EP236: The Microbiome Connection: Optimizing Health from the Inside Out - Jason Hawrelak, ND, PhD
In a Nutshell
Dr. Jason Hawrelak explains that the microbiome is a modifiable ecosystem that influences every body system, with dysbiosis—marked by low diversity, depleted butyrate producers like Faecalibacterium and Bifidobacteria, and elevated Proteobacteria—driving most chronic Western diseases. The most effective interventions target ecological factors: lowering colonic pH with prebiotics like lactulose, increasing fiber and resistant starches to boost butyrate production, and using selective antimicrobials like pomegranate husk to reduce LPS-releasing organisms without harming beneficial species. These changes can dramatically shift microbiome composition, resolve symptoms across conditions like IBD, SIBO, and autoimmune disease, and prevent the generational loss of microbial diversity occurring in Western populations.
These notes were generated by AI and may contain inaccuracies.
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Welcome to episode 236 of the Better Health Guy podcast. If you are seeking new ways to create better health, I might just be your guy. Today we explore the microbiome connection, optimizing health from the inside out with my guest Dr. Jason Hawrelak. He is a researcher, educator, western herbalist, and naturopathic physician with over 25 years of clinical experience. He earned his PhD examining the capacity of probiotics, prebiotics, and herbal medicines to modify the gastrointestinal microbiota and teaches worldwide on the topics of microbiota modification and gut health. He has published extensively in these areas, including 20 textbook chapters. He serves on the medical nutrition council of the American Society for Nutrition and is a fellow of both the American College of Nutrition and the Naturopaths and Herbalists Association of Australia. He maintains a busy telehealth practice as lead clinician at the Hawrelak Gut and Microbiome Clinic. He is chief research officer at Probiotic Advisor, which offers a searchable database that enables evidence-based prescribing of probiotic products. He also founded and serves as lead educator at the Microbiome Restoration Center, an online educational platform devoted to training health professionals to become microbiome clinicians through its flagship courses, naturopathic and functional medicine approaches to gastrointestinal disorders and advanced microbiome manipulation.
It was actually in my final year of my naturopathic training and there was a lecture put on by Professor Steven Myers who's a medical doctor and a naturopathic physician and a PhD scientist and he gave a talk on the role of dysbiosis and leaky gut in chronic disease. This is back in 1999. And he's like piecing together all this stuff which was more so animal studies and things like that at the time. But it just something about the topic is like going hey you know naturopaths have always said it all comes back to the gut. Hippocrates said it all comes back to the gut and here we're piecing together with you know research going yeah it's supporting that and then right after and that was essentially it's coming towards the end of my training and I was like okay I approached him right after the lecture and said I want to research this I want to contribute to that body of the connections between leaky gut dysbiotic you know bacterial ecosystems and chronic disease and so I subsequently did my honors degree and then PhD looking at the role of dysbiosis and we chose a condition that in the late 90s had a bit of research showing there's a dysbiotic ecosystem associated with and that was irritable bowel syndrome. And that was kind of the poster child of dysbiosis back in the '90s. You know, you look at the literature, the stuff on some IBD, the stuff on IBS, but IBS had research from 1980s showing like dysbiotic changes in the ecosystem and you had had probiotic studies going back 1950s showing efficacy for treatment of IBS. We're like, okay, let's choose that as our poster child of dysbiosis and really just gave me a chance to spend, you know, my honors degree was one year. Australia honors degree is like a research degree and we were at clinical clinical trial in that first year you know and then you my PhD went for four years five years of just like full-time just doing microbiome research and reading all the papers and at that time you could read all the papers on the microbiome I think that's the incredible thing is where we've gone from you know I think it was 300 papers published a year on the what we call the microflora back in the day and probiotics and prebiotics you know that topic was you know four or 500 papers a year is quite achievable to read as a PhD student. It's not a big ask. But you go forward now to 30,000 papers published year. It's a different story and it just shows how much that area has boomed at the end of any time.
But it's still I said that that lecture just of his and he became my PhD supervisor later on and he guided me through that sort of process. But yeah, I'm just lucky that I chose a topic that I was one passionate about and two becomes this you know everyone's talking about the microbiome now which was not necessarily the case back in the '90s early 2000s. With naturopaths, it was functional doctors. If we had doctors that were talking about the importance of the microbes and conventional medicine for the most part was just ignoring all everything to do with the microbiome like ah they're just bacteria it doesn't matter if you kill them you know it makes no difference at all and there's a small group of microbiome researchers even then who said this stuff is these bugs are important you know it does matter if we kill them antibiotics do have long-lasting impacts beyond just like the short impact on the microbiome composition etc and that you know went from you relatively small group of microbiome researchers now there's like tens of thousands around the world which is really again adding to why we've got such a huge body of knowledge now around the microbiome compared to what we used to have.
I was and I maintained my clinical practice as I was doing my you know honors and PhD I still practiced too because I wanted to make sure I didn't put my clinical training to waste so to speak. But also it's like I think it floats into each other well because you read studies hey look at this intervention it worked great tried it in the real world does it like sometimes it does you know work sometimes it totally doesn't and you're like my god that you know the studies so it works but in reality doesn't work nearly as well as what it shows in the studies or you get these other sort of side effects at the time frame it comes on so I think it's merged well having that research hat as well as a clinical hat because I think it also brings you bring clinical reality into research too because you see some researchers who just been researching scientists for 30 years and they just don't know the reality of engaging with patients or what patients do for patients, how to implement things. Like sometimes I go to microbiome research conferences and you just look at the food that people are eating. You're like, you know heaps more about the microbiome than I do in certain little facets, but you don't know how to actually take your findings and clinically apply them in a way that's actually going to make, you know, people's lives different or your own life different sometimes, too. The first microbiome conference I went to Italy, I was Italy, too. I was just shocked at the food that was being served. I was like, "Yeah, these guys are going to be all over the microbiome. They're going to have such microbiome supportive meals for everybody in the breaks and at lunch. It was like totally not." And that was my Yeah.
