 I'm thrilled to see so many people here interested in microbiome. I only have about 30 minutes, but I'm hoping to impart some key insights into microbiome testing and therapeutics, and hopefully challenge a few paradigms along the way. For those not familiar with my background, I'm an MD-PhD student at the University of Illinois. I just recently defended my thesis on the effects of diet and exercise on the gut microbiome. I've also worked for Chris Kresser for the last four years as a senior research associate, and I also founded my own blog two years back to explore a lot of gut microbiome research and the latest literature, which you can find at ngmedicine.com. I'm going to talk a lot about different myths and misconceptions about the microbiome today. I'm going to cover a lot, so I'll provide a link to my slides at the end of the talk. So first, I want to make it very clear that I do not have any financial affiliation with any microbiome testing or supplement manufacturing companies. I decided a long time ago that I wanted my loyalty to remain with the evidence. So I think it's safe to say that everyone in this room is rid of the microbiome, yes? So I'm not going to bore anyone with a basic overview. It's truly amazing to see the gut microbiome getting so much attention. And of course, we know that the gut microbiota plays several important roles in our health. It feeds in digestion, synthesizes different vitamins, outcompetes pathogens, stimulates the immune system, and regulates gene expression. And we also know that the gut microbiota is strongly implicated in a number of chronic disease states. And mechanistic studies have even shown that in some of these cases, you can transplant the gut microbiota into mice that have been raised in sterile isolators and show that it recapitulates the disease. So interestingly, to our group especially, is that some researchers have hypothesized that the loss of ancestral diversity in the gut microbiome is what's potentially driving these chronic diseases. So a theory triumphed by Dr. Martin Blazer suggests that the loss of particular ancestral microbes may impair the normal metabolic, cognitive, and immunological development of the host. And changes are cumulative across generations, and they're associated with increased disease risk. And some studies estimate that we've already lost about 50% of our diversity. So you can see here, they looked at four different populations. This is with increasing socioeconomic development, we see a reduction in the alpha diversity of the microbiome. Of course, there's a number of reasons for this. One that most of you are probably familiar with is the overuse of antibiotics. Antibiotics were no doubt one of the greatest discoveries of the 20th century and have revolutionized medicine saving innumerable lives. But now they're widely overused and they devastate gut microbial communities. And what we've seen from studies is that the recovery of the microbiome is often incomplete. Not only this, but a number of non-antibiotic medications alter the gut microbiome. So a study done in 2018 showed that 24% of non-antibiotic medications alter the gut microbiome. So in other words, these pharmaceuticals may cause negative shifts in the gut microbiota that further perpetuate the cycle of dysbiosis, gut permeability, and disease. So the other reason that we may have this lost diversity came out in a paper in 2017 where they did a study of the microbiome of Hadza hunter-gatherers. And they found that the microbiota directly reflects the seasonal availability of food. And there were striking differences between the wet and the dry season with many taxa dropping to undetectable levels during one season and then coming back and flourishing in the other season. And interestingly, these same microbes that tend to oscillate are rare or entirely absent in industrialized populations. So everyone's interested in the microbiome because of this loss of diversity, because of the connections to chronic disease. So now anyone can buy an at-home microbiome test, as I'm sure many of you are aware, or walk into a grocery aisle and be faced with an entire wall full of probiotics, prebiotics, and herbal supplements targeted at the gut microbiota. But are these tests accurate and do these interventions actually work? In this presentation, I'm hoping to dig down to the real evidence of modulating the gut microbiota and dispel some common myths and misunderstandings. So the first thing I really want to touch on here is that there's a lot of companies that are still using culture-based stool tests. For decades, study of gut microbes relied on culture, staining, and microscopy, which was basically all we had at the time. The problem is that only a small fraction of the microbes in the human gut can actually be cultured. And culture also dramatically skews the relative abundance of microbes. So there's several popular stool analysis companies that are still using culture-based techniques, despite the fact that we know that these are not entirely accurate. So what we should be using