Oh, that's my icebreaker question. We're going to put everyone on the spot. I know. Seriously, hold on.
All right. The room is filling up. Good morning, everyone. Good afternoon.
Good morning. Hello, hello. Thank you for being with us. We're going to give a few minutes to... the room to fill in and let everyone check in.
And as is tradition in our Microbiome Labs webinars, I always like to ask an icebreaker for us all to connect for a second. And one of my favorites is, what did you have for breakfast today? If you have broken your fast, what have you had for breakfast today?
I've had some eggs and coffee. eggs and coffee okay and half a banana that my daughter didn't finish uh-huh yes yes lots of people fasting already nice lots of eggs gotta love eggs oh poached salmon that's very love that wow some people have really fancy breakfast jennifer florida has poached salmon with lemongrass tea someone has venison chili with sweet potatoes and broccoli i love that people have time for this i unfortunately don't that's enough for that i guess bison and kraut like oh my gosh do you guys have personal chefs or something i love it oh very good very good all right this is always fun beef stew and eggs yeah i'm happy to hear we've got like hearty breakfast this is winter we gotta have hearty breakfast Well, good, everyone. Thank you for playing with us.
So let's get started. My name is Angelica. I am on the events team with Microbiome Labs.
And we're so honored that you're here with us today because we just began this series towards the end of 2023. And we're now in 2024. And we are continuing with our clinical science liaisons. We have four brilliant ladies. Oh, wait, is it five brilliant ladies on our team? And they are showing up live with you twice per month to educate you on the foundations of the microbiome and the digestive tract and to teach you clinical applications with applied microbiome science, which you can use in your clinic.
So you can be in the know when it comes to microbiome-centered care for your patients and your clients. Today, we have our foundations webinar. Nope, we don't.
This is our webinar. Oh gosh, you guys. I'm like, we're at the end of the month now. It's our clinical applications day.
Yes, it's our clinical applications day. And Kara Seidman is with us. She's going to be talking about becoming a microbiome expert by introducing you to BiomeFX, which is Microbiome Lab's own patented technology and stool test.
So I'm going to tell you a little bit about Kara, and then I'm going to let her take it away for the next hour here. All right, so Kara Seidman is one of our... Lovely, lovely clinical science liaison.
She's a registered dietitian with a wealth of experience and knowledge in microbiome and digestion specific dietetics practice. She has been a registered dietitian for 13 years. Most recently, she spent the last eight years working in a large gastroenterology practice, building a program that integrates functional medicine and nutrition into the patient care model.
With a strong focus on the microbiome and overall health, Kara has guided many patients on a journey to reclaim their health and well-being. And a fun fact about Kara, she is a very bubbly and vivacious woman. You're going to find out really soon.
But she said when she was nine years old, played on Wheel of Fortune. Is that right, Kara? Not when I was nine, but nine years ago.
Nine years ago. I didn't know you had fun facts about me yet. That's probably... My claim to fame is that I... From your bio.
And she kicked everyone. Took the winnings to go travel for a year. So she's obviously a smarty-pants. Well, I don't know how smart you need to be on that show, but I am competitive when it comes to...
You have to be strategic. That's for sure. Okay.
So without further ado, I will let Kara take it away for the next hour. Awesome. Well, thank you so much for that introduction.
I didn't know there was a fun fact on there. So how cool. Well, thank you everyone for joining us for our kickoff of BiomeFX webinar and series. Can you guys hear me okay on my side?
Someone said poor microphone quality. So I'm going to try to do my best to speak up. Okay, cool. Thank you for Valerie for giving.
Okay, good. Thank you guys. Okay, so please, if you have any questions throughout the webinar, please make sure you put it in the Q&A box.
One of my colleagues, Alicia, is on and she's going to hopefully answer some of the questions throughout. And then we'll have time at the end for a little Q&A. But we just want to make sure that we can get to everyone's questions as best we can.
But like I said, thank you so much for joining us for our kickoff webinar. This is a four-part series that's focusing on biome effects, which is a functional microbiome analysis. So for those of you who aren't familiar with it, this is a stool test, right? It doesn't only look at who is in the gut, but what we're going to learn and what becomes very important is what are microbes doing? And so this is why, you know, different stool tests differ from one another.
