OPTIMIZE YOUR GUT to Fight Disease (Busting Common Gut Health Myths) with Dr. Jason Hawrelak

Content By: Ari Whitten

In this episode, I’m speaking with gut health and microbiome expert Dr. Jason Hawrelak about his absolutely fascinating research on how to best care for your gut and feed your good gut bacteria. Dr. Hawrelak is the most well-informed (and humble!) gut specialist I’ve ever spoken with. 

After this introduction, be sure to explore our new Gut Health Optimization Program, a comprehensive (and highly practical) 16-module course led by Dr. Hawrelak…and unlike any gut program you’ve ever experienced!

Table of Contents

In this podcast, Dr. Hawrelak and I discuss:

  • Three fascinating ways your gut health is connected to your energy levels (or LACK of energy!)
  • The 1 gut problem you should be aware of that can lead to weight gain, insulin resistance, autoimmunity, brain fog, and even Alzheimer’s disease and cognitive decline
  • The connection between your microbiome, dietary fiber, and…brain health!
  • A major probiotic myth that Dr. Hawrelak has been trying to bust for over 20 years and why you might be wasting your time (and money!) on probiotics that aren’t right for you
  • The amazing effects of prebiotics and when to use prebiotics versus probiotics 
  • Dangers of the Carnivore Diet trend and why your gut, microbial, and system-wide health might suffer long-term
  • Dr. Hawrelak’s top 3 gut health tips…including one I didn’t expect!

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Ari Witten: Hey everyone. Welcome back to the Energy Blueprint Podcast. I’m your host, Ari Witten, and with me today is Dr. Jason Hawrelak, who is the Head of Research at probioticadvisor.com. His passion for gastrointestinal health, the microbiota, and probiotics was ignited during the final year of his undergraduate training. Subsequently, he did his honors, first class, and PhD degrees in the areas of gastrointestinal microbiota, irritable bowel syndrome, and the clinical applications of pre and probiotics. He’s written extensively in the medical literature on these topics, including 20 textbook chapters, and his research has been cited over 1200 times.

I will say also on a personal note, that I’m taking a course with him right now. I’ve been absolutely blown away by his knowledge, I’ve learned a ton myself and I think– I’ve interviewed many, many gut health experts on this podcast and friends with many gut health experts personally and I will say that he is absolutely in the crème de la crème. The highest echelon of everybody that I know and in my opinion, probably the single most knowledgeable gut health expert I’ve ever had the pleasure of learning from. I’m very excited to share his knowledge and wisdom with you guys. Welcome to the show, Dr. Hawrelak. Such a pleasure to have you.

Dr. Jason Hawrelak: You’re very welcome. Thank you for having me. Thanks for those kind words too. I’m humbled. I think it’s the right word.

The gut health - energy link

Ari: Yes. I think as a general starting point, broad question, maybe as an entry point, especially given this is the Energy Blueprint Podcast, we could talk about the relationship between gut health and energy levels, and some of the key mechanisms there, maybe the gut-mitochondria access or any other aspects you want to talk about, the gut-brain access. Any of the key mechanisms that you see linking gut health with energy levels.

Dr. Hawrelak: That’s a great way of introducing the area actually because I think for me when I’m looking at this, and I’m looking at gut health in general, there’s probably three components, broad components I look at. Number one would be gut motility, and how long it’s taking food to go make its way through, and essentially around colonic motility, or more likely lack thereof. When people actually have fecal loading or constipation.

When we get the situation where fecal matter is in there for a fair period of time, and for some people this can be 10, 15, 20 days, actually transit time from mouth to toilet bowl, as I tell my patients. It’s an easy thing you can test at home, and I think everybody should be totally on to this and be aware of this, but you can have some corn on the cob, or some red quinoa, black quinoa, or even some green peas, don’t chew them particularly well, don’t choke, but don’t chew them all that well, you want to be able to see them come out the other end.

Just take note, write down when you actually ate it, keep track and look at your bowel movements in great detail over the coming days and see when it starts coming through. I’ve had patients who were doing a lovely type four stool, which is a Bristol stool, which somebody would call the perfect poo, every single day and never missed a day and it took 10 days for the corn to come out the other end. I’ve had other patients who were only pooing every two or three days, there was 26 days before the corn came out the other end.

If you could imagine how much you’re reabsorbing from that. It’s something that Hippocrates said, “Death sits in the bowels,” since all disease begins in the gut. I think this is one of the concepts around that, is that when we have– Older [unintelligible 00:04:05] called this bowel toxemia and that we’ve got this old fecal matter there that’s constantly leaking bacterial toxins into the system.

That’s one of the key things we look at, is looking at transit time and if transit time is slow, then we’re obviously absorbing through the colon mucosa a lot more of those toxins. Particularly what I’m referring to is endotoxins or also known as lipopolysaccharide, which is part of the cell wall of gram-negative bacteria, which is a group of bacteria in the gut. One consideration is that, is transit time. Two is microbiome composition. This is also fits in with the endotoxin or lipopolysaccharide.

Because people’s ecosystems they’re all unique. My ecosystem will not look like yours. You can take 1000 people and there’ll be some similarities obviously, but there’ll be market differences. Just like your fingerprints are unique, your microbiome signature is unique and more similar to your siblings and your mom, probably than anyone else in the world, but it’s still quite different. Within that individual composition, there’ll be certain ecosystem traits that you’d see as pro-inflammatory, depending on the composition.

If your ecosystem contains greater amounts of what we call gram-negative bacteria, but that’s specific grouping of that called proteobacteria. They’re much more problematic from an inflammatory perspective. 80% of the cell wall structure of gram-negative bacteria is lipopolysaccharide, or endotoxin. This isn’t a toxin that the bacteria is secreting it to make us ill, it’s like, we grow hair, we grow fingernails, it grows lipopolysaccharide. It’s just what it does. Just when they die, they release that lipopolysaccharide into your gut lumen.

Now, some people only have– Like I had patients yesterday with a 0.4% proteobacteria, then I’ve had other patients who are 50% proteobacteria, to probably give the two extreme ends of that. Most people are not in either of the two extremes, but the amount of proteobacteria that’s present, has a huge contributor to potential inflammatory load, essentially because when you’ve got greater amounts of proteobacteria present, and other gram-negative bacteria– There’s other groupings, like bacteriaodities, or verrucomicrobia, that also have endotoxin involved that they grow to, but it’s far less inflammatory. It’s really proteobacteria that we really clue in with because it’s a super inflammatory compound.

We look at the composition there, and we know that lipopolysaccharide essentially works as a- it’s an immensely pro-inflammatory agent. It can cause damage to the gut itself, so cause a leaky gut, but when it reaches the circulation, this is where we know can impact things like blood sugar regulation negatively. Decreases insulin sensitivity, it can damage the blood-brain barrier. It changes with neurotransmitters we produce, and it causes inflammation in the brain and it interferes with mitochondrial function.

