Speaker 1:

Welcome to the SIBO Doctor Podcast, hosted by Dr. Nirala Jacobi. Medical experts join us to discuss functional digestive disorders, clinical practice, and research as it relates to SIBO and associated conditions. This podcast is intended for SIBO-treating practitioners and aims to help educate how we may best serve our SIBO patients. Head over to thesibodoctor.com and sign up to the SIBO Mastery Program and take your SIBO knowledge to expert level. If you're a patient, you can sign up to the SIBO Success Plan and beat SIBO for good. Please note, this podcast series is not intended to diagnose or treat medical conditions. Ask your doctor before initiating any new treatments. And now over to Dr. Jacobi and the latest episode of the SIBO Doctor Podcast.

Nirala Jacobi:

Welcome to another episode of the SIBO Doctor Podcast. Today, I'll be talking to Dr. Steven Sandberg-Lewis who's a very familiar guest on this podcast because his incredible insight over 40 years of being in practice or probably longer by now. So today, we'll be talking about H. pylori, which surprisingly, we haven't really covered in depth on this podcast over the three and a half years that we've been doing this. So I'm really excited to talk to Dr. Sandberg-Lewis, who is really Dr. Functional Gastroenterology himself. He wrote the book Functional Gastroenterology. And a really incredible wealth of knowledge on all things gut, so welcome Steven.

Steven S-L:

Thank you. My pleasure.

Nirala Jacobi:

Okay. So H. pylori, it's got a long history. I would like to cover in our conversation where we've been, where we are now, what's happening with diagnosis and treatment, and hopefully get some really good insights for practitioners as to what's the current status of H. pylori. Take it away.

Steven S-L:

Well-

Nirala Jacobi:

Where are we at right now with it?

Steven S-L:

I think we're in a kind of a mess, that's where we are. And as we discussed a little earlier, the two of us, I think that part of the problem is that it's assumed that the dictum is test and treat. So if anyone gets tested, it's expected that they are then going to be treated with standard therapy, triple therapy or quadruple therapy. And there's lots that we can talk about how that's losing effectiveness. And there's lots that we could talk about how the idea that if you find H. pylori on a breath or a stool or a blood antibody test, you're expected to eradicate it as if the only good H. pylori is a dead H. pylori. And I have a two-hour lecture that I do on that and I often call it that. I say the only good H. pylori is a dead H. pylori, right? And the answer is, not necessarily.

Steven S-L:

So first of all, a book that I think all physicians and anybody else who wants to should read is the book Missing Microbes by Martin Blaser. Dr. Martin Blaser is the head of the microbiome research lab at New York University Medical School. And it's a great book, explains the research that he and his group and others have been doing for almost 40 years now on the essential place that H. pylori takes up in the gastric microbiome. He calls it basically the center, the most important organism of what he calls the ancient dominion organisms of the gastric microbiome, which sounds very poetic, which I enjoy.

Steven S-L:

But the research says that H. pylori has been in the human stomach for at least 60,000 years, maybe 100,000. And so I usually say 80,000 just to be fair. And then basically, throughout the entire world, H. pylori was the central organism in the stomach for 100% of mankind and womankind. And then we've been trying to kill it off since 1995 or so when it was accepted after being initially ridiculed. Now, it's the dictum, test and treat. What I really want to focus on is who not to test because if you test them and you find it, it may be just the commensal H. pylori.

Steven S-L:

And if I find H. pylori in someone who doesn't have symptoms that would have required that they should be tested, meaning symptoms of an ulcer, peptic ulcer, or a very high family risk of gastric adenocarcinoma, or the third thing would be just the rare situation that someone has gastric lymphoma, also called MALToma. That's a situation where I'd always agree, if someone has H. pylori and they have MALToma, gastric lymphoma, they should be treated, and certainly if they had recurrent peptic ulcers, especially duodenal ulcers. I think that makes total sense. But very little else do I think makes sense to treat for H. pylori. And I certainly have seen a handful at least of patients whose H. pylori triple therapy was the beginning of their SIBO problems. You probably have as well.

