker 2: interview of Barry Marshall, which is what our first stand
Speaker 2: account was extracted from. So we'll definitely post all of
Speaker 2: those and the other articles as well.
Speaker 3: Excellent.
Speaker 1: Yeah, you can find all those on our website This
Speaker 1: podcast will Kill You dot com under the episode's tab.
Speaker 1: You can find all of our sources from this episode
Speaker 1: and every episode, and.
Speaker 2: What about you, any sources? None?
Speaker 1: I mean I shouted out the one and I'll post
Speaker 1: links to all of them, so okay, yeah cool.
Speaker 2: Thank you to Bloodmobile for providing the music for this
Speaker 2: and all of our episodes.
Speaker 1: And thank you all of you listeners. We love telling
Speaker 1: you about disease and we love hearing from you about
Speaker 1: your diseases and the diseases you want us to cover. Eventually,
Speaker 1: we have the longest list ever and it just keeps growing.
Speaker 3: And thanks. We love you.
Speaker 2: Yeah, thank you. Okay, well with that, wash your hands
Speaker 3: You filthy animals.