We’ve got this situation where we’ve got these bacteria, they’re releasing these toxins, and some people are releasing a lot more of those, and there’s certain dietary choices that we make, that actually can enhance or decrease the absorption of that endotoxin as well. You’d see that you’re having these mitochondrial poisons that you’re absorbing 24 hours a day, and then sometimes with certain meals, you get a spike of lipopolysaccharide hitting the bloodstream, and that’s termed into toxemia now, or metabolic endotoxemia, to be a bit more specific. That’s the other aspect, is looking at microbiome composition from a pro-inflammatory perspective.

Then conversely, we have other species in the gut that we would see as having the opposite effect of anti-inflammatory compounds. Those have capacity to promote gut healing. You might put species like most people are familiar with, like bifidobacteria is one that we would see as having anti-inflammatories and the gut healing qualities. There’s others that are less well-known, like Akkermansia muciniphila is also a species that we see as helping promoting gut health and gut integrity and subsequently helps with blood sugar regulation, and even helps determine your metabolic rate, which I think is super cool, too.

There’s another bigger group that we call butyrate-producing species. I think you can see butyrate is almost the counterpoint of lipopolysaccharide in that butyrate has a healing, anti-inflammatory effect in the gut. It is the main food source for your colon cells. Many people, we’ve been aware of that aspect of this for a long time, but I still think it’s pretty amazing to think that we’ve evolved, relying on bacterial production of this compound to feed a certain group of ourselves that are really key for our good health.

The issue here is, if we don’t have enough butyrate-producing species, we don’t make that much butyrate as a consequence of that. That any butyrate we do make in the gut is avidly consumed by our colon cells and none of it reaches the body-wide circulation. It’s only when we make enough butyrate that exceeds our colon cells capacity that butyrate reaches the systemic circulation, floats through the area, and then we get the anti-inflammatory effects body-wide of butyrate and it has a healing effect on the blood-brain barrier, decreases neuro-inflammation and improves mitochondrial function, improves blood sugar regulation, improves metabolism.

It’s a pretty amazing substance actually, butyrate. The more we research it, the more stunning we actually find that it is is. We’ve got these little factories in us. All of us do. The population can vary dramatically too. The lowest I’ve seen is 2% of an ecosystem being butyrate-producing species, and the highest I’ve seen is like 65%. Again, a huge variation there that can determine how much of an anti-inflammatory effect we’re getting from that microbiome versus the pro-inflammatory effect that we get when it’s more proteobacteria and more lipopolysaccharide.

I think the third thing to look at is gut integrity. When the gut is what we call the leaky gut or intestinal hyperpermeability. We have more of the lipopolysaccharide that actually leaks through into our systemic body-wide circulation. We get more of the negative aspects to our health. Essentially, inflammation that goes everywhere, but people will have their own weak areas where I think that inflammation will become more manifest.

That will differ a bit per person, where some people with endotoxemia will start developing insulin resistance, some people start developing weight gain. Other people, I think it’s going to roll personally with autoimmune conditions as well. Some people get brain fog. We know that endotoxins are pretty pivotal role with something like Alzheimer’s disease and cognitive decline. There’s been some very cool research where they’ve done autopsies of the brains of Alzheimer’s patients, and they’re super rich in endotoxin. People who do not have Alzheimer’s, it’s not rich with endotoxin. It’s not in their brains. Nowhere near as this degree.

For me, it’s those three areas that I’m always looking at. It’s like, what’s gut integrity like, what’s the microbiome composition look like, and what’s your transit time, because alterations in any of those three things can certainly play a pivotal role with essentially your inflammatory status. I think that flows into cognitive function that flows into just levels and energy I would suggest too for that matter. Then people got two out of three or three out of three not working well, or are balanced. Then we get major problems.

Butyrate for brain (and gut) health

Ari: Good stuff. I want to mention you’re on your number two point about short-chain fatty acids and butyrate. I interviewed Datis Kharraziani and Dr.  Kharrazian recently, a few months ago, and he actually listed butyrate as his number one compound for brain health as far as supplements he was recommending. I was a bit surprised by that. I was expecting maybe curcumin, or polyphenols, or something like that. Centrophenoxine. Who knows? [unintelligible 00:12:46]. He went with butyrate, and he just raved about the effects on brain health in particular. This is widely regarded as one of the world’s top brain health experts who was saying that.

Dr. Hawrelak: That’s very cool, yes. I remember there was a paper published, I think was 2016. That was one of the earlier ones in a neurology journal talking about how do we improve brain health. Let’s give people fiber. It’s like, that was pretty mind-blowing. I think seeing that in a mainstream neurological journal was great because it just means that it’s people, particularly the top research experts are totally concluding to this, but their message is seeping out. I think that’s pretty amazing that’s the number one. I think it’s so cool because we actually have these butyrate-producing factories already there. We just have to make sure that we’re feeding them to actually get that benefit.

What to look for in probiotics

Ari: Yes. Actually, that’s a point I want to circle back to, fiber and butyrate consumption, later in the podcast. Let’s talk about probiotics. This is a huge area of passion for you, and something a ton about, and I’ve already learned a ton from you on this topic. Things that I didn’t know. For example, the importance of strain specificity. I was blown away by a lot of the research you presented on that topic, which is something I’ve historically brushed off as unimportant.

I thought it was mostly a marketing gimmick that had people say, “Oh, this strain of Lactobacillus rhamnosus versus that strain.” I’m like, “Ah, they’re the same species. How different could they possibly be?” I’ve seen from a lot of research that you’ve presented, they are very different in many cases. First of all, can you talk about what a probiotic actually means? Then I want to talk a bit about some common probiotic myths, and then the strain specificity.

Dr. Hawrelak: Most of us have a vague idea what probiotics are. Beneficial microbes. I think the strict definition is live microbes that when administered in adequate amounts and confer a health benefit. I think you can see that as having a few different components of the definition. Is, one, they’ve got to be alive. If you’re having a supplement that contains dead bacteria, and it can still be very helpful, but it won’t be a probiotic at that point. In fact, it should be termed a postbiotic, technically speaking.

The other aspect is that it confers a health benefit too. There’s certain parts of the world and certain research scientists in this field who take that very seriously. Whereas if you have a strain of Lactobacillus acidophilus or Lactobacillus rhamnosus that has no research on at all, they wouldn’t call it a probiotic. They’d be like, “Okay, that’s a bacterial strain that may or may not have any therapy benefit.” I think that’s the other interesting aspect of that definition as well as adequate amounts.

This is where this does differ a bit per strain. That there’s some pretty amazing research on Lactobacillus reuteri strain DSM-17938, which is sold around the world is BioGaia. The research studies often use 100 million CFU, so colony forming unit. It’s 100 million microbes. It gets these great results. It’s not good for everything, but it’s good for a lot of different things. From viral gastroenteritis, preventing antibiotic-associated side effects, even prevention of SIBO in people who take proton pump inhibitors.