instead, and this is going to be a little bit more geared towards the practitioners in the room, but I promise we'll get to more microbiome therapeutics in a minute. So we have a number of tests where you take the DNA from the microbes first, and then we can do a number of downstream sequencing techniques. So the first is called 16S-RRNA gene sequencing. This is popularly used by companies like Ubiome and Thrive. We also use it in the research lab as well. You can think of this as essentially like a bacterial fingerprint. So we're sequencing this one, this one gene of all the bacteria so we can get all the bacteria at the genus level by comparing them to established databases. The only downsides is that there's no species or strain info, so it doesn't get quite as granular. There was also no archaea, fungi, or eukaryotes, like parasites, and it's subject to primary bias. So there's a little bit of air in the results that you get. The second would be targeted QPCR, which is commonly used by GIMAP, if some of you are familiar with that test. This essentially uses targeted probes for the microbes of interest, and it has improved sensitivity, accuracy, and speed of results over 16S sequencing. But you do need a probe for each microbe of interest, meaning that you can't usually target quite as many microbes as you would with 16S. And then lastly, we have metagenomics, which captures all of the microbes at the species and strain level. So essentially, in this case, we're grinding up all the DNA sequencing every single gene in that sample. And from this, we can get information about all the microbes that are there at the species and strain level, and we can also tell their functions. This is currently kind of prohibitive because it's quite expensive, but it's rapidly dropping in costs. And I think that increasingly research is moving towards metagenomics, and I think that clinical practice will as well. So I wanted to provide an example of the results of culture versus sequencing for the same stool sample to really dry this point home of why we shouldn't be using culture-based tests. So some of you may recognize tests that look like this. This is a culture, a bacteriology culture. And you can see that they use a semi-quantitative scale from no growth to four plus, and they kind of rank the bacteria based on that. So the problem is when we match this up to what we get from 16S sequencing, you can see I took all of the microbes that were present in the culture-based sample, and I basically pulled them out of the 16S spreadsheet to determine what their actual relative abundance in the gut microbiome was. And we could see that less than 4% total of human gut bacteria were actually captured by the culture result. The other thing is that it skewed bacterial abundance. So I want to direct your attention to enterococcus here. You can see that it comes up as four plus on the culture-based test, but when you look at enterococcus here, it's less than 0.01% of the ecosystem. So this isn't a huge problem here because this enterococcus is considered a beneficial or commensal species, but if you had a four plus come up for pseudomonas aeruginosa, you might treat that when in reality it is only 0.01% or less of the ecosystem. So this is why we really need to move towards sequence-based tests. So the second myth is that we know exactly what a healthy microbiome looks like. So it's generally believed that diversity and community stability are key components of a healthy gut ecosystem. This is kind of the most widely touted measures we can look at, but even these have been associated with disease states, so there are definitely exceptions to that rule. The other thing is that keystone beneficial species that are generally recognized to be crucial for microbiome health, such as Bephidobacterium, are absent from the guts of traditional cultures like the Hadza. In general, also the gut has a very high degree of inter-individual variability. So on average, two people only share about a third of their gut microbes, and it's a complex network of interactions. So the abundance of a few microbes does not tell us the health of the network interactions and how the microbes are interacting in the gut. So I actually did an independent analysis of popular stool and microbiome tests. I unfortunately don't have time to go into all of the results today. Essentially, which stool test is best kind of depends on what you're looking for, but I will point you to, if anyone's interested in looking at that more, you can find that on my website. What I'm using currently with my clients, I'm using GI map and UBIOM. So I use GI map to look at bacterial pathogens, yeast, parasites, and gut health markers. And then I'm using UBIOM to look at bacterial abundance and the relative balance between microbes. Given what I said about how we don't exactly know what a healthy microbiome looks like, I'm mostly using UBIOM at this point to look for major red flags in the gut microbiome. So really high abundance of proteobacteria, for example, has been associated with inflammation. And other kind