So, let's set the stage then with kind of an overview of the microbiota or the microorganisms living within us. How many organisms live within us compared to our human cells? How are the types of organisms in the stomach different from the small intestine and again different from those in the colon? What do we more commonly expect to find in each when we kind of move from top to bottom? Again, no pun intended. And how many different types of microbes does an optimal microbiome contain as compared to what most people today likely have? So, start from the top again. I mean, I suppose looking at the microbiome, it's like 100 trillion cells. And there was a time in which people there was this figure thrown around in the microbiome literature that was like 9 to 1. We had nine times more sort of microbial cells than we did human cells. That's sort of reevaluated somewhat to so you see different different amounts thrown out in literature, but it's probably 2/3 microbe, one/3 non-microbe, I think is probably kind of the area that we've kind of more settled at, which is really quite striking. And I think it's really shifted. As I said before, we go from being microbes not being important to researchers going, "Hey, these aren't bugs aren't important. These should be seen as a separate microorganelle to your overall health." And then that skip all the way through to where we're converging now to that we are holobiont or meta organisms composed of human cells and non-human cells that make us who we are and how we influence those non-human cells influence ex how every single body system works. And that has become super clear over the last 20 years from just okay these things impact what's happening to the gut. It's like it's happening. What happens to the gut changes what happens everywhere. What change what we do to change the microbiome composition changes functionality everywhere which is both like it's striking but it's also on one hand it can be worrying in terms of what impacts we're actually doing on our health through altering that ecosystem because it is relatively you know fragile to certain influences and on the other hand it's great. It's super empowering because we can change that.
Yeah. It's me mentally change. We can't change our genes, for example. We can change how they're expressed, but you can't change some of the structure. We can totally change the microbiome composition. If you're willing to change your diet, willing to change lifestyle, implement prebiotics supplementation, you can make massive changes and completely turn around, you know, a microbiome. That's some easier said than done with some patients, which is, you know, the clinical reality that you and I face is like, yeah, in theory, do this, this, this, and this, the micro would change a lot, but hey, we can't do this, this, and this now because of these other factors there. Yeah. So, and I think what again that the connections between the gut microbiome and every sort of body system has now become super clear that we can change how the immune system works. We change how the nervous system works, how the brain works, how metal functionality works. Now we got like, you know, gut brain kidney axis, gut brain mitochondria axis, gut brain, you know, like all these different sort of gut microbiome axes, kidney axis, skin axis, all these things now because we're tying all these things into what's going on in the gut. And even I was at a conference in South Korea a couple weeks ago, microbiome conference, and they're talking about the most common the things they're finding in the human bloodstream. The most common thing are microbial metabolites, which makes sense. And we're still teasing out naming these things, you know, seeing what they might actually do. But there's a huge amount of microbial metabolites in our bloodstream. Most of which are uncharacterized to date, and that's the microbes communicating with us and producing things that are impacting us. Yeah. Because we're I mean, they're part of us really is the best way of really kind of describing it. Yeah. And as ecosystem you know kind of shifts the oral system is relatively micro microbial it's quite rich in number of microbes okay you get different microbes there cuz you get some oxygen exposure but there's different ecosystems between like the gum pocket and your top your teeth etc too and the oral microbiome is not really my thing you know I know little bits about it little bits of how to influence it but my influence my main focus has always been on the colonic microbiome yeah so we go the stomach relatively small number of microbes you know people estimate like you know 10 to maybe a thousand microbes per mill of intestinal of sort of gastric contents. These are ones generally we swallowed. They could be streptococci or lactobacilli some veillonella that we swallowed from our saliva but usually the stomach acid kills the majority of those those things that that we reach into our into our stomach. Yeah. Then move into the small intestine and the first bit of small intestine is microbial you know not very d you know rich but as you move towards the end it becomes much more so. So people talk about maybe towards the end of the small bowel maybe 10 to the 8 bacteria per mill and then boom you go over the valve and you get 10^ the 11 10^ the 12 10^ the 14 in some papers are saying now in terms of microbes you know so so far more micro mass per sort of milliliter of content and diversity also increases as we go you know from stomach being the least diverse to small first intestine being a bit more diverse then as you make your way through the small bowel more diverse and then in the colon it's like major improve increase in diversity from from that point.