A decent spread of applications. All of that very tiny dose. Where some people go, “There’s nowhere near enough. We have to give 100 billion on 10 different strains to get any impact.” It’s clearly not the case from research. I think that’s one of the probably flow into this particular myth that sometimes there’s a mythology that we have to give mega doses, or it has to be mega high potency multi-strain to get any sort of positive impact. That’s clearly not the case. Then we’ve got hundreds of research studies showing single strains even at relatively low potencies of 100 million or one billion microbes having therapeutic effects clearly in the literature.

The probiotic strains matter

Ari: Very, very interesting. As far as strain specificity, can you give a few examples of how that plays out in some specific studies about specific species of bacteria for specific outcomes?

Dr. Hawrelak: Yes. This is an area like when I did my training, I trained it at– My [unintelligible 00:17:18] training was in the late ’90s, we didn’t cover strains really at all. It was like very superficially. Mostly stuff was talking about species. It’s only when I started delving into it part of my PhD, it was like, you become familiar with these new concepts of, I delved into prebiotics, which I really only knew superficially, delved into probiotics, and it’s like, “Oh my God, there’s actually dramatic differences in terms of characteristics of qualities. Never mind therapy actions. Strangers in the same species.”

For those people who are less familiar with the concept of strain, I think a good analogy here is like breeds of dog. All dogs are Canis familiaris. They all have certain traits in common, but there are differences, but they’re all the same species. With bacteria strains within the same species, we don’t have the same physical characteristics that look different, but we know that we can subject them to different exposures, and they will react differently. Some strains within a certain species will tolerate stomach acid, and some won’t. Some will tolerate bile. Some won’t. Some will attach to your gut. Some won’t. Some will stay in your gut for a few days. Some will pass straight through.

Just to name a few those are the basic characteristics that we’re often looking for with probiotics. We’ve known for a long time you can go back to research in the 1970s that we’re looking at. Let’s isolate 15 strains of Lactobacillus acidophilus and let’s expose them to the gut stomach acid. You can see even then that some strains could tolerate those things, some things did not.

I think it was a study in 2010 where they took, I think it was 90 strains of lactose– I think from memory was fermentum. They said, “Okay, let’s expose these 90 strains to stomach acid. Let’s expose some to bile. Let’s see how many to tolerate both those things well.” I think it was, from memory, is 4% of those starting materials could actually tolerate stomach acid and bile to the point that they could their theoretically survived transit to the upper gut. The rest would have all died. I think that’s one of those clear examples.

There’s looking at another species, Lactobacillus reuteri. There’s certain strains of Lactobacillus reuteri that can produce an antimicrobial compound called reuterin. Reuterin is effective against fungal pathogens, is defective against bacterial pathogens, but we can’t assume that all strains produce it, because they don’t. Only some strains do. Even if it has the name Lactobacillus reuteri, it does not mean it produces reuterin. Those strains that do not produce reuterin are very unlikely to have the same benefits from a microbiome alteration perspective. Either against fungal dysbiosis or bacterial dysbiosis as those that produce reuterin.

Then the strain that we know that’s probably the biggest from the research base, is the one I mentioned before the DSM 17938, which is in BioGaia. Which has got this cool study where they gave it to essentially kids who are taking a proton-pump inhibitor, which is the class medications that probably many of your listeners are familiar with and gosh, a lot of people take. In Western nations, it’s huge because it suppresses stomach acid output. It’s used to treat reflux disease essentially, also peptic ulcer disease, but that’s usually a shorter period of time.

A high proportion of people who take his medication, they develop SIBO, small intestinal bacterial overgrowth. There’s some debate about how much that is, whether it’s 50, 60, 70% of these people will develop it, but it’s pretty the marked anyway. This study was, “Okay, well, what happens if we give a probiotic alongside the proton-pump inhibitor, will it prevent SIBO from developing?”

This is what the study did. They gave a placebo, they gave this particular strain of a Lactobacillus reuteri. I think SIBO developed in 56% of those in the placebo group versus 6% of those in the probiotic group. I think what’s interesting here is that there’s another study using a combination of two different probiotic strains at maybe 10 or 20 times a dose, the same similar model.

Let’s give it to people taking proton-pump inhibitors. It did not work, it didn’t actually stop people from developing. It’s not something that all probiotics do. This particular strain we know produces reuterin, and reuterin works against fungal and bacterial pathogens and prevented the overgrowth from occurring. Which I think is one of the things that’s pretty amazing and it means we just have to make sure that the strains that we’re choosing for tags has got the qualities and actions that we’re after.

One of the few studies that actually directly compared two different strains in the same study was for viral gastroenteritis. Which is something that all kids end up getting. All of us will often dig it from our kids when they bring it home from daycare. It’s immensely common. This condition generally is short-lived, but it can result in hospitalizations and dehydration, and death in kids. It often does still, even in Western nations because of the dehydration aspect, even though it’s not, directly causes death is more indirectly via dehydration. Having treatments that shorten the duration, and decreases severity, are extremely welcome.

In this particular study, they compared these two probiotic strains, the same species, Lactobacillus rhamnosus, one with Lactobacillus rhamnosus GG, one with Lactobacillus rhamnosus lactophilus. Gave these kids one of either the two. The kids that took the LGG, they got better 24 hours sooner. 24 hours is big. If you’ve got a kid that’s got vomiting and diarrhea, you will notice 24 hours less of vomiting and diarrhea. It also enhanced secretory IgA production, one of the main immune markers, the way that the immune system was dealing with, pathogens like viruses in the gut. Whereas the other lactophilus rhamnosus did not.

This is again, the same species, just different strains. There’s a lot more examples in terms of other characteristics that we could go into as well. I think it is very clear if you look at the literature it’s definitely not a marketing thing. I hear you because I think there’s a lot of [unintelligible 00:23:22] and I think this is partly because the industry promotes that idea. Some in the industry do. Generally, the companies that are-

– supplements that don’t have research yet. That’s right. They don’t list their strains or they use strains with no research base. They don’t want people to know about the strain specificity, they want to cloud at the waters and they do that effectively. This is something that I’ve been trying to bust for seriously 20 years. I’ve been trying to let practitioners, clinicians, and the general public, but mostly I work with training clinicians this information so that they can really see through that the cloudiness that’s being put out there because the research is clear if you look at it. That there are generally big differences.

Now for certain conditions, it may not matter so much, well, in maybe the similarities of the capacity of if bacteria strains to produce acetate, and that all of them probably will share within any given species. Although there will still be differences in terms of how I’d say produce certain food substrates, they all produce acetate, for example. That might mean for certain conditions it won’t matter as much. You might put, maybe post antibiotics trying to restore a bit of gut health, something, maybe it won’t matter quite as much, in that case, because maybe just a change in pH it’s all that’s required to help in that case.

Now that said, it matters heaps when we’re actually giving it alongside the antibiotics, where we know that certain probiotics make no difference. There’s this cool study that was published in the Lancet, it’s a huge medical journal in terms of reach and how high it is from an impact factor perspective that used, I think it was 60 billion CFU of four different probiotics strains to try to prevent antibiotic-associated diarrhea. I think it had like over a thousand patients. It’s a big study. Did not work. Yet we’ve got other strains where you can give– We’ll go back to that Lactobacillus reuteri DSM 17938, 200 million CFU. It works to prevent antibiotic association diarrhea.