of bigger picture traits like that. I will say that this is a constantly evolving space and I'm continuously evaluating new companies that come out in this space. And I think soon I'll be switching to metagenomics as the cost drops and becomes more reasonable, especially for repeat testing when you want to test, do an intervention, and test again. All right, so now I wanna transition a little bit to talking about microbial therapeutics. So I already mentioned antibiotics earlier. Obviously that's not the best microbial therapeutic as we know that it's generally detrimental to the gut ecosystem. I'm also gonna talk about diet and exercise, which has been the focus of my research, The Blast Four Years. I'll touch very briefly on herbal antimicrobials and then discuss probiotics, prebiotics, and fecal microbiota transplants. So we know that diet rapidly and reproducibly alters the gut microbiome. So not only does your long-term dietary pattern impact what your gut microbiome composition looks like, but you can actually have diet, short-term changes in diet, alter the gut microbiota composition within 48 hours. This seminal study by David had also found that diet alters microbial gene expression, and this paper has been highly cited over 2,700 times. And I'll mention why that's relevant in just a second. But first, I kinda wanna transition into this other myth that a high-fed diet is bad for the gut microbiota. And I know there were a lot of questions at the keto panel yesterday about what keto does to the gut microbiome, and so I'll touch a little bit on what we know about that now. So the first thing is that a lot of people who are saying a high-fed diet is bad for the gut microbiome are relying on animal studies. And this is extremely misleading. So in rodents, a high-fed diet, as is commonly termed in the literature, is in reality a diet high in refined soybean oil, lard, refined sugar, and very low in fiber. The natural diet of a mouse is also low in fat and high in carbohydrates. They don't metabolize fat the same way that we do. And additionally, the lab mice of choice, which is C57 black six mice, are genetically selected to gain weight in response to a high-fed diet. So we really can't rely on animal studies to tell us whether a ketogenic diet is appropriate for gut health. So what's interesting is that this study that I just showed, when you actually look at the supplementary data of this highly cited 2,700 citations study, the animal-based diet that they used in the study, when they showed that the switch from a plant-based to an animal-based diet shifted the gut microbiota, the animal-based diet was ketogenic. And they actually measured urine ketones to ensure that the participants were in ketosis. So I'm gonna kind of dig into the results here. So essentially you can see they were on kind of more of a plant-based diet. They went on an animal-based ketogenic diet and their diversity in the gut microbiome actually increased the beta diversity. Of course, like I said, diversity isn't everything. There were a number of other changes that occurred in the gut microbiome. And then it kind of returned to baseline levels pretty quickly after shifting back to the initial diet. So this essentially points to the metabolic flexibility of the gut microbiome and kind of back to this idea of seasonality. And I know this is a lot of text, but I just wanted to share, this is actually from the discussion of that paper, but is not widely talked about. So they said, our findings that the human gut microbiome can rapidly switch between herbivorous and carnivorous functional profiles may reflect past selective pressures during human evolution. Consumption of animal foods by our ancestors was likely volatile depending on season and stochastic foraging success with readily available plant foods offering a fallback source of calories and nutrients. Microbial communities that could quickly and appropriately shift their functional repertoire in response to diet change would have subsequently enhanced human dietary flexibility. So I think this is a really important point because we're talking about whether ketogenic diet could be bad for the gut microbiome. The truth is, it's probably just the microbes that are responding to our dietary changes and essentially enhancing our dietary flexibility. So the other thing, diving further into this myth, the other concern is usually around butyrate. So we know that dietary fiber is well known to have effects on the gut microbiota and it's fermented by colonic microbes into metabolites called short chain fatty acids. The three most abundant short chain fatty acids in the human gut are acetate, propionate, and butyrate. And butyrate has gotten perhaps the most attention and it's the most well known because it helps maintain gut barrier function. So gut drive butyrate increases mucus secretion, epithelial proliferation, and turnover. And this is because it's the primary fuel for gut epithelial cells. It makes up about 70% of their energy they get from butyrate. It also promotes the release of antimicrobial