Now in terms of you know what's a normal level of ecosystem richness you know because richness I mean diversity is a metric that has two components you one is the richness of the ecosystems like how many species are present or how many genera are present and two is evenness so how dominant are they or how how spread out they are ideally want to have it like not be too dominated by one or two species or three species you want to have a nice spread of things yeah so you want it to look like a tropical rainforest rather than a plantation essentially is what I always tell my patients. It's like, you know, you could have, you know, 150 species of trees and an acre of rainforest, but if 80% of those are one species, it's not going to look like a rainforest. It's going to look like a plantation, but if it was actually have, you know, 10% this, 8% that, 12% that, 2% 2% 2%, it's going to look like a diverse rainforest. That's kind of what we're aiming for from microbiome perspective. So, the diversity metrics we we often will see like the Shannon index, we'll be looking at, you know, both those components, for example. But in terms of richness getting at like a number of number of species present you know there's one paper looking at westerners at you know maybe 160 anything below 160 is abnormally low looking at a couple of the labs that are doing shotgun metagenomic sequencing which is you know say the kind of the highest stand the best technology to assess microbiome composition that we have access to today unlike tiny health in the US for example with a lab that offers that and they less than 145 species they'd see is low and here in Australia we have a called micro with the shotgun sequencings too and they have about 110 species or less would be considered to be low. So for me it's like they're not too 110 to 160 in that range between the published literature and what the different labs are saying. So you can kind of have that as your baseline. Anything below for me anything below 160 you know I'd see as is abnormally low from a species perspective and I'm also looking at number of genera present too. So most of your listeners are probably familiar with it you know species genera stuff but you know lactobacillus is the genera lactobacillus acidophilus or lactobacillus rhamnosus those are the species so you can have numerous you know species within a genera but I I look at both those bits I look at the number of species present but I look number genera present too and I'm aiming for what you see in westerners often is 100 to 150 different genera yeah that's what I'd say is where I'd say the norm for westerners so the people who are below that point or ideally we're trying to aim for for above above that point in terms of spectrums that I've seen in clinical practice lowest I've seen is 12 in someone who is on long-term vancomycin and they were all e.coli klebsiella like really nasty microbes as well although there's a little bit of lactobacillus to to the highest being like 700 some now of that sort of spectrum yeah and and these are you know people in western western nations but definitely those that have had in my practice the most diver rich species rich and genera rich ecosystems are those that you grew up in a more sort of rural setting outside of cities and avoided antibiotic use as kids and they were like born vaginally. They were breastfed, not given antibiotics when they were kids, grew up eating a whole food diet, avoiding processed foods, you know, and not much antibiotic use of any in their their sort of more adult years or little. And those ones have got the the richness there that still still exists. And I suppose it's also, you know, we inherit it from our parents, too. So you know if we you know if our parents take a ton of antibiotics growing up before they had kids then that impacts what they can pass on because you can only pass on what microbes you have. Yeah. So if you actually have 150 species that's all the best you can pass on is that you know and most of us will be gifted you know let's say we're gifted 200 species and then antibiotics here antibiotics there this that western diet you know time we have we might time to have kids we might only have you know 160 of that 200 species left for example you and that's what we typically see and then that mean that's why we're seeing this dwindling of the microbiome in terms of richness over time in western nations because you know each generation has less microbes to start with to pass on to the next generation and then or you know exposing it to the you know western diet antibiotic use etc which which reduces it further with every single yeah generation.
I think that we commonly think about the gut as being somewhat self-contained and we don't think about the broad-reaching implications of our microbiome. You already touched on some of these different axes that affect the entire body. So when we're thinking about the microbiome, the microbiota, the organisms within us, are we more concerned about the pathogenic organisms being present? Are we more concerned about a lack of sufficient beneficial organisms and microbial diversity being present? And then how significant are imbalances in the development of chronic health challenges? What are some of the types of issues that we might see when the microbiome is dysbiotic? All right. Well, I mean in essence all those those factors you mentioned before like for some this will differ per patient and in terms of what we will deal as clinicians in western nations it's all those for some people it is you know Crohn's disease patient recently did a microbiome assessment they were like 55% you know proteobacteria which is mostly E.coli klebsiella citrobacter and enterobacter is like that is not good in terms of gut health is not good in terms of overall health because they're they're actually absorbing a huge amount of endotoxins and you're spot on. is the Alessio Fasano has famous for saying, but I think it's very apt is like, you know, what stays what happens in Vegas stays in Vegas, but what happens in the gut does not stay in the gut. It's such an easy way of trying to remember just keep that in mind is it totally doesn't, you know, and the more research we're doing, the more we realize that these bacterial components, both positive and negative, are being absorbed in our bloodstream all the time and totally influence all of our different systems. Yeah. And this is becoming more and more clear in terms of the disease states we now associate with dysbiosis. like there's almost no chronic disease that we will see in clinical practice is not now associated with the dysbiotic ecosystem that's that's driving it and that can be very high levels of proteobacteria like I mentioned before like e.coli klebsiella etc that have very pro-inflammatory endotoxin on them and they they grow endotoxin like we grow hair and nails it's not like they're it's not a toxin they're actively secreting although they they can sometimes do that too it's just something that they grow and they're just releasing as they die and as they live they live a little bit they die releasing more and it's just happening 24 hours a day, 7 days a week, you just have this, you know, very pro-inflammatory driver coming from the gut. And that that level of proteobacteria in someone's gut can go from like 55% which is, you know, the very high end of the spectrum to zero% in in other patients, which is very low end of the spectrum. And then you have, you know, the lack of of beneficial species playing a role too. You you have the ones that making short chain fatty acids particularly we talk mostly about butyrate for good reason because I mean a bit of a super molecule that has such wide ranging effects not just in the gut in terms of it's the the main food source for colonocytes totally is body it's working systemically to have anti-inflammatory effects and heals a damaged blood brain barrier improves insulin sensitivity reduces neurological inflammation helps generate new neurons improves mitochondria function helps induce mitophagy it's like it's a really amazing substance butyrate and that's just one of the the better characterized compounds that are coming through the microbiome and and we're as I said we're just kind of scratching the surface there currently and um next watch the next 15 20 years it's going to be focusing on what metabolites bacterially find in the bloodstream will be the next area of booming research rather than just you know what bacterial species are in the gut which you know this obviously still going to be important because they're driving that but it's just we're going to be teasing out more mechanisms of of how these interactions you know are are occurring. Yeah. So definitely you see high levels of of problematic bact species and then you have high levels what we call pathobions as well. So pathobions you know so we've got I told my patients we have like the good bad and the ugly is nice easy way of remembering you've got you know you got beneficials which generally except for extreme cases are going to be beneficial in your gut you know like yes you have like 80% of it might be problematic but it's like a rare scenario like bifidobacteria would be a classic example here lactobacilli faecalibacterium are three that I'd put in that that distinctly into that category as as positives that you know it's very rare for them to get to points where they're are problematic in terms of their their comp their their amount in the gut and the consequences like I've seen it lactobacilli I've seen it twice in my you know 26 years of practice in people that had Crohn's and abdominal surgery and had short bowel and they had like you know 20% lacto in their gut instead of the usual 0.01% and they developed D-lactic acidosis. It's like yeah you can find the rare example where this can occur but in like real life practice with typical persons you'd put those three in the sort of beneficial camp and then you have the ones that are clearly problematic like you might put klebsiella and citrobacter salmonella shigella a bunch in that sort of pseudomonas into that category as well as other things like giardia too for that matter like you know um sometimes amoeba too you put as like
Pathobionts are microbes that perform beneficial functions in appropriate amounts but cause harm when present in excess or deficiency. Examples include certain species that shift from being solely beneficial to problematic in specific contexts. Akkermansia has shifted into the pathobiont category based on research from the last 5-10 years. While most Western populations have insufficient levels, some individuals show excess amounts causing thinning of the mucous layer, leaky gut, and increased bacterial translocation. This has been observed in Parkinson's and multiple sclerosis patients. The normal target range is 1-3%, though many patients present with levels as low as 0.001%. Akkermansia has a wider therapeutic window than other mucus-degrading organisms.