We know [unintelligible 00:25:33] antibiotic strains definitely do matter, but there will be some applications where I think, probably after antibiotics, well we’re just trying to get more, change the pH of the environment to help indigenous populations that we want to support to grow back a bit more quickly, may not matter quite as much.

Ari: Got it. The big picture summary of this is strain specificity, not just a marketing gimmick, often matters in a massive way and can be the difference between something working exceptionally well versus not working at all even within the same species. Like a Doberman and a Chihuahua are the same species. One is a really good guard dog one is not such a good guard dog.

Dr. Hawrelak: That’s exactly right. You might have a catalog or something that’s good for certain tasks, but not good for other tasks. That’s what we tease out with research on these strains is that one is good for antibiotic-associate diarrhea but completely useless for depression or one might be good for antibiotic-associate diarrhea and not good for preventing urinary tract infections. Then we’ve got that clear example of strains within species that are already out there. I think that the dog analogy is helpful in a couple of ways.

Ari: Absolutely. It was helpful for me when you presented that, I was like, “Wow. Yes, I never really have considered that.” They’re all the same species and they are radically different as far as their function. I have a couple of Australian Cattle Dogs and they’re built for a certain function and they’re not good for a certain function. If I’m laid out in bed or I have an elderly person in my house who just needs a companion to lay by their side in an apartment all day, this is a really bad choice of dog for that purpose.

Dr. Hawrelak: It is.

Ari: It’s used to be out running around all the time.

Dr. Hawrelak: I used to have a Red Kelpie and they’re bred to run like 60 kilometers a day or something like that. They’re just like little battery cells, there’s never run out of energy. Not good for keeping your elderly relative company.

Ari: Exactly.

Dr. Hawrelak: No, but very good for the other tasks. Definitely.

ProbioticAdvisor - key to finding the strains to help your condition

Ari: It might be worth mentioning. You’re the Head of Research of ProbioticAdvisor. This is a company that I learned about through you and I signed up for, and I have been absolutely amazed by that. I didn’t know a tool like this even existed where I can go in and type in a particular condition. For example, my two-and-a-half-year-old, since we potty trained her started suffering from some constipation and instead of having a bowel movement every day, it became every two or three days.

I can look up probiotics specific to that function or probiotics specific to hand eczema or antibiotic use. How do you minimize certain complications when you’re on antibiotics? It brings up the search results of all the specific research on specific strains of probiotics that have actually been shown to be affected in that specific context. It’s an amazing tool that I didn’t even know existed until I started taking your course.

Dr. Hawrelak: Ah, thank you. It started off with just some paper documents is how that started. Seriously it was probably in 2001 when I first started teaching. I probably started my research process, and when first started teaching and it’s like, “Okay, I’m going to pull together these resources and India with three different documents and with 30 pages long or 40 pages long. It’s like, “Okay, I need to put this into a searchable database on bits of paper in the old way.”

I think we now have that capacity to really look at the research because research is built up so much over the last 20 years that we can, we don’t have to guess we don’t have to take the supplier’s word for it, which is what many of it people were doing before.

It’s like, “This company says, it’s good for this.” I’m like, No, don’t, look at the research.” This just makes it easier, because yes, you can do a search of Medline, and I think we should still all be doing that frequently, but this as a tool just makes things easier. You can just type in that condition and brings up the strains and it tells you what products in Canada or the US or Australia contain those strains just to again, make things easier because That’s the added bit on top is like, yes, this is a great stream, this great research study, but where do you get it? Sometimes those bits of information are not easy to come by.

Ari: Yes, absolutely. One other thing related to probiotics that I want you to speak to is colonization. I think this is also a widespread myth. People have the assumption. They take a certain probiotic and they think it goes in there and it just starts it’s colonizing the intestinal tract and then starts reproducing.

Now you’ve got huge quantities of this particular species of bacteria. What is the deal with that? Is there any species that colonizes– I know this is probably something that you could talk about for five hours, but how could you simplify into a few-minute-long answer

Dr. Hawrelak: Simplify? Generally no? Generally we don’t get colonization from current generation probiotics. We’re talking about lactobacillus strains, bifidobacteria strains, even the E. coli strains we currently have Saccharomyces probiotics, and I would say the bacillus type strains too they don’t permanently colonize. They’re all temporary visitors. This has been clear for also like 40, 50 years. For me, the interesting thing is that we there’s this conception that one of the five-R points is reinoculate and people think that they can just take antibiotics and then just pop a pill and everything will be replenished from that and forever onwards. It’s good to know that that’s not true. It’s rubbish.

It does not happen because I think it makes you appreciate and care for that ecosystem differently when that it’s actually– One, it is unique. It’s yours. It’s been passed down your family line and we should respect it as such. Two that it’s not as simple as that. It’s not reality. If we wipe out our bifidobacteria, we can’t replace it with one in the supplement. It doesn’t stay. Again, you go back 40, 50 years is like a good probiotic strain will last a week or 10 days in there versus ones that just pass straight through ones that die in the stomach or small intestine.

We’ve had studies showing this time and time again is we just don’t get long-term colonization as a general rule. There is the odd exception. There’s the odd study. I think there’s one using a strain of bifidobacterium, there’s AH1206, which isn’t commercially available now, but that was able to colonize, I think in 30% of people for six months afterwards. That is an immense rarity because you can just–

If you delve into literature, you’ll find that they last for five days, two days, 10 days, 14 days, but you can see their populations just diminish. If you take daily stool samples that goes down all that time. You can investigate this yourself too. You can do a stool test whilst you’re taking that probiotic and then two weeks later do that same stool test and keep every other variable the same. You’ll see that maybe a bifidobacteria was here and then it’s not there anymore. It’s pretty clear.

As someone that’s done a lot of stool testing over the couple decades of my practice using accurate, assessment techniques is, you clearly see that they do not colonize in these patients. I think it really cheapens the thought of the ecosystem and care of the ecosystem if we think it’s easily replaced just by popping a probiotic pill because it’s not.

Can probiotics stand alone?

Ari: What do you think of- and this is something I don’t believe that I’ve heard you mention in the course. I believe it’s Bacillus subtilis [unintelligible 00:33:34]-based probiotic that is in products from Microbiome labs and they talk about it. it does colonize and that it takes up residence there and also that it has an impact on modifying other species of bacteria that are present in the intestines. What do you think of those claims about that?

Dr. Hawrelak: I think the latter one, we know that probiotics do have some impact on the gut ecosystem. Now I would put that in general as relatively minor. You compare that to changes in diet. You compare that to prebiotic usage. The alterations we get from a probio are relatively small. They’re not none often and that can be bigger. If it’s right after chemotherapy or right after antibiotics, you’re going to get bigger changes from probiotic usage in that case because the ecosystem is immensely disrupted and it’s more flexible in terms of how things shift at that point.