Steven S-L:

So, in addition, it turns out that every mammal on earth that's been tested has a Helicobacter in their stomach, whether it be whales or cheetahs or pigs, there's a Helicobacter specific species for each type of animal that's a mammal. So we expect it to be there. And so, to kind of give you the last chapter of the book Missing Microbes, spoiler alert, is that what Blaser really thinks will happen in the future, because in the US, we're down to less than 5% of children having H. pylori, and that's when it does really all of its essential function as a commensal in the stomach to fully develop the immune system in the gut. He thinks that in the future, once our FDA allows it, because right now, it would be total heresy and never accepted, we would have multi-strain H. pylori probiotics that we would give to newborns because maybe 4% of newborns have it now and kids have it, which is creating a lot of immune problems for us as doctors that we have to treat, and it's going to get worse.

Steven S-L:

And then maybe when they get into their forties or fifties or sixties, if they develop a very reasonable H. pylori-related problem, then it could be killed, but you want people to pass it on during their reproductive years to their kids. Or if they don't have it, and less than 10% of adults have it now, using these kind of probiotics. But we don't have that at this point. So a lot of immune dysfunction is being passed on and developed in early life.

Nirala Jacobi:

Yeah. He really goes into that in the book as well. I often recommend this book as an educational tool to practitioners, so they really can understand the significance of H. pylori as well. And so just to summarize also for those who are listening who are not practitioners that H. pylori, when we say commensal, we mean it's a normal organism that's supposed to really be there in small amounts and have a symbiotic relationship with us. And so what you're saying is, there's a few things actually I want to kind of unpack a little more, so when you say that when somebody is symptomatic for H. pylori, and H. pylori obviously can cause inflammation, can ultimately, at some point, the risk is development of, like you say, gastric cancer, and so the recommendation has always been to treat it if you find it. And the symptoms that you think require testing, that's a bit up for debate because a lot of people get tested just when they have heartburn or reflux, rather than just the classic ulcer symptoms. So would you not test somebody that simply has reflux, for example?

Steven S-L:

Yeah. I think that that is a terrible idea to test people with reflux who don't have ulcer tendency. It makes no sense because the predominance of research into H. pylori and reflux is that it protects against reflux if you have it in your stomach, and it protects against the complications of reflux, such as Barrett's esophagus and cancer of the esophagus. And they think that because there's been such a reduction in H. pylori, and then now in children, the incidents of reflux and its complications, Barrett's esophagus and cancer of the esophagus, have gone way up since the 1980s when we started to do this. And of course, Blaser's research also shows that, at least in mice, repetitive courses of antibiotics, single antibiotics, not triple therapy, over a lifetime often gets rid of H. pylori as well, unintended. So that's-

Nirala Jacobi:

That's why we're seeing the decline in H. pylori and, well, this real dramatic decline, as you say, if all mammals are supposed to have some species or some form of H. pylori and we're down to 4% of newborns having it, it's a dying ancient species that we don't even know, really, the repercussions of wiping it out. But back to this idea of somebody testing positive that just has reflux. This is where the conundrum lies, is what we started the conversation with, because if you test positive at that point, there is sort of this obligation by the physician to treat this organism, which may or may not be part of what's been happening. Is that right?

Steven S-L:

Yeah. So let me break it down a little bit more. So, according to research, when basically anybody has H. pylori in their stomach, initially they have a reduction in acid. They have hypochlorhydria, at least for the first three months. And that may be part of what reduces the risk of reflux is that they have less acid, but there are other factors because reflux could be neutral as well, it doesn't have to be acid reflux. But there's basically two patterns that I'm aware of in the research with H. pylori gastritis. So gastritis, peptic ulcer, stomach cancer, adenocarcinoma, and lymphoma of the stomach, those are the four classic H. pylori-related conditions in the stomach. And when gastritis occurs, it almost always occurs if H. pylori is there, so there's some thought that gastritis, a mild gastritis, may be a normal state. In fact, it may be part of the priming of the immune system by having this low-grade inflammation, which we know occurs throughout the entire gut, a low-grade inflammation. And that's what tells the immune system what's going on, like there's an interface there that is monitoring what's going through the digestive tract.

Steven S-L:

So, two patterns of gastritis predominately. One is antral-focused gastritis. And for those who aren't physicians, antrum of the stomach is the bottom of the stomach leading to the pyloric valve, it's like the little entryway into the pyloric area. And antral-focused gastritis tends to cause hyperchlorhydria, hyperchlorhydria. And that is because, for those who are interested, the G cells in the antrum, which are the cells that produce gastrin, which is the major stimulus for stomach acid production, when you have a gastritis there, the G cells, I guess, get kind of irritated and they produce more gastrin, hypergastrinemia. High levels of gastrin in the blood are typical in this case.