And so biome effects, right, we call this a functional microbiome analysis. And it comes down to really the type of technology that's being used. And we'll get into all of that nitty gritty. And it's because of that difference in technology that we can really get into the functional profiles of our microbiome. So with a functional microbiome analysis, by understanding the functional capabilities of the microbiome, you can actually start to uncover some potential links between specific microbial functions and various health conditions.
So this knowledge. really opens up the door to personalized medicine and personalized interventions, you know, targeted supplements, targeted dietary support, which can obviously improve our overall health and prevent and treat certain conditions. Okay, so just to go through a few of the highlights of functional microbiome analysis, we'll test utilizes what's called whole genome sequencing. And we're going to get into what that means as we get throughout this webinar. And the goal of the test is really to provide valuable insight into the gut microbial ecosystem to paint a picture of the overall strength and resiliency and the overall health of the microbiome.
And it does this by reporting not only who is in the gut, but what are they doing there and their function. So how are these microbes interacting not just with each other, but the human host as well. And so...
this will also give insight into the impact that our diet actually has on microbiome. So this valuable insight directs our treatment plans and can really help to ultimately restore that balance to the microbiome, rebuilding strength and resiliency, you know, offering specific dietary changes, lifestyle changes, supplement changes to strengthen the microbiome. So let's first get into a little bit of a background.
You know, if you've been to microbiome webinars, if you've listened to our foundation, we know that the microbiome is extremely important. And it becomes even more important to actually look at the microbiome and assess it. And I think that's something we all here can agree upon, that the microbiome has to be common and is often a focus when we're working with our patients.
And so the microbiome, I like to think of this really as the foundation of our health, almost like we think of the foundation of our health. You can have, you know, you can go look for homes and find the most beautiful home in the world that has everything that you've ever wanted, all the bells and whistles. But all of a sudden you get that report back saying, oh, there's an issue with the foundation. Now, my question would be, would we still buy that home? Would we still want to move into that?
And so we really want to view the microbiome as the foundation of our health. As we go through life, we experience, you know, different microbiome disruptors or these disruptions that can, in fact. drive crafts and our foundation.
So why is a healthy microbiome important? It's because it impacts our overall health and it produces very important postbiotics, performs functions that benefit our health. There we go. We know that a healthy microbiome contributes to a well-functioning intestinal barrier, which we all know is extremely important.
We'll talk about a healthy microbiome has a low inflammatory load. And we know that a healthy microbiome builds a more resilient environment that's less likely to experience chronic disease. So let's just review. For those of you who've been to any of our webinars, we use this schematic a lot. So I just want to review what it means to have a healthy gut, because if you go through the research in looking through PubMed and what's considered a healthy microbiome.
There really isn't a consensus, but what we know is there's key characteristics, which include having good microbiota diversity, so high diversity and having a high diversity of those protective strains. We know we want to have a... whoops, a high production of short chain fatty acids, as well as those well formed tight junctions so that we can protect our immune system. When we have leaky gut, or there's dysbiosis, right, this is a term that we use a lot, we essentially have an imbalance of that microbial ecosystem. And we essentially see that we have low keystone strains, we're going to talk about these later on.
These are what we call our group likes to call these the Instagram influencers of the microbiome. They don't take up a lot of real estate, but they have a disproportionate effect on the influence on the overall health of the microbiome. So it's not a good thing when we have low diversity of these keystones like acromantia and faecal bacterium and bifidoloma.
So as we lose diversity of these keystone strains, these protective strains, we start to lose that production in short chain fatty acids. And essentially, we end up with a disrupted mucosa. We see disrupted immune response.
And essentially, we have a dysfunctional gut barrier. And we find that all these inflammatory byproducts and bacteria can enter into circulation and activate the immune system. And this can essentially impact us beyond.
So it becomes so important that we actually can visualize and see what's happening within one's microbiome. So when we talk about what impacts the microbiome and what starts to drive those cracks in the foundation, what I like to think of as the hurricanes, the winds, the earthquakes, the bomb cyclones, like all these things that we know can essentially affect our foundation. We call this dysbiosis risk factors or what's been termed the exposome.
So everything from medications and natural antimicrobials to infections and excessive alcohol intake, smoking and stress and lots of lifestyle, right? Travel. Of course, our diet, right? Standard American diet. We know environmental toxins like glyphosate, heavy metals impact the microbiome.
Of course, a lack of sleep, even intense exercise. And so more importantly, when we're exposed to these microbiome disruptors, ultimately our goal and what we want to start to think about is how do we begin to restore that ecology and environment within the microbiome? So I'm just going to pause for a moment.