The mucus layer serves essential barrier functions and feeds microbes, with some organisms residing within it. Ruminococcus torques and Ruminococcus gnavus also inhabit the mucus layer and counterbalance Akkermansia. Most people have one or the other, though Western populations often show dominance of the Ruminococcus species with low Akkermansia. These organisms have a much smaller therapeutic window - tiny amounts are beneficial, but excess thins the protective mucus layer. Lower fiber diets commonly trigger blooms of Ruminococcus torques and gnavus, leading to mucus layer thinning that drives autoimmune disease and other chronic Western conditions through increased gut permeability.
Treatment strategies for pathobionts depend on the specific organism, its abundance level, and clinical impact. Bacteroides exemplifies this category - important for health at appropriate levels but pro-inflammatory when excessive. The target is generally below 20% of the ecosystem, where the greatest health improvements occur. Ecological approaches include increasing dietary fiber and prebiotics, as Bacteroides is particularly sensitive to pH changes. Lactulose proves most effective for reducing colonic pH, causing a thousandfold decrease in bacterial populations, including thousandfold reductions in E. coli and Bacteroides counts, while increasing lactobacilli tenfold and bifidobacteria thousandfold.
E. coli demonstrates the pathogen-pathobiont spectrum. Normal strains provide benefits including vitamin K production and oxalate breakdown, but toxin-producing strains (shiga toxin, hemorrhagic strains) require elimination as true pathogens. Elevated non-toxigenic strains may still warrant reduction using both pH-changing strategies and targeted herbal antimicrobials. A clinical case demonstrated successful elimination of shiga toxin-producing E. coli from 6% to 0.06% within 5 weeks using combined herbal and ecological approaches, resolving bloody diarrhea and normalizing calprotectin and lactoferrin.
Bilophila and Desulfovibrio represent key hydrogen sulfide gas producers. Small amounts of hydrogen sulfide gas are beneficial and colonocytes can detoxify moderate increases, but excess causes various health issues. These organisms commonly overgrow in Western populations due to dietary factors and can often be managed through dietary modifications alone without requiring herbal antimicrobials.
Microbiome testing has progressed from culturing just 4-5 species (E. coli, Lactobacillus, Bifidobacterium, Enterococcus) to DNA-based methods. PCR testing expanded detection to 12 species but remains limited to known targets and better suited for pathogen identification than ecosystem assessment. 16S sequencing provides genus-level accuracy and reveals the entire bacterial ecosystem proportionally, enabling richness and diversity calculations impossible with PCR or culturing. Shotgun metagenomics offers species-level identification plus detection of viruses, fungi, archaea, and bacterial pathways for functions like oxalate breakdown, hydrogen sulfide production, or histamine synthesis.
Testing intervals for chronic conditions should be no less than 2 months, with 4 months often showing greater shifts. When targeting organisms like Akkermansia, initial improvements may bring levels from undetectable to 0.5%, requiring additional 2-month periods to reach target ranges of 1-3%. Follow-up testing may occur after 12 months if stable, or sooner following antibiotics, high stress periods, dietary changes, or lifestyle disruptions. DNA techniques require only tiny stool amounts compared to culturing methods.
Stool tests assess colonic populations only and provide no direct information about small intestinal microbes. However, when combined with positive SIBO breath testing showing elevated E. coli or Streptococcus in stool, clinical assumptions can be made about likely small bowel overgrowth organisms. SIBO cannot be diagnosed from stool testing alone, and mucosal microbes are not well represented in standard stool analysis.
Microbiome testing provides clinically valid results for guiding dietary changes and interventions. Long-term clinical use demonstrates measurable improvements in both microbiome composition and patient quality of life and disease state outcomes.
Genus and species level data provides the most valuable information. Phylum level data (the five major phyla) offers clues about inflammatory load. The clinical approach involves examining diversity first, then phylum level data, then genus and species details.