Steven S-L:

And because the focus is only in the antrum, the body of the stomach, which is the major, bigger part of it that's higher up toward the esophagus, that's where you have parietal cells, cells that can actually be stimulated by gastrin to make more acid. So if you have a antral-focused gastritis, you have more stimulation to make acid and you have cells that can do it. So that's one type of H. pylori gastritis, and seems like everything points to that smaller group of people that have antral gastritis are the ones more likely to have ulcers, peptic ulcers, because they produce excessive amounts of acid.

Steven S-L:

Now, the more common type of H. pylori gastritis is pangastritis. The entire stomach lining is inflamed, mildly or more so. In that case, that gastritis leads to atrophy or shrinking of tissue. And a lot of that is parietal cells, which are in the body of the stomach. So you actually lose parietal cell mass, you have fewer parietal cells, and it doesn't matter whether you have a lot of gastrin in your blood or not, they can't respond. So you tend to have long-term hypochlorhydria in that group, the people with pangastritis. And they're not going to get ulcers, they're more prone to stomach cancer over decades, and it's less than a 1% risk, it's not a high risk. But these are the folks that are more likely to get stomach cancer.

Steven S-L:

So certainly, I think an approach would be, if your patient has peptic ulcer disease, and they're hyperchlorhydric, and they have H. pylori antral gastritis, it makes a lot of sense if their ulcers keep coming back after treatment. It makes a lot of sense to treat them because it fits. If they just have reflux, which we know H. pylori is protective against, it doesn't make any sense to even test them because then you're expected to treat them and then they're more likely to have more complications and negative effects and more likely to have reflux, even if they didn't have it before treatment. If you just test everybody, you just do stool testing on everybody, and check them for H. pylori, I don't use those tests. I use stool tests that don't check H. pylori because I don't want to know because then I'll be expected to treat them. All these people with commensal, not very many, but maybe 10% of the population that has commensal H. pylori is still present. Is that enough to chew on for right now?

Nirala Jacobi:

I have a few questions about this, and we'll get into the different types of testing in a moment. But one thing to clarify is, how does H. pylori protect against reflux? That's one. And two, what you were mentioning was really interesting to me was serum levels of gastrin could be indicative of hyper and hypochlorhydria. So, I mean, you always got to go with the symptom picture and I have some patients that are severely hypochlorhydric with high gastrin levels, and what you're saying is, at least in the initial stages, you could have high gastrin as a result of just having this antral gastritis.

Steven S-L:

Yeah, or even pangastritis. But in that case, like you said, in that case, you have fewer parietal cells and you're not going to get hyperchlorhydric, you're probably going to be hypochlorhydric with the same stimulus. But the body in its wisdom is still trying to get some acid production, so it's stimulating gastrin. The same thing occurs when patients take proton-pump inhibitors, they end up with hypergastrinemia, which is thought to be the mechanism behind rebound hypersecretion.

Steven S-L:

So I didn't know about this, I just looked at a study a couple of days ago that showed that they did a study with people that didn't have heartburn, didn't have hyperchlorhydria, they gave them proton-pump inhibitors for just one month, and a good percentage of them, significant percentage, developed heartburn and hyperchlorhydria because of the rebound effect. You get high levels of gastrin when you're taking a PPI, and then when you stop taking it, you still have high levels of gastrin, but now, your stomach parietal cells, their proton pumps can respond because you're not taking the inhibitor and now you're going to have excessive acid and you may have many symptoms from that. So they were actually showing that you could have iatrogenic reflux in people that didn't previously have it.

Nirala Jacobi:

So how does H. pylori protect from reflux?

Steven S-L:

Well, it just depends what mechanism you want to create in your mind, because I don't know it's been proven, but I think that the easiest explanation is the hyperchlorhydria, the, excuse me, hypergastrinemia that occurs from H. pylori antral gastritis irritating those G cells that produce the gastrin in the antrum and the levels in the blood getting very high because it's a hormone, right? It's secreted by these G cells into the blood and it's a blood hormone. But then when it gets back to the stomach, if the parietal cells can respond, they'll respond to it. Goes all the way around the, I guess, it goes all the way through the whole circulation, comes back to the stomach, and it can have effects if the parietal cells can respond. So I think the hypergastrinemia from H. pylori antral gastritis explains-

Nirala Jacobi:

Yeah, I'm still unclear about how it protects.