And I want everyone to kind of take a step back. think about. You can even put it in chat if you want.
But how much of the exposome or how many of these things do we encounter in our day to day life? I'll throw myself on the spot. So I have to travel monthly for work.
Sometimes there's excessive alcohol intake, which I put here more than one drink per night for women, two drinks for men, which, you know, sometimes on the weekend, I like to have a couple of drinks, lack of sleep, I have a one and a half year old that likes to talk really loudly in her sleep, you know, stress. So all these things that I think about, think about that I am exposed to, and I'm not someone who generally has GI disturbance, I would say I'm pretty healthy. But what impact is this having on my microbiome as I continue to move through life and progress through my day-to-day living?
Because ultimately, and I think everyone here would agree, and if you've come to our foundations webinars, and if you haven't, we're going to repeat them. But if you've come to our foundations webinars, we really focus on the overall microbiome impact. impact that our microbiome has not just in our gut, but beyond.
Because we know that it can provide clues into how we can even start to prevent potentially future issues from taking place or link us to what's driving conditions outside of the GI tract, right? Because our microbiome is our foundation. And this is really at the crux of what the gut organ access. And this intricate picture here really explains that there exists these many bi or multi-directional pathways between the gut and our non-gastrointestinal systems. They run along various nerve pathways through the portal vein, you know, directly through the intestinal epithelial barrier.
And microbial metabolites or these byproducts can actually act as biochemical signals that travel through the various axes. And that's essentially what modulates functions in the tissue. And so it becomes important that we start to understand the role that it's playing. So ultimately, we want to figure out how can we get a glimpse into how the microbiome can be impacting us beyond our gut. Because we know we're exposed to these risk factors, we know that we're exposed to these disruptors throughout our life.
So measuring dysbiosis, we can actually help pave the path to how we need to clinically sort of move through and clinically work with our patients. Because we know that different types of bacteria perform different functions, those postbiotics and functions being performed in the gut can become altered when there is dysbiosis. And so the only way we can really look at that is to... start to explore and assess the microbiome. And that is where we're going to talk about our biome effects, which is a functional microbiome.
So I want to bring up this idea, it's sort of a paradigm shift. Because when we talk about different types of stool tests on the market and different types of microbiome tests. We're ultimately talking about different tests. A functional microbiome analysis is using different types of technology.
So when we're thinking about stool tests, a lot of times we're usually thinking more of something like a parasitology or a stool chemistry test, which we'll talk a lot about these differences, but different technology or techniques. are used. And so it's like, we can't really compare apples to oranges, right? Yes, they're both fruit. Yes, they both have carbohydrates, but they have different vitamins and minerals, they taste different, they look different.
So for our rest of our time today, we're really going to learn how a functional microbiome analysis differs. And what can we glean from the type of from that information to potentially, you know, to help sort of guide our treatment plans that we cannot glean from other tests. So we'll go into that differentiation.
Okay, so this next slide, I'm going to take a few moments to just go through kind of broad, sort of high level overview of the difference between traditional stool tests and biome effects, which is a functional microbiome. Because the real difference being this sort of paradigm shift in the way we're actually looking at the microbiome, and not just how we're looking at it, but also how are we using that information to start to restore balance and build resiliency to start to build or, you know, fix up those cracks in our foundation. So I'm going to walk us through this chart.
And if you know, again, if you have questions, please put them in the q&a. But not to necessarily say one is better than the other. They're just different tests.
So I do want to put that out there that I want us to really start to understand how these tests differ. So a traditional stool test, where we might see something like a stool chemistry where, you know, SIG A or, or fecal fat, a microbiology or parasitology class. or tests, these may actually give us information on, you know, few microorganisms, but they don't necessarily provide a detailed picture of who is there and more specifically what they're doing. So without that information, without knowing what our microbes are doing within the microbiome, we're really missing an important, you know, piece of information that can actually help better direct our treatment plan.
So it's often geared towards, you know, probing for a specific diagnosis with the intention generally to treat. meaning who are we trying to eliminate or who do we need to eliminate? So it's a little bit more, it can be for some of us and, and, and especially as you know, we're starting to learn more about the microbiome, but it can often be a little bit more one directional and don't get me wrong, right? Everyone, we want a diagnosis. Like everyone wants a diagnosis.