Proteobacteria indicates significant inflammatory potential due to highly inflammatory LPS, particularly from Enterobacteriaceae (E. coli and related species) and Gammaproteobacteria. An 8% Proteobacteria level warrants investigation as a potential major inflammatory driver.
Bacteroidetes (now renamed Bacteroidota) are gram-negative bacteria that release LPS, though their LPS is approximately 1,000-fold less inflammatory than E. coli LPS. When present at 50-80% of the ecosystem, these bacteria still contribute to inflammation. High Prevotella or high Bacteroides have been identified as drivers of chronic fatigue syndrome, with symptom resolution occurring when levels are reduced.
Verrucomicrobia (the phylum containing Akkermansia) provides basic presence/absence information, though genus-level analysis is more informative.
Faecalibacterium prausnitzii serves as a key indicator for butyrate production capacity. Low levels indicate reduced butyrate-producing capacity with downstream effects on gut health.
SIBO represents both a consequence of initial drivers and a cause of ongoing pathology. Once established, SIBO bacteria release LPS that drives brain fog, fatigue, mitochondrial dysfunction, depression, and anxiety. An 8-year-old patient developed fatty liver, metabolic syndrome, and obesity from SIBO-related pathology.
Common initial drivers include:
- Antibiotic usage
- Traveler's diarrhea or food poisoning events
- Opiate usage for pain management, which impairs motility
Food poisoning and traveler's diarrhea can cause damage to motility nerves, leading to long-term motility impairment and bacterial overgrowth.
Treatment approaches depend on the underlying driver. When methane-producing organisms are present, addressing the microbial overgrowth itself often resolves the motility issue. For hydrogen-dominant SIBO following food poisoning, focus shifts to reducing prolonged nerve inflammation.
Therapeutic options include:
- Morinda citrifolia (noni) curcumin extract
- Boswellia (frankincense)
- Ginger as a prokinetic
- Magnolia bark (traditional Chinese herb) with research demonstrating capacity to regenerate interstitial cells of Cajal, restoring functionality after damage from food poisoning
IBD conditions (Crohn's disease, ulcerative colitis, collagenous colitis, microscopic colitis) are microbiome-driven rather than autoimmune diseases. Evidence includes an 11-fold increase in ulcerative colitis over 40 years with no genetic changes, and immediate incidence increases when individuals from low-incidence regions (Japan) relocate to high-incidence areas (America, Australia).
Clinical outcomes in IBD respond to microbiome alterations through dietary interventions primarily, with herbal medicines as adjunctive support. Patients with 50% Proteobacteria and active Crohn's disease show dramatic responses when microbial drivers are addressed. Higher Faecalibacterium proportions correlate with better responses to all interventions (steroids, anti-inflammatories), confirmed by both research and clinical experience.
Fungi normally comprise 0.01% of gut microbial mass compared to 99.99% bacteria. Individual fungal species typically number 100-1,000 microbes per milliliter of stool at normal levels, making detection difficult with current testing technologies.
When fungi appear on stool tests, they are typically abnormally elevated. Candida is the most common concerning species. Saccharomyces commonly appears but is rarely clinically significant. Dietary sources (blue cheese, Camembert) can introduce fungi that appear on testing but are temporary visitors rather than indigenous populations.
Treatment combines microbiome optimization with environmental modification. Lactulose reduces Candida counts by feeding beneficial bacteria whose metabolic byproducts suppress Candida growth through pH changes and antimicrobial compounds. Lactobacilli produce compounds with antifungal properties.
Candida behaves differently based on pH: more acidic environments favor the budding form (less aggressive) over the hyphal form (more problematic). Current testing limitations prevent definitive thresholds for problematic versus acceptable levels.
External mold exposure does not consistently correlate with fungal overgrowth in the gut based on shotgun sequencing results. Sinus and lung colonization from environmental mold is more likely than gut colonization. PPI use removes stomach acid's protective effect against mold and yeast, potentially allowing growth in specific populations. The gut environment (temperature, pH, oxygen dynamics) differs significantly from sinuses and lungs, making gut colonization less probable.
Organic acids testing has limitations including incomplete food databases for compounds like arabinose, potentially leading to misattribution of metabolites to microbial sources rather than dietary intake. Clinical correlation with history, environment, and symptoms improves interpretation accuracy.
Hydrochloric acid supplementation is rarely used due to lack of evidence supporting low stomach acid in GERD and documented cases of harm (esophageal ulcers) from inappropriate use. Long-term H. pylori infection causing definitive damage to acid-secreting cells represents the primary indication for HCL use.
Stomach pH plays a critical role in killing incoming microbes; PPI use allows mold, yeast, and other microbes to colonize the stomach.
Colonic pH fundamentally determines microbial composition and metabolic output. pH 7 supports different microbes and byproducts than pH 5.5-6. Most pathogens prefer neutral pH while beneficial organisms prefer acidic conditions. Faecalibacterium, Akkermansia, and Bifidobacterium (butyrate producers) thrive below pH 6.5.
Bacteroides at pH 6.5-7.5 produces beta-glucuronidase and ammonia, but below pH 6 ceases these activities while remaining present in the ecosystem. This demonstrates how pH modification can suppress pathogenic behavior without eliminating organisms entirely, analogous to changing growing conditions for plants (shade versus sun exposure).
Changes in pH and oxygen dynamics in the colon represent the most significant ecological shifts that can be made to the gut microbiome. These two factors allow for dramatic and selective ecosystem changes that encourage beneficial organisms while discouraging problematic species, without requiring direct antimicrobial approaches.