Steven S-L:

Oh, I'm sorry. How does it protect against-

Nirala Jacobi:

Yeah.

Steven S-L:

Oh, sorry.

Nirala Jacobi:

Against reflux, yeah.

Steven S-L:

Sorry. So the majority of H. pylori gastritis is pangastritis. Because of that, it's sort of nature's own proton-pump inhibitor.

Nirala Jacobi:

Mm. That makes sense, yeah.

Steven S-L:

So even though it causes hypergastrinemia, relative, depending on how much gastritis there is. If it's mild, then that's probably not the case. Yeah, the parietal cells can't respond, so you have less acid. And now, of course, I'm writing a book on reflux, right? So I'm-

Nirala Jacobi:

Oh, great. Excellent.

Steven S-L:

Yeah, I hope it'll be done by the summer. But certainly, we know that you can have reflux symptoms even if there's no acid in your stomach. There's such a thing as neutral and even alkaline reflux, which can cause many symptoms, but the kind that we're normally talking about that leads to erosive disease in the esophagus and all of its complications is usually either acid or acid plus bile, which are very erosive. So having a nature's own proton-pump inhibitor could certainly reduce that tendency toward erosive esophagitis.

Nirala Jacobi:

That makes a lot of sense. And for those of you who are listening, Dr. SSL and I did a podcast on reflux a little while ago, so you can review that, where we talk about bile reflux and Barrett's and all of that, but this podcast, I really want to rein into just touch on H. pylori because there's so much to talk about. Let's talk about testing before we go into treatment. So really, just as a take-home from that section is, for those of you who are listening, if you only have reflux, then just testing for H. pylori isn't the right approach, is what you're saying. Unless you have... Can you just briefly talk about the symptoms of peptic ulcers just so that people understand the difference between just reflux and those symptoms?

Steven S-L:

Yeah. It'd be simpler if I hadn't studied this and dealt with this with my patients so much. The truth is, according to most of the literature, only about 50% of people with peptic ulcers actually have the classic symptoms. You can actually have no symptoms at all, especially if you're diabetic and not well controlled, you can have sort of silent ulcers, just like you can have silent heart attacks where you don't actually have the typical symptoms because autonomic neuropathy changes in the autonomic nerves in the GI tract. But the classic symptoms of, let's say... So peptic ulcers, a general term, it's whenever you have an ulcer in the digestive tract related to peptic juice, meaning stomach acid and stomach secretions, right? Yeah, acid and enzymes. So you can have gastric ulcers in the stomach, and if they do occur, they're typically in the lesser curvature, toward the middle, toward the bottom of the stomach, or duodenal ulcers, which are in the first portion of the small intestine. That's the most likely location of first or second portion, first half of the duodenum.

Steven S-L:

The typical symptoms, which maybe only occur 50% of the time when you have them, the typical symptoms of a gastric ulcer would be pain when you eat food. In other words, pain, I always like to say for my students, the typical pain in ulcers is, the pain is where the food is. So if you have a stomach ulcer, when you eat food, the food is where the ulcer is in the stomach, and so it triggers acid and enzyme production, and that causes irritation to the ulcerated area. So, symptoms could be anywhere from pressure or a gnawing kind of pain, like a little mouse is chewing in there, anything up to really severe sharp pain, if they have the typical symptoms. And it would be typically when there's food in the stomach, so especially the first couple of hours or right after eating.

Steven S-L:

Whereas, if it's a duodenal ulcer, the classic symptoms that might occur only about half the time would be pain that comes on when the stomach is empty, when the food's not there in the stomach, it's now in the duodenum, which is where the ulcers are, right? So duodenal ulcers are aggravated when the stomach empties, which is anywhere from, if someone doesn't have gastroparesis, anywhere from two, three, four hours after a meal. So people often wake up at night with stomach pain, upper abdominal pain, similar to what I just talked about, gnawing or pressure or more extreme, like a burning or sharp. And it's better by eating because when you eat food, unless it's some crazy irritating food, but good food, eating food delays gastric emptying, right? As soon as you eat, we know that shuts off the migrating motor complex, which includes gastric emptying. And so, for several hours, you're not going to have much emptying of food into the duodenum. And if the food isn't where the ulcer is, it feels better. You have less acid leaving the stomach, irritating the ulcer, all of that.

Nirala Jacobi:

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