peptides and helps to maintain physiologic hypoxia in gut homeostasis. So a lot of people are worried whether keto will reduce their production of butyrate. But there's a metabolite of protein fermentation called isobutyrate which they found can actually stimulate the same receptors as butyrate in the gut so it can actually potentially have the same signaling functions as butyrate. And then second is that acetoacetate and beta hydroxybutyrate are the two primary ketone bodies. And these potentially can supplement colonocytes, the cells in the colon. So this is the epithelial cell of the colon. You can see that it can either get butyrate from the lumen to go down this pathway to get energy or it can get ketones from the blood that feed in even later in this pathway and provide energy for replication. So ketone bodies are actually an intermediate in the butyrate metabolic pathway. So the idea that a loss of butyrate if you have high levels of ketones might not necessarily be a bad thing and this might be an adaptive mechanism, this pathway. It's also important to note that the inflamed gut actually has impaired butyrate uptake such as an inflammatory bowel disease. So if you have mucosal inflammation you're not gonna get as much butyrate uptake but you could still potentially get ketones from the blood. And there's a number of people anecdotally and a few preliminary studies that have suggested that a ketogenic diet might be beneficial for some people with IBD. So kind of to summarize my take on that myth, I know I expanded on that a lot but I know there was a lot of interest in that topic. There's no evidence that a well-designed ketogenic diet is detrimental to gut health at the moment. And in fact, some studies suggest that ketogenic diet induced changes in the gut microbiota and gut barrier function may even be the reason for some of the benefits of ketosis. So they've shown it in at least one study with multiple sclerosis where they've, they showed that the ketogenic induced changes in the gut microbiome was responsible for the benefits for MS. I wanna put a huge caveat here. I know I talked a lot about this. I'm not fully on a ketogenic diet. I did it for a while. I kind of cycle in and out. I don't believe the ketogenic diet is right for everyone but, and especially not necessarily right for everyone with a gut issue. But I definitely just kind of wanted to set the record straight about where the evidence is at this point. You can definitely do a keto in a way that does not support gut health and you can probably do it in a way that does support gut health. So lots of non-starchy vegetables and quality meats and fats could definitely still feed your healthy gut microbes without causing detrimental changes. If you're interested in this more I also have this blog article that I wrote that outlines all this research in detail and has all of the references. So before I leave the diet section I know I focused a lot on keto but some of you may have heard Angie, Rob and Mickey talk about this yesterday. But we have an upcoming study where we're gonna look at the autoimmune protocol and how this impacts the gut microbiota and short chain fatty acids in eczema and psoriasis patients. So I'm very excited about this and I will be recruiting this coming week. We'll also be directly measuring gut barrier function with the double sugar electrolose mannitol test. So we're gonna be able to see does the autoimmune protocol improve gut barrier function essentially reducing leaky gut. So next I kind of wanna pivot to talk about exercise since this has been a major focus of my lab research. And our laboratory and others have demonstrated that exercise has independent effects on the composition and function of the gut microbiota. In animal models we've shown that exercise tends to increase microbial diversity and increase butyrate producers. It also increases sequel short chain fatty acid production and the abundance of lactobacillus and bifidobacterium which we typically think of as healthy in the mouse gut microbiome. In cross-sectional studies where they've compared essentially compared athletes and non-athletes, they found that again athletes tended to have higher microbial diversity, higher abundance of fecalibacterium prosnitsi which is one of the main butyrate producers in the western gut. Increased levels of acromanzia musinophilia which is an important mucus associated bacteria that's been associated with the lean body mass. And increased carbohydrate turnover and short chain fatty acid production. We also in 2017 performed the first longitudinal study of exercise on the gut microbiome. So we actually took sedentary individuals and put them through an exercise intervention to see if that had effects independent of diet. So we kept their diet the same throughout the study to kind of get over the issues with cross-sectional studies where athletes are eating very differently from non-athletes. And in those longitudinal studies we found that exercise increased fecal butyrate and butyrate producers particularly in lean individuals. We're still