Digestive enzymes play a role beyond nutrient assimilation. When digestive capacity is inadequate, undigested food reaches the lower GI tract and feeds less desirable organisms. Protein malabsorption is particularly problematic, as malabsorbed protein in the colon feeds pathogenic and problematic microbes, contributing to colic cancer-type metabolites and increased bacterial activity. This occurs regardless of protein intake levels, as a proportion of protein is always malabsorbed.
In conditions like celiac disease with recent diagnosis, where villi are flattened and pancreatic function is compromised, digestive enzymes provide dual benefits: improved nutrient assimilation for healing and reduced amounts of undigested material reaching the colon. While unabsorbed lactose may increase bifidobacteria without causing dysbiotic changes, unabsorbed protein definitively causes dysbiotic shifts. Data on unabsorbed fat is less clear but may increase Proteobacteria.
Beneficial microbiome organisms are predominantly anaerobic and thrive in low-oxygen environments. Hyperbaric oxygen therapy and oxidative therapies negatively impact the gut microbiome, with data showing increased Proteobacteria levels in patients receiving hyperbaric oxygen. This effect occurs because oxygen leaks through from the bloodstream into the gut lumen.
Approximately 99.99% of beneficial bacteria in the colon are so oxygen-sensitive that they die upon exposure, which explains why these organisms could not be cultured until DNA technology was developed. Pathogenic organisms including E. coli, Klebsiella, and Candida thrive in oxygen-rich environments, making oxygen reduction a mechanism for shifting microbial dynamics.
Oxygen levels cannot be directly measured and must be assessed indirectly through microbiome composition. High levels of oxygen-loving organisms like Streptococcus, Enterococcus, E. coli, Klebsiella, Citrobacter, and Veillonella, combined with low or undetectable butyrate producers, indicate an oxygen-rich environment.
The therapeutic intervention involves increasing fiber and resistant starches to boost butyrate production. Colonocytes oxidize butyrate, which pulls oxygen out of the gut lumen. Low-fiber Western diets and therapeutic low-fiber diets prevent butyrate production, allowing oxygen to accumulate and shifting the ecosystem toward oxygen-rich species.
Supplemental butyrate can address oxygen-rich environments by feeding colonocytes, which then oxidize the butyrate and pull oxygen from the environment. Butyrate supplementation does not suppress butyrate producers and may slightly increase their populations, particularly in disrupted ecosystems.
Daily butyrate production on high-fiber traditional diets is estimated at 7,000-10,000 milligrams. Typical supplemental doses of 150 milligrams twice daily may be insufficient, with therapeutic doses potentially reaching 3-5 grams daily to more closely replicate healthy gut conditions.
Postbiotic preparations like sterilized fecal material may be particularly useful for patients on severely restricted diets who cannot tolerate prebiotic foods. These provide bacterial metabolites that support colonocyte function and help normalize gut functionality when dietary interventions are not yet possible.
Shotgun sequencing can detect viruses, though not all laboratories provide this analysis. Research on viral-bacterial interactions is emerging, with dedicated conference streams appearing only recently. Protozoa like Blastocystis hominis have shifted from being viewed as pathogens to protective organisms that eat bacteria and correlate with better metabolic and ecosystem health outcomes.
Prevalence varies significantly: approximately 6% in the US versus 55% in Australia and 40-50% in Ireland. The organism is rarely problematic, with symptoms typically attributed to other gut issues rather than Blastocystis itself.
Worm exposure was historically normal for humans, with some evidence suggesting beneficial immune-modulating effects. Pinworms are the most commonly encountered in clinical practice. Treatment is warranted in cases of failure to thrive, sleep disruption, or migration causing secondary issues, but not all worm presence requires intervention.
H. pylori and Blastocystis represent organisms that may be overtreated in modern medicine. H. pylori presence is associated with reduced risk of esophageal cancer and reflux disease, having occupied an ecological niche in humans for hundreds of thousands to millions of years. Only certain strains with virulence factors tend to be problematic.
Treatment is indicated for upper gut symptoms like burping, discomfort, lack of appetite, gastritis, or peptic ulcers. However, H. pylori detected on PCR tests without corresponding symptoms or virulence factors does not warrant treatment. Concerns exist that eradicating H. pylori may allow more problematic organisms to occupy the vacated ecological niche.
LPS (lipopolysaccharides) from gram-negative bacteria drive inflammation and chronic disease including Alzheimer's, Parkinson's, multiple sclerosis, cognitive decline, brain fog, chronic fatigue syndrome, depression, anxiety, cardiovascular disease, and fatty liver disease. Three key factors influence LPS burden: proportion of gram-negative bacteria particularly pro-inflammatory producers like Enterobacteriaceae, gut permeability, and colon transit time.
Longer colon transit times increase LPS absorption as material remains in contact with the gut wall for extended periods. LPS itself causes gut damage and increases permeability, creating a vicious cycle.
Gut permeability and colonic permeability represent distinct mechanisms that can both contribute to endotoxin absorption. When transit time is slow, there's increased opportunity for absorption from a slow-moving colon even with lower levels of LPS-producing microbes. Conversely, individuals with high levels of LPS-producing microbes but intact gut integrity and normal bowel movements experience less of an issue. All three factors must be addressed: healing the small intestine, ensuring adequate transit time, and reducing levels of LPS-releasing microbes in the gut.
Selectivity of antimicrobial agents is critical for protecting beneficial microbes. Early microbiology work from 2001-2002 demonstrated that berberine-rich herbs like Coptis and goldenseal killed beneficial Bifidobacteria at the same doses that eliminated pathogens. Garlic showed selective action that didn't harm beneficial species. This led to a philosophy of using tools that can correct dysbiotic changes without killing beneficial bacteria.