If you take someone who’s more stable ecosystem, you give them a probiotic whether it’s [unintelligible 00:34:34]-based or otherwise the impact will be relatively small, not nothing but relatively small. If you change their diet markedly, you give them a couple of prebiotics, you’ll see dramatic changes in that ecosystem. In terms of the long-term colonization, I haven’t seen research to suggest that that’s the case. Now it’s possible that I’ve missed that study showing that there’s long-term colonization.

Again, doing lots of stool testing over the years, I can’t even recall seeing the bacillus showing up on stool tests, very commonly at all, when people are taking that supplement, which makes me, whereas I do see bifidobacteria, I do see lactobacilli, that populations do go up and down and people are taking the supplement versus not, that makes you just think those show up on stool tests where they haven’t really seen that with Bacillus which makes me less– At least at detectable levels, it seems less likely to me that would be occurring.

Do we inherit our microbiome?

Ari: Okay. You said a couple of things in the last couple of answers that I want to maybe clarify. You said something really interesting which is that kind alluding to our microbiome is subject unique to us as an individual something passed down through the generations from our family. Along with this idea that we could take probiotics, but it doesn’t really have much of an impact, they don’t really colonize, it almost paints a picture of the microbiome as this static unchanging thing.

On the other hand, you also alluded to other lifestyle factors, nutrition, prebiotics, things like that, that do have a big impact on it. How do we reconcile the degree of plasticity of our microbiome? Is it highly changeable or is it more? It stays unique to us and it’s this thing we get from our parents that we can’t do much to change it?

Dr. Hawrelak: There’s a limitation with how much we can change it, I would say because we get gifted it from previous generations for sure. There’ll be unique strains passed down your family line, which I think is amazing. I think what’s even more amazing is, women’s breast milk contains unique sugars. They’re unique to her that feed that family line Bifidobacteria for example, that don’t feed other Bifidobacteria nearly as well.

It’s a pretty amazing process when we go into the finer details and you just get to really appreciate the uniqueness and nuances when you delve into it more. It also makes you worry about alterations of that ecosystem to a far greater degree too, because it’s not easily fixable. I think that thing of custodianship of your familial line of microbes if you take that on board, it really changes your choices in life in terms of what you’re going to do to that ecosystem.

We get it. We inherited this ecosystem and then we can change populations within that through dietary factors, lifestyle factors, and medications. Medications like antibiotics can cause extinction events to that. Many people would argue that with every course of antibiotics, our ecosystem gets less and less diverse.

We can only pass on what we’ve got. I would be able to pass on less than what my mom passed to me, for example, sadly, because I was dosed tons of antibiotics when I was a kid. I grew up in the seventies where every single sniffle or cough or sneeze, or like take antibiotics. It was really only when I was in my 18, when I moved out of home and discovered the world and discovered health that was like, oh, I’ve had almost no antibiotics since then, but it’s like, yes.

Ari: I can still taste the amoxicillin if I just conjure the memory of every time I had a cold that was given amoxicillin.

Dr. Hawrelak: Yes. I can remember that.

Ari: The viscosity of it, the flavor of it, the pink look of it.

Dr. Hawrelak: Yes. I know. I’ve got that very clear my memory too, sadly. There’s this cool study published in got a couple of years ago where they were looking at one person’s ecosystem, essentially taking almost daily stool samples and the ecosystem was immensely stable without any change of diet or lifestyle. Gave them a single shot in the bloodstream intravenous antibiotics. Nine species went extinct.

Ari: Wow. Even through the blood, through an injection, that’s crazy.

Dr. Hawrelak: Yes. From a single dose of an antibiotic. To me that was just mind-blowing that we can lose nine species from a single antibiotic exposure. It caused massive disruptions in this ecosystem. In fact, there was a species that went from like 0.02% up to 96% the day afterwards that they hadn’t named before, and then they named it up to themselves as researchers often do. [unintelligible 00:39:33] or something like that, a very funky name.

One of the interesting things was, how much dynamics there was for the first week or two afterwards. It was crazy dynamic that ecosystem. It settled into a new pattern a few weeks after that a different pattern than was beforehand. I think the thing for me is two years afterward still nine species were missing. You’re like, Ugh. How many antibody courses do we get? I had a child patient the other day that had 14 by the time they’re 3. You’re like, “What’s happened to their ecosystem.” It’s like, we’ve narrowed it down so much.

We have things like that, we have proton pump inhibitors. It’s a widely used class of medications that I’ve mentioned before, increased SIBO risk hugely, but there are selective antibacterials, too, that they actually kill bacteria. They actually decrease the diversity of the ecosystem dramatically. We’ve got people taking these for years on a daily basis and again, we’re just narrowing this population. What we were gifted from our previous generations, it gets narrow and narrow in that situation. We can obviously make certain proportional changes with dietary fact interventions or our dietary choices, pre-virus can make pretty major shifts in proportions of microbes.

We know that we can have temporary increases in diversity by spending time in nature and going out for a lovely hike in the woods or in the rainforest, organic gardening, all these things will temporarily boost diversity. If we’re doing it daily then we get these lovely [chuckles] continual boosts of diversity that come with that, but they’re generally just temporary visitors again.

It’s not to say we don’t pick up microbes because I think we’ve always picked up microbes from a fecal-oral route. If you go back, before we had such clean water supplies, we were always picking up microbes from people upstream from us. [chuckles]

Ari: We were bathing in polio.

Dr. Hawrelak: Yes or bathing but in other people’s gut bacteria and if they didn’t have gut diseases, it’s like, that’s a good way of passing on microbes. When I was visiting Sri Lanka, they have this amazing system of canals that were set up 1,300 years ago that go for like hundreds of kilometers. People out there, their feces and their laundry and stuff goes into that canal. It’s the way it’s been for 1,000 years and people downstream are bathing in it, [chuckles] that same water.

Yes, if they’ve got giardia or salmonella or something that’s obviously going to be a bit problematic. It is an occasion, obviously, but it’s also a way of passing on microbes. There are ways of getting some species back in that we’ve lost, but it really comes to feces exposure whether that’s accidental or whether that’s intentional when it comes to things like fecal transplants where we can regain species in a more permanent way that way.

Ari: Yes. I’ve been to Sri Lanka and I’ve been to India, and I’ve seen some of these scenes of people bathing and doing their laundry in a river with literally corpses floating through the river, and obviously, sewage pouring into the river and things like that. I picture this as almost the opposite end of the spectrum of what we do in the West of giving the antibiotic courses that you were just talking about. These are people being exposed to all kinds of crazy microbes on a daily basis, whether they colonize it or not, there’s exposure happening and immune training and all. Who knows what other complex physiological responses there are to that exposure?

Dr. Hawrelak: Yes, totally. Thankfully in Sri Lanka, I wasn’t seeing the dead bodies floating [chuckles] downstream. That’s another level of microbial exposure for sure.