not quite sure why that is but potentially diet has a greater impact in obese individuals and exercise just can't move the needle as much in the gut microbiome. But we certainly need future studies in larger populations. And if anyone's interested, I have a recent review paper that was published in exercise sports science reviews that covers all of the research on exercise in the gut microbiome. I do wanna cover a few myths related to exercise in the gut microbiome. So a lot of people think that strenuous exercise is always better, no pain, no gain. So we've actually shown in mouse studies that this can be really detrimental to the gut microbiota. So a student in our landmark Cook a few years back did a model where he did, there's a number of ways to exercise mice for studies. The first is forced treadmill running, which is a single bout acutely about 60 minutes long where they're running on a treadmill. The alternative is to do voluntary wheel running where you basically just put a wheel in the mouse's cage and they enjoy running throughout the day, they hop on and off. And what was really interesting is that we found that the forced exercise training increased colitis outcomes and gut inflammation, whereas the voluntary exercise training, the wheel running, reduced colitis outcomes and inflammation, suggesting that the modality of exercise really matters and potentially how you feel about it affects the response to exercise. Interestingly, another student in our lab, Jacob Allen, followed up on this in 2015 and showed that the different modes of exercise also differentially altered the gut microbiome. So this is a PCOA plot is essentially the groups that cluster together tend to have more similar microbiomes and if they cluster separately, it's distinct microbiomes. So we found that these different modes of exercise had different effects on the gut microbiome and we wondered, okay, is the difference in the gut microbiome what's responsible for the differences in the colitis outcomes? So we did a really cool study where we transplanted the microbes from either a sedentary mice or mice that had voluntary wheel run into a notobiotic or germ-free mice. So these mice are raised in sterile isolators. They've never seen a microbiome in their lives and this is a key way in microbiome research that we can get it causality, get closer to causality. So we can transplant a gut microbiome into these germ-free mice and see what happens afterwards as a result of the microbiome. And so we transplanted the sedentary or exercise microbiota into these germ-free mice. We allowed colonization to occur for a while and then we induced an acute colitis insult and we found that the exercise microbiome, attenuated body weight loss, which is one of the hallmarks of colitis, it also reduced colonic shortening and clinical symptoms. So this was really interesting to us that actually changes in the microbiome from exercise are what's potentially conferring benefits on gut health. All right, now I wanna briefly touch on herbal supplements. This could probably be a whole presentation in its own. But one of my major concerns is that across the blogosphere, there's lots of people who are convinced they have candida or they think they should do a parasite cleanse once a year and they really don't know what's in their gut, first of all, that they're treating because they haven't tested. And they're using these herbal supplements, some of which are potentially detrimental to the gut microbiota. So herbs really have great potential to beneficially modulate the gut microbiota and I think it's an area that we need a lot more future study because there's definitely a lot of potential there for them to both inhibit pathogenic overgrowth and to act as prebiotics, stimulating the growth of beneficial bacteria. And there's been some herbal formulations that have already been shown to do this. But they also potentially have great ability to do harm. So some research by Jason Horlach has shown that in vitro, grape seed extract, which is commonly used, it's one of the most popular herbal supplements for treating candida and gut dysbiosis in general, was actually worse than the antibiotic clindamycin in terms of affecting beneficial bacterial populations. And it didn't even inhibit the pathogens that we would expect it to. So more studies definitely need to be done. Most of the studies done to date are using culture that's been inoculated with human fecal material. So we really need more clinical trials to be able to understand how herbal antimicrobials impact the gut microbiome and whether they're safe to use long-term. All right, next I have a number of myths I wanna cover on probiotics. For those not familiar with the definition, probiotics are live microorganisms which when administered in adequate amounts confer a health benefit on the host. And the first myth and probably the most prevalent is that strain doesn't matter if you know the probiotic species. So when we're looking at probiotics, we have genus, species, and strain. So here's an example, lactobacillus ramnosis