Pomegranate skin and husk serve as selective antimicrobial agents used in Ayurvedic medicine for 2,000 years and traditional Chinese medicine for 1,800 years for gut infections. Pomegranate increases Bifidobacteria counts, has neutral effects on Lactobacilli, increases bifidogenic microbes, but kills a range of pathogens including Candida, Giardia, E. coli, Klebsiella, Citrobacter, and Pseudomonas. It also provides anti-inflammatory effects on the gut.
Green tea extract containing EGCG feeds beneficial bacteria, reduces pathogen levels effectively, and provides anti-inflammatory and anti-cancer properties. These tools can selectively target Proteobacteria populations that release LPS causing gut damage. Giving glutamine and zinc carnosine to heal leaky small bowel becomes ineffective if LPS continues to be released.
Severe die-off reactions occur when targeting high levels of Proteobacteria, particularly when patients are 40-50% Proteobacteria. These reactions become more extreme when patients are constipated because killing bacteria releases LPS that remains in the colon for days. Ensuring patients are pooing well prevents reabsorption of endotoxins.
Long-term berberine use for metabolic syndrome and insulin resistance raises concerns about microbiome effects. For motility issues, coffee enemas can help move material out of the intestine to minimize lipopolysaccharide and endotoxin exposure. The preference is working from the inside out rather than down out, though coffee enemas have a time and place for extremely slow bowels.
SARS-CoV-2 can cause meaningful microbiome composition changes in some individuals but not others. Some people show no impact while others experience dramatic shifts with beneficial bacteria decreasing and pathogenic bugs increasing. The pattern typically includes reductions in butyrate producers and Bifidobacteria, with increases in E. coli, Proteobacteria, and Bacteroides. People who develop long COVID or severe COVID infections show greater microbiome impact.
The pattern of insufficient butyrate producers and Bifidobacteria with increased E. coli, Proteobacteria, and Bacteroides represents a common dysbiotic state underlying most Western diseases including Parkinson's, multiple sclerosis, and Alzheimer's.
Loss of Bifidobacteria appears as a defining feature of the modern microbiome. FUT2 genetics and secretor versus non-secretor status do not appear to have significant connections to microbiome changes based on larger studies. Human milk oligosaccharides (HMOs) appear inferior to lactulose, GOS, and FOS for restoring Bifidobacteria, though they may be appropriate for individuals sensitive to gas formation.
Ketogenic diets kill off Bifidobacteria, with ketones themselves directly killing these bacteria. High protein, low carb diets and high fat, low carb diets both reduce Bifidobacteria counts. Antibiotic use and the Western fiberless diet also contribute to low Bifidobacteria levels. Levels below detectable limits can often be restored unless someone has been on carnivore diets for extended periods like 5 years.
When Bifidobacteria is truly extinct rather than just below detectable levels, feeding it up won't restore it. The only methods for restoration are intentional or accidental fecal microbiota transplantation. Probiotics rarely persist and colonize, with only one documented case in 25 years of practice requiring daily supplementation for years alongside three different prebiotics and homemade yogurt.
If Bifidobacteria is truly extinct and cannot be restored, daily supplementation or consumption of fermented foods containing Bifidobacteria is recommended. Bifidobacteria represents a keystone species with limited functional redundancy, making its absence detrimental to gut function and important for health span and longevity.
Microplastics, heavy metals, environmental chemicals, and plasticizers consistently reduce Bifidobacteria and butyrate-producing microbes while increasing Proteobacteria and Bacteroides. Recommendations include eating organic foods, avoiding plastic food storage, and buying from local farmers markets.
Restricting plant food diversity reduces gut microbiome diversity. Oxalobacter only consumes oxalates, so complete oxalate elimination starves this bacteria. Other microbes like E. coli can consume oxalates with built-in redundancy, but many people rely on Oxalobacter as the key oxalate-consuming microbe.
End-stage carnivore patients represent one of the hardest groups to work with due to starvation of beneficial bacteria, high visceral hypersensitivity from hydrogen sulfide gas production, and sensitivity to any gas production. The ecosystem shifts toward hydrogen sulfide gas producers including Bilophila and sulfate-reducing bacteria.
Fermented foods aren't essential for gut healing. The amount of bacteria in even half a cup of properly fermented homemade yogurt remains tiny compared to colonic bacterial populations. VSL#3 at 450 billion organisms doesn't produce substantive microbiome changes even with daily long-term use.
Slow transit time drives histamine sensitivity through increased histamine production in the colon and increased DAO consumption. Patients may report daily Bristol type 4 stools but have 10-day transit times, with some showing 26-day transit times. All patients should complete stool diaries and bile transit time tests using corn on the cob, canned corn, black or red quinoa, or whole grains.
Whole black or red quinoa and whole sesame seeds (black and white) serve as effective markers for measuring gut transit time. These substances are visible in stool and do not significantly impact gut motility. Charcoal should be avoided as it slows transit time despite being easy to see in stool. Beets speed up transit time and will give artificial results. Some people use synthetic blue food dye, though this involves ingesting synthetic compounds.
Most patients use corn or quinoa for transit time testing. Slow transit time is often present even when people report one bowel movement daily without bloating or distension. Symptoms like fatigue, brain fog, and food reactivity may indicate underlying transit issues.
Probiotics and fermented foods are overhyped for microbiome optimization. Prebiotics prove far more effective at changing the microbiome in significant ways. Probiotics do have specific clinical applications including improving mood, sleep, transit time, small bowel healing, and immunity, but their impact on changing the microbiome composition is minimal except after acute antibiotic exposure, chemotherapy, or radiotherapy.