When to use prebiotics

Ari: One other thing I wanted to ask you was– So you’ve mentioned prebiotics a couple of times. How do we know when to use prebiotics versus probiotics? It’s interesting what you’re saying in the sense that most people I think are under the impression that probiotics are really what matters. Probiotics are the things that I need to take that are really going to have an impact on my gut.

While this is trending in a good direction, most people, in general, have brushed off prebiotics as unimportant. Whereas what you’re saying, it sounds almost like the opposite. How do people know, how should they prioritize pre versus probiotics?

Dr. Hawrelak: Yes. I think you’re spot on there in that, and I think it is changing, too, as I think you flag too, is there’s a growing understanding of the importance of fiber [chuckles] and prebiotics in terms of tools that we use to make a more substantive shift to the ecosystem. I don’t want to come across as anti probiotics because I’m not. I use probiotics every day in my clinical practice, but I think it’s important that we frame what they do well and what they don’t do.

If you’re after optimizing your gut ecosystem, prebiotics are far, far more effective at doing that. They’re far better at increasing levels of beneficial species and decreasing levels of what we call pathobionts or pathogens. Pathogens are– People are more familiar with their bad bacteria. Pathobionts are ones that, in the right amount, are helpful to us, but when they overgrow they’re problematic and cause harm. We’ve got a number of those in our gut.

What I love about prebiotics is their capacity to lower levels of pathobionts and pathogens, and at the same time, increase the levels of beneficial bacteria. I think that the selectivity of their impact on the ecosystem is just brilliant. Since I learned about them really, which goes back to 2000 -2001, they’ve been a core part of my clinical practice since then. They really have been core because I think their capacity to shift the ecosystems in dramatic ways is you can see that. You do the right stool test, and you can see dramatic impacts after two months of use on a prebiotic.

If you took a probiotic for that two months, you would not see that, there’d be some little shift. It’s not to say that probiotics can’t help with speeding transit time, they can help with healing up a damaged gut, they can help with decreasing inflammation. There’d lots of good reasons to use specific probiotics, but if you’re after shifting that ecosystem dramatically, prebiotics or a change in dietary approach will produce far greater shifts.

Ari: Very, very interesting. That was a very strong statement that you made that I think if people really hear that it will blow a lot of minds and change a lot of perceptions and make people realize that prebiotics, that they’ve really been neglecting, and underappreciating the value of prebiotics. I know that that was even true of me prior to going through your course. I had already read a lot about prebiotics. I can supplement prebiotics, but I still was blown away with how you rate the magnitude of effect size in changing gut microbiota [unintelligible 00:46:48] [crosstalk]–

Dr. Hawrelak: Yes, and if you do lots of microbiome assessments with patients pre and post, you see it [chuckles] firsthand, and you see how that correlates with the shifts in their energy, their cognitive capacity, and their gut symptoms. It can be dramatic.

I remember I’ve got one patient who, when I started working with her, she was essentially bed-bound. She could barely sit up, she couldn’t feed herself. She had to have people feed her and then to working on a microbiome-only level. Now I wasn’t giving mitochondrial support or other things, just microbiome stuff. We couldn’t do much with diet because it was restricted because she wasn’t in control of her food. She was at in an institution and she just got institutional food, which isn’t good [chuckles] as you would know.

We just worked with prebiotics and probably some [unintelligible 00:47:35] something as an anti-inflammatory as well, but mostly with prebiotic work. Geez, I spoke to her just the other week, and she is now in a wheelchair, she is going outside daily, and she’s able to feed herself, be able to sit up, and it’s just like the difference for her. That might sound like a relatively small thing. It was huge. Huge in so many ways, and she’s getting better at each progressing week or month. More functionality is returning, and that tweets one of those cases that demonstrates the huge potential impact that we can get if we change the ecosystem.

Her ecosystem was very despotic, had very high levels of proteobacteria and very low level– Which are rich with the endotoxin that we started off talking about, and very low levels of beneficial anti-inflammatory butyrate producers. It was rife for the changing. We did a full-up stool analysis and we reduced the proteobacteria by half, and we’d increased beneficials pretty dramatically.

Even though we weren’t able to implement all the things because we had to do very tiny [chuckles] doses, stepwise increase because her system was so sensitive. Even within that context, there was a dramatic change, but you can see it. I think that’s the thing, too, is you can clearly see the impacts and how dramatic they could be by using a good stool analysis pre and post.


Fiber in the diet - Key to gut health

Ari: Cool, because I have a million questions more that I want to ask you. I won’t have time to ask you all of them, [chuckles] but I’d like to ask a few more. I think a natural segue from what you were just talking about, and you’ve made a couple of allusions to the importance of fiber in the diet for maintaining the gut microbiome and prebiotics. I’m curious, are you aware of the carnivore diet that is trending in some circles right now? I’m curious what your thoughts are on it.

Dr. Hawrelak: Yes. I think it’s probably effective at reducing certain gut symptoms short-term like gas-related symptoms because you essentially produce a lot less hydrogen gas when you eat only meat because it does get fermented. In fact, this is called putrefaction when meat gets fermented in the gut and it does produces maybe one-third [unintelligible 00:50:03] gas level is what you get when you’re fermenting fiber or carbohydrate compounds.

I think it can definitely help with these symptoms but I think there’s a major trade-offs [chuckles] with that because you’ve got to be aware that most, if not all the beneficial species in our gut, are fiber or oligosaccharide or carbohydrate consumers. If you start feeding them, their population dips. Not surprisingly if you stop feeding something it goes down, and at a certain point, you’re going to reach the point of extinction if you stop feeding things long enough, and there’s not enough food for them, their populations will eventually just go out. It’s impossible or really hard [unintelligible 00:50:43] the fecal transplant to bring them back.

As someone who’s worked with people that have been on the carnivore and are really unwell and try to get them back, it’s really hard work because part of the other issue here is what they are feeding. We know they’re not feeding butyrate producers, they’re not feeding bifidobacteria and that’s really problematic. What they are feeding is hydrogen sulfide gas producers because they quite like eating protein, and they quite like eating bile. There’s a lot of that in reaching the gut in that dietary approach.

Hydrogen sulfide gas causes gut leakiness, but it causes also visceral hypersensitivity, which is when the nerves in the gut are hypersensitive. You can start feeling even little bits of gas moving their way through, little bits of fiber compounds [chuckles] moving through. You start feeling it.

Ari: Which logically, it would make sense then that there’s a possibility that someone who adopts that diet and then tries to reintroduce plant foods might be way more sensitive to them. Therefore, almost insidiously, then even more convinced that those foods are harming them.

Dr. Hawrelak: Yes, exactly. This is where it’s really hard to get people off of that because their gut has now become so inflamed and so there’s such severe visceral hypersensitivity that even a tiny amount of a substrate fiber, [chuckles] plant-based food, or that they used to tolerate fine, or prebiotic actually causes them excruciating pain now and discomfort. It’s like, “Okay, how do we work forward?” It’s really, really slow going because you have to try to deal– This is where you might use supplemental butyrate because we can’t feed the butyrate producers yet [chuckles] because the degree of inflation is so severe. We have to use lots of gut antiinflammatories to get to the point where– And we have to use things that help with detoxification hydrogen sulfide gas to try to– Initially before we can start introducing prebiotics to shift the ecosystem more positively, but it’s really tricky.