GG. So a lot of probiotic supplements will simply list lactobacillus ramnosis and they won't actually tell you the strain. But two strains of the same species can have very different characteristics. And I could put six slides up here of evidence to demonstrate this, but one clinical example is that they've shown that one strain of lactobacillus plantarum actually improved symptoms of IBS and another tends to increase bloating in abdominal pain. So there's definitely very different effects based on the probiotic strain. Most probiotic formulations do not provide this information or they have secret strains and will tell you it's proprietary information when you contact them. This is really concerning because if they're not willing to share the strain, the likelihood that they haven't selected it carefully or that clinical trials haven't been done on it is pretty likely. So I only recommend probiotics that provide strain information and that have demonstrated advocacy and safety in human clinical trials. Myth number seven, and I know this might turn a few heads, fermented foods, myth number seven is that fermented foods have all of the health benefits of probiotics. So fermented foods include kombucha, sauerkraut, kimchi, yogurt, kefir, lactoferments. These may contain a diverse community of microbes that are not well-defined. Strains may differ from batch to batch and lack specific therapeutic qualities. So these wild ferments are not harmful. There's definitely a tradition of use but we can't just rely on these for specific therapeutic effects. So if you have a gut condition and you're just saying, well, I'm just gonna throw a bunch of fermented foods at it, it might help, but it might not because the strains are really gonna differ from batch to batch and won't have as specific of a therapeutic effect as if you were to find a probiotic strain that's been shown in clinical trials to help your specific condition and take that in an isolated form. So they're not the same as probiotics containing standardized, thoroughly researched strains. Myth number eight is that probiotics help recede the gut microbiota. So some of you may be aware of this myth. Most probiotics do not permanently colonize the gut. Some appear to transiently colonize for a week to up to several months, but most do not colonize at all. However, this doesn't mean that probiotics are useless. You might have seen a lot of media coming out after some studies recently that suggested that probiotics often don't colonize. Well, we already knew that and probiotics are definitely not useless. They still confer benefits while in transit through the GI tract. So they're known to ultra gene expression, modulate the immune system and outcompete pathogens among other benefits. Myth number nine, this is one I covered in detail recently is that you should always take probiotics after antibiotics. And most people think that this is absolutely, you take antibiotics, no question, you should be taking probiotics. There was a recent two papers published in Cell that I covered on my blog and on Chris Cressor's podcast, suggesting that the probiotics actually delayed the return of the native commensal gut microbes when they were taken after antibiotics. And particularly they delayed the return of butyrate producing microbes, which we know are particularly important to health. So it's possible that other varieties, such as Saccharomyces bulardi, which has been studied for antibiotic associated diarrhea, or other probiotic formulations that they did not use in this study, they only used one formulation of 25 different strains. It's possible that those others may be effective, but we really need more research to be able to say definitively that we should be taking a probiotic after antibiotics. So I get a lot of questions now about what should we be doing if we have to take antibiotics. And this is something I've really been exploring lately and will be publishing on my blog soon. But there's evidence lately of an oxygen dysbiosis connection. So the normal healthy colon is supposed to be an anaerobic environment without any oxygen. And so you can see here, this is a healthy colon cell. So you can see that there's fiber that's being converted into butyrate in the gut lumen. And that butyrate comes in and actually activates this target called P-pargamma. And that fuels the beta-oxidation of the butyrate and all this oxygen gets used in that beta-oxidation. But when you have an inflammatory profile where you have butyrates that's been depleted by antibiotics or by another insult, essentially you don't have that activation of P-pargamma. And you're not getting as much beta-oxidation. So instead you have to rely on glucose from the blood and you're getting this fermentation process to lactate and a leakage of oxygen into the gut. And this is really important because oxygen and lactate in the gut can fuel the growth of pathogenic microbes. So this is potentially the mechanism by which antibiotics induce dysbiosis. And so like I said, this down regulation of that P-pargamma shifts the gut