Six months after such insults, probiotic impacts become minor. Prebiotics can cause 100 to 1000-fold increases in bifidobacteria populations after gut insults. The bifidobacteria stimulated by prebiotics represents indigenous populations carried in family lines for thousands of years.
When taking prebiotics, the indigenous bifidobacteria populations that have been carried through family lines are being fed, rather than bacteria from someone else's family line. Most probiotic bacteria supplements originated from healthy individuals' stool samples. While probiotics are still used clinically, encouraging optimization of one's own populations feels more aligned with long-term family microbiome matching than supplementing with external bacterial strains.
Postbiotics like butyrate or sterilized stool preparations have a niche role in end-stage carnivore diets or severely damaged guts with high oxygen-tolerant microbe populations and very low butyrate producers. These represent their primary clinical niche.
Prebiotic tolerability depends on transit time, visceral hypersensitivity, and SIBO presence rather than feeding pathogenic organisms. Symptoms from prebiotics represent feeding beneficial bacteria, not pathogenic ones. When transit time is slow with 5 days of stool accumulation, sudden gas production causes discomfort that people may misinterpret as feeding bad bacteria.
In SIBO cases, the small bowel has reduced diversity with predominance of organisms like E. coli or Klebsiella. These organisms lose competition for food sources like GOS, FOS, or lactulose when beneficial bacteria are present. In the colon, these populations decrease with prebiotic ingestion, but symptoms may occur if visceral hypersensitivity or slow transit exists.
Partially hydrolyzed guar gum (PHGG) is often the safest prebiotic for sensitive populations and SIBO patients. It feeds bifidobacteria, normalizes stool form (softening hard stools, hardening loose stools), and has bidirectional effects on transit time. Not all patients tolerate it, but most do.
HMOs and acacia fiber can be better tolerated in some people with gas-related issues. GOS sometimes shows better tolerability, with studies demonstrating decreased gas output in IBS patients, though individual responses vary. Start low and go slow with dosing.
Lactulose and inulin are more likely to cause gas production and hydrogen output. When gut function is optimal, this manifests as increased flatus for the first week. When gut function is impaired, pain, discomfort, or worsening constipation may occur.
Worsening constipation with prebiotics typically indicates methane issues that need addressing. Hydrogen gas produced by prebiotic fermentation has health benefits, comparable to those sought from hydrogen water machines.
Probiotic characteristics are strain-specific rather than species-specific. Some effects like lactic acid or acetate production may be species-specific, but many therapeutic effects are strain-specific. The database compiles research on specific strains, summarizes studies, and shows commercial availability in Canada, the US, and Australia.
Lactobacillus plantarum PS128 was isolated from Taiwanese fermented mustard greens and demonstrates GABA-increasing effects. This specific strain has been studied in Parkinson's disease, insomnia, and children on the autism spectrum for mood and irritability balance. Not all L. plantarum strains have these effects.
Korean research identified specific kimchi-derived lactobacilli strains with MAO-inhibiting activity from 200 different strains tested. Targeted probiotic selection based on specific symptoms or conditions yields better results than random high-CFU approaches.
FMT risks are relatively small when donors are well-chosen. The primary risk involves matching the best donor to recipients. One case involved a child on the autism spectrum who showed dramatic improvement (verbalization, eye contact, name recognition) within 24 hours of FMT from one donor, with continued improvement for 6 weeks. Switching to a different donor caused regression within 24 hours to baseline function.
Most children on the autism spectrum show either significant help, modest improvement, or stability with FMT. Positive FMT research exists for IBD, metabolic syndrome, type 2 diabetes, type 1 diabetes, lupus, Parkinson's, Alzheimer's, cognitive impairment, and ankylosing spondylitis.
Ideal FMT donors would be vaginally born, breastfed, with minimal childhood antibiotic use, grown on organic whole food diets, and no adult antibiotic use. Such individuals represent approximately 1 in 100,000 to 1 in 500,000 people in Western nations, making them rare.
C. diff treatment showed that donor quality mattered less because any FMT was better than the recipient's condition. For other conditions, donor quality significantly impacts outcomes. Current donor criteria often only exclude antibiotics in the last 3 months and known disease, which may transfer unhealthy ecosystems.
Human data on GLP-1 effects on the microbiome is limited, with only one or two human studies in a 2023 systematic review. Animal studies don't always replicate in humans. Different GLP-1s show varying microbiome impacts - liraglutide increased Akkermansia in one study, while others may decrease bifidobacteria. Unlike metformin, where microbiome alteration appears to be the core mechanism, GLP-1 microbiome effects are not established as primary mechanisms.
Peptides like BPC-157, KPV, or larazotide are not easily accessible in Australia. Existing protocols using glutamine, carnosine, and Saccharomyces effectively heal damaged small bowel with documented pre- and post-testing validation. Research on peptides remains early-stage, and quality concerns exist with peptide sourcing.
Sunlight exposure has shown positive microbiome impacts in at least one study. Connection to traditional environmental exposures through sunlight and outdoor time likely provides microbiome benefits alongside other health advantages. Being in nature and gardening increases microbiome diversity through environmental microbial exposure.
Daily meditation for 35 years supports stress axis function. Diet consists of mostly plants with wide diversity and rainbow colors, sourced from local farmers markets and personal organic garden. Climate was changed by moving 2,000 km closer to the equator for better growing conditions and year-round farmers market access.
High-fiber, primarily plant-based diet with rainbow colors represents key microbiome enhancement principles. Regular beach running and ocean swimming provide year-round outdoor activity in the current climate.
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