This is where I really worry about is that for a week, yes, not a big deal, but you start doing this for months is you start making more longer-term impacts to the ecosystem but also just the environment and the inflammation level that are hard to come back from.

Ari: Do you think that there’s a possibility along the lines of what you were talking about with antibiotics, there’s a possibility of extinction events for certain species of bacteria that maybe you can never get back?

Dr. Hawrelak: I would think, yes, but it would probably be time duration dependent. Again, for a short period of time, probably not extinction, their populations will just go down but there’ll be a point at which you expect there to be extinction events because if you just– The extent, [chuckles] there’ll be a consequence.

I can remember working with one person who is just eating two chickens a day, that’s all this person ate. Looking at that guy ecosystem, it was like so high in hydrogen sulfide gas producers, so high in bile eaters, who create secondary bile acids, which are also pro-inflammatory in the colon, and no bifidobacteria bacteria, no faecal bacterium. I was surprised there was 2% [chuckles] of butyrate producers in that ecosystem which is I think the lowest I’ve ever seen.

Through a lot of work, we’re able to expand things and eventually diet too, for that matter. I still think that there are some species that we’ll never recover because she’s on that diet for long enough that I think there’d be extinctions, and the diversity was never going to be as good as what it would’ve been otherwise.

Ari: Based on what you’re saying, it seems like it has the potential to be a pretty insidious thing in the sense that a person might adopt this diet and experience only benefits initially-

Dr. Hawrelak: Initially.

Ari: -and therefore be convinced that they’ve discovered the best way to eat, and it’s making them lose weight, they’re feeling good, they have way less abdominal symptom, GI symptoms. The subjective conclusion from that feedback is I’ve found the magic best human diet that is going to make me kick butt. Only later will they start to develop all kinds of other problems, which they probably will not then attribute to the diet that they are convinced is the best diet.

Dr. Hawrelak: Yes. No, I think you’re totally spot on.

Ari: Maybe the last [chuckles] but 20 things I wanted to ask you about. The last thing that I want to cover is probably SIBO. SIBO has become somewhat of a controversial thing. I have personal friends on both sides of this who some people are in the mainstream functional medicine camp, so diagnosing everybody and everybody with SIBO based on hydrogen breath test.

I have other friends, for example, Dr. Alan Christianson, who has written an article that caused quite a stir in the functional medicine community, basically attempting to debunk SIBO as a thing. He had multiple lines of evidence and logic that he presented to essentially conclude that the evidence doesn’t support that SIBO exists and is a cause of IBS-like symptoms and that sort of thing.

I went through two hours of lecture of yours on this topic so I know it’s something you can talk about in enormous step. [crosstalk]

Dr. Hawrelak: Probably three hours. [chuckles]


Ari: How would you speak to the legitimacy of SIBO and maybe problems with a lot of the testing that goes on with it?

Dr. Hawrelak: I actually came from the very skeptic camp, too, to be honest, because I was doing my PhD in the role of dysbiosis and irritable bowel syndrome when this idea– This is looking at chronic dysbiosis and all the research was around chronic imbalance. Then, this researcher, Pimentel said this idea of small intestinal bacteria playing a role and antibiotics may be helpful for IBS.

Before that, all the research were showing that antibiotics were a common cause of IBS occurring. I was immensely skeptical when that first came up. I will [chuckles] flag that and like, “It doesn’t really fit just the broader literature around that.” The only discussion of SIBO was really, before Pimentel stuff, was essentially in people that had short bowel, people had gut surgery, part of the small bowel removed, and they would have raging SIBO and they’d end up in the hospital.

There were cases of SIBO discussed in literature but it was very much research with abdominal surgery. That was the thing that we saw with SIBO up until Pimentel’s ideas started coming forward. I was cautious and hesitant about it too because my area was IBS and it was dysbiosis. Those are my areas so it was like, “This was just–“

Also, lactulose as a tool to diagnose it was peculiar to me too because it was like, “I’m using lactulose as a prebiotic, and as we know it’s a selectively fermented substrate that only some bacteria can eat and a whole bunch can’t. You’re not going to see if those bacteria are present in a small bowel because they can’t eat it. [chuckles] That’s going to pass through. That’s why I’m skeptic towards that as a diagnostic tool as well.

You fast forward to 2022, [chuckles] here I am. I actually do believe in SIBO and I do use breath testing. I treat patients with SIBO and their IBS symptoms get better long term, and you can cure people of their IBS symptoms.

I think, for me, an interesting journey that’s gone all along the way as researchers changed, as you start trying different things clinically and seeing things. Now, I don’t use antibiotics to treat SIBO, I use selectively acting antimicrobials, I use probiotics, I use prebiotics. It’s a way of altering that ecosystem.

I think, for me, it’s clear that there are people who do get overgrowth of bacteria in their small intestine and we treat that and their symptoms go away. Not only gut symptoms but some people who have brain fog, they get fatigue, aches, and pains, those things go too. I see this every single week in practice. No matter how much somebody says, “I don’t think this condition exists.” [chuckles] I would say, “I see it.” [chuckles] I can do pre and pros breath testing, and breath testing isn’t perfect.

I think if we relies totally on lactulose, we’re actually getting false positives and we’re getting a lot of false negatives, which it’s really problematic if we only use lactulose, which is, for me, one of the reasons I was so distrustful of lactulose as a diagnostic tool that I started using– I was always using glucose breath testings the very beginning, and I started using fructose breath testing, and then I started doing triple breath testing on every single patient I suspected of SIBO over the last ten years. You can actually start seeing patterns and start seeing which sugar substrates, I think, are more effective for diagnosing SIBO.

I would actually argue from a clinical perspective that fructose is actually a more accurate sugar than other lactulose or glucose. I generally will do at least fructose and lactulose, or all three if I really want to get the best chance of seeing it’s there or not. What we can see is, let’s say, we have this early rise on fructose, so there’s a breath gas spike at the 20-minute mark. It’s extremely unlikely that fructose has reached the colon in 20 minutes.

Is it possible in some people? Yes, but in most people in that situation, it’s not the case. We can treat that person for that apparent bacterial overgrowth with those selective reacting herbal antimicrobials, pre and probiotic combinations. Their symptoms go and we can do a retest and they no longer have that spike in gas at any time point. We get this objective data showing that that is no longer the case and we get this subjective improvement of symptoms that go with that. As I said, that’s something that I see on a weekly basis, so I’ve a hard time thinking it doesn’t exist [chuckles] when I can see scenarios like that.

I also share some of the concerns that people have about the broader SIBO field and that not everybody’s got SIBO. I think I have issues too, with saying everyone with IBS has got SIBO and that’s clearly not the case, looking at the data around that.