towards this inflammatory colonocyte profile. And I'm exploring a lot of the implications for this that perhaps targeting P-pargamma during antibiotics could potentially prevent this dysbiosis. And one of the things that we know activates that P-pargamma of course is butyrate. So if you don't have your own, if your butyrate gets wiped out by the antibiotics perhaps supplementing with butyrate while you're taking antibiotics could maintain that activation and prevent this process where you're getting an expansion of pathogenic microbes. So, and that's actually something we're hoping to study in our lab soon. All right, I wanna touch a little bit on prebiotics. So prebiotics of course are substrates that are selectively utilized by host microorganisms conferring a health benefit. So it's the substrate that the gut microbes feed on rather than the microbes themselves in the case of probiotics. So myth number 10 is that prebiotic supplements work the same for everyone. So prebiotics are surprisingly the third most common and fastest growing non-vitamin dietary supplement in the US. So there's a lot of interest on them. You can find them in almost any grocery store now. So there's, I see lots of people that are testing their gut microbiome seeing that they have low abundance of certain microbes and then looking for certain prebiotics that might boost those particular microbes. And this is an interesting strategy. The problem is we've seen in many studies now that prebiotic supplementation, the response to it is highly individualized and very much depends on your baseline gut microbiome. So for instance, resistance starch is a prebiotic that's supposed to increase production of butyrate and on average it does. However, some people actually go down in butyrate production with the resistance starch supplementation and this has been demonstrated in several studies now. And unfortunately this doesn't leave us with great solutions at the moment. There's a number of groups that are currently working on in vitro diagnostic tools. So essentially you'd submit a fecal sample, they'd test it in a 96 well plate with different prebiotics and they'd be able to measure how much butyrate you produce from each of those, your gut microbiome produces from each of those prebiotics. So they're currently testing how much those in vitro diagnostic tools will actually predict your response if you take that prebiotic. So that'll be really interesting in the future to look out for ways to personalize prebiotic therapy potentially. The last one, I wanted to make sure I touched on fecal microbiota transplant because there's a lot of hype about it. It has excellent efficacy for recurrent C. diff, nearly 100% and is currently being explored for a wide range of other conditions under investigational new drug applications. Still, there's a lot we are missing with current screening techniques, viruses on characterized microbes and there was actually a recent FDA report of two patients that contracted severe infections, one of whom died from an FMT that contained a multi-drug resistant organism. So I just wanted to stress for all of you trying to modulate your own gut microbiomes that it's always best to find an experienced clinic that is carefully screening donors. And I'll also mention that none of what I presented today should be construed as medical advice, so please make sure to always confer with your own physician. In summary, microbiome modulation has enormous therapeutic potential but we need to follow the evidence and make sure that we're constantly looking at it and evaluating new evidence. We should be very wary of tests and supplements that lack evidence, have secret strains, are not willing to provide that information about how they're manufactured. There are many companies in this space, unfortunately, that are taking advantage of the hype around the gut microbiome without any understanding of the literature. I can't tell you how many probiotic companies I contacted to ask them about their strain info and they just told me the genus and species, thinking that was the strain. And I said, no, that's the genus and species, what's the strain? And they still couldn't tell me because they weren't familiar enough with the space to understand what was in their product. So that's definitely a concern. And there's lots yet to be understood and discovered so I'm really excited to be a part of this field and I think we'll have a lot to share in future years. If you want to learn more, this is my blog here, ngmedicine.com. I have a monthly newsletter and I'll also have a new ebook release very soon that will have all of the research that I covered today. So if you subscribe, you can be notified when that's ready. And then you can also get a copy of this presentation at this link here. I really have a wealth of resources on my blog related to these topics. I didn't even have a chance to touch on SIBO today but there's a lot of recent paradigm shifts in SIBO for those who are interested in that. And you can also follow me on Facebook or Instagram at NextGen Medicine.