I still don’t think we’ve got the ideal ways of diagnosing SIBO or defining SIBO. I think there are still areas that are open for improvement. I do think there are people who have this early rise in breath gases on sugar substrates. Breath testing and [unintelligible 01:01:51] guts to go with that, that when we treat that and the breath normalizes and the gut symptoms go away.

Should you avoid prebiotics if you have SIBO?

Ari: You said something else in there that I want to flag as interesting. I think it was the case for me and it’s the case for many, many functional medicine practitioners that I know, that there is a general fear over prebiotics when dealing with SIBO because these people have dysbiosis and bacterial overgrowth in the wrong place, that’s leading often to this reaction to certain prebiotic fibers. The tendency in thinking if I can generalize, is towards maybe the elemental diet, is towards reducing fiber and avoiding any fiber that could feed the bad bacterial overgrowth.

Your course really presented a big shift in thinking because you pointed to all this research, basically showing that certain prebiotics are actually highly beneficial and can help resolve SIBO. Can you just speak to that, maybe trend of thinking, and why it’s wrong and why prebiotics are not something to fear?

Dr. Hawrelak: Yes, I think we could even put probiotics in that, too, in that the general consensus has been don’t give probiotics in SIBO because you’re already just adding more bacteria to an already overgrown system. Then you look at the research data, [chuckles] it’s very clear that probiotics are helpful. There is individual studies, but then there were the meta-analysis published a few years back that looked at just grouping all probiotics together, which I think is problematic, but it can still give a general idea about how it’s brought effectiveness.

There’s a 50% rate of curing of SIBO with probiotic. Given that rifaximin in the antibiotic use it’s something where between 50% to 70% effective, depending on which [unintelligible 01:04:41] you read. It’s not markedly different than that, yet we still have people saying, “Don’t give probiotics because of the theoretical consideration,” but they don’t look at the research that says, “Look at the research. It’s very clear.” There are some strains that have better efficacy than 50%, but that’s just when you get them all combined.

I think too, you look at the research around prebiotics. Let’s look at partially hydrolyzed guar gum, which is a fairly unique prebiotic substance because it particularly targets butyrate-producing species, I would say. A little bit of bifidobacteria, but mostly butyrate-producing species. We know if we give that alongside, let’s say, rifaximin for the treatment of hydrogen-dominant SIBO, that we improve essentially the cure rate from 67% to 87% by using a prebiotic alongside the antimicrobial.

We have methane overproduction, which can happen in the small bowel or colon, or both. We know that giving partially hydrolyzed guar gum decreases methane output with continued use. Following on from that, we know that other prebiotics can decrease methane as well like galacto-oligosaccharides.

Now, we’re limited with there’s not that much human research around tools to help decrease methane, but we do have that one study with partially hydrolyzed guar gum. We have research on the– We’ll go back to the BioGaia DSM 17938 strain of lactobacillus reuteri, which has been found to decrease methane output as well. Here we have these tools that some people would just biased say, “No, we can’t use pre and probiotics” despite the fact we have clinical trials showing that they’re actually helpful.

I think that’s what I find frustrating is that when people get stuck in very rigid thoughts around conceptions and theories that they can’t accept the evidence that is being published and right there. It just means the patients get some optimal care because of people being closed and too rigid and not open to new evidence when it comes out.

3 keys to start optimizing your gut health today!

Ari: Fascinating stuff, Dr. Hawrelak. I really want to thank you for your time. This has been absolutely wonderful. Thank you for going over our hour of allotted time. The last thing I want to ask you to wrap up with is– And this is maybe a hard question. If you were going to generalize how to best take care of one’s gut health, what would be your top three recommendations that you want to leave people with?

Dr. Hawrelak: Avoid antibiotics as much as you can. Make sure you check if they’re actually needed. They’re still used far too often for viral infections. [unintelligible 01:07:13] I wish they weren’t but they still are, number 1. Two, eat predominantly plant-based. It doesn’t have to be completely plant-based, just mostly plant-based, and eat a variety of different plant foods, so you’re having legumes, whole grains, nuts, seeds, fruits, vegetables, multiple colors. That’s what’s feeding a diversity of microbes. Mostly, species in there are fiber and polyphenol consumers. If we’re eating some purple carrots, if we’re eating some black rice, some black beans, we make sure we’re feeding a wider diversity than if we’re eating orange carrots only, brown rice only, or white rice only.

I think those are probably the most important, but I would actually tag on exercise in nature [clears throat] as a way of linking two things we know are important. One is, getting [unintelligible 01:07:59] amount of exercise is important for diversity. Two, being in nature is another great way of increasing your ecosystem diversity. If you can join those two together, hiking in the woods or running through the woods, that I think, would be my third on that list.

Ari: Beautiful. Thank you so much. The last thing is just where can people get a hold of you, follow your work, get in touch with you if they want to work with you, or where do you want to send people?

Dr. Hawrelak: Probiotic Advisor is a good port of call, in that I’ve got a number of courses online, mostly geared for practitioners but others, for the health-conscious general public as well. I’ve also practiced through Goulds Natural Medicine, which is a clinic in Hobart, in Tasmania in Australia, even though I don’t actually live in Hobart now. It’s all virtual these days, but I practice still and I’m still researching, too.

I think I love all those aspects of things because I think they all feed it into each other really well. I think working with those patients and seeing the impact is immensely important. Trialing things you see in research and going, “Does it work in the real world? How do we implement it in the real world to get the benefits?” I think is really important. I think those [crosstalk]–

Ari: Do you work with patients all over the world, or just [inaudible 01:09:17]? [crosstalk]

Dr. Hawrelak: I do. For the last 5 or 10 years, it’s been mostly all over the world.

Ari: If somebody wanted to work with you one-on-one, they can contact you. Let’s say, they’re in Canada, or in States, or in Europe, or something like that and you could potentially have them get certain testing done, and then you can evaluate the testing and then work with them?

Dr. Hawrelak: Yes, very much so. I would say at least half of my patient load is in North America or Europe now.

Ari: Excellent. Thank you again so much. On a personal note, I’ve really, really enjoyed your course and benefited hugely from it already. Thank you so much for coming on my podcast and sharing your wisdom with my audience. I’m really appreciative of everything.

Dr. Hawrelak: You’re very welcome and it’s lovely to chat, actually. I enjoyed it thoroughly.

Ari: Yes, me too. [chuckles]

Show Notes

00:00 – Intro
00:52 – Guest intro
08:19 – The gut health – energy link
18:47 – Butyrate for brain (and gut) health
20:14 – What to look for in probiotics
23:32 – The probiotic strains matter
34:11 – Probiotic Advisor – key to finding the strains to help your conditions
36:45 – Do probiotics colonize?
39:55 – Can probiotics stand alone?
42:00 – Do we inherit our microbiome?
50:00 – When to use prebiotics
55:25 – Fiber in the diet – Key to gut health
1:01:50 – SIBO
1:08:10 – Should you avoid prebiotics if you have SIBO?
1:11:58 – 3 keys to start optimizing your gut health today!
1:15:38 – Outro


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