I always, you know, sort of joked working in GI that I never worked with a group of people that wanted to be diagnosed with something more because they needed something. They wanted something to explain why they. feel so bad. And this is really why the term even functional GI disorders got changed to disorders of gut-brain interaction, because it almost sounds right.
People view functional as less legitimate. But as we know that when we're talking about microbes, we can't diagnose based on microbes. And as you progress through these Biomeffects webinars, we're going to get into microbial patterns and patterns we may see with specific conditions like leaky gut or inflammation or upper GI disorders, but we can't create a diagnosis. we can't diagnose based on. And as we know that sometimes people, there isn't a diagnosis because it's what's happening in the microbiome that's driving a lot of their symptoms.
So I just want to sort of kind of paint that picture. That's the paradigm shift, right? That we're looking at the microbiome a little differently. So with a functional microbiome analysis, we're getting a better gauge of diversity and we're also getting the microbial function.
So we're gaining information about the overall strength and resiliency. And I really like this for people who maybe aren't experiencing GI symptoms, but as we know, and what we saw in that previous slide, that the microbiome impacts beyond the gut itself. And so this can be actually helpful and give better clues into how the microbiome is driving symptoms beyond the gut. And that's really, you know, why a functional microbiome analysis is necessary and how it's actually different, because you're going to get that overall ecology.
So with a functional microbiome analysis, We're looking more at who do we need to support by increasing or decreasing or balancing, because we know that the microbiome is so much more intelligent and complex than just focusing on microbes in isolation. And again, like I mentioned, you can often see clues on a functional microbiome analysis that can help you capture even potentially reverse conditions before they ever even become symptomatic. It could, again, looking at metabolic health and autoimmunity and liver health. So they're just two different tests. So how can we differentiate a functional microbiome?
So with a functional microbiome analysis, we're going to focus on functions by products of microbes and how that impacts symptoms and health conditions. So we're going to get insights into things like ammonia and hydrogen sulfide and short chain fatty acids, the strobilum. And we'll go into more detail about this. This can often help sort of lay the path of what needs to be done next.
And it can often help guide some of that clinical judgment. We want to focus on creating a healthy ecosystem that naturally limits pathogens. So this is where we get into the conversation a lot of times about.
building versus killing. And we will discuss this more, but I like to sort of use this and understand the microbiome because it can help provide that insight into when it's appropriate to potentially do a kill protocol or help us answer questions like, can my patient's microbiome even handle the use of antibiotics and antimicrobials? And as we know, killing is absolutely necessary. It's part of treating, it's part of certain conditions.
But we want to know if someone's microbiome lacks the resiliency and the strength to respond the way we want them to when using antimicrobials. And so we'll talk more about that. You know, we don't want to make things worse, essentially. We don't want to necessarily kill off microbes, because if you kill the bad, you also kill the good that continue to drive the issues that we're dealing with.
And we know that dysbiosis impacts the gut organ access. We know it plays a role in conditions outside of the. the gastrointestinal tract.
So functional microbiome analysis can benefit patients with and without GI symptoms. So let's start our very first step to becoming a microbiome expert. Let's take a look at what's inside a biome effects test.
So when we look at a stool analysis, or we're looking at a microbiome test, we're really looking at sort of three main questions that we're wanting to get answered. So one is who is in the gut? And that's looking at what is the relative proportion of community members?
You know, how rich is the community? How evenly distributed? And we'll talk, we'll go into more depth with each of these sections. We're also looking at what are they doing there?
So what functional chemistry is actually being carried out? And how do they interact with the environment and each other to carry out those functions? And we're looking at is there balance?
We all understand balance is key in the microbiome. You know, there is always a thing as something being too good. And we're going to go through that with each section. So balance is...
is necessary. And then finally, you know, why is all this important? Because if we don't focus on building that strength and building resiliency in the microbiome, catching up those cracks in the foundation of their gut, the patient will most likely continue to experience decline in their health or potentially start to develop, you know, symptoms along the way.
So how can we make these microbiome disruptors, this exposome, less impactful and less damage-causing? So looking at Inside a report, we're going to look at gut microbial composition, diversity, alpha and beta. And this is the only test actually with the functional microbiome analysis that will report both alpha and beta. And we'll go into the difference.
Something known as resistome occurrence, pathobiome. Now, these three markers, these are really a marker for strength and resiliency. So they really kind of lay down some of the foundation of what you'll see throughout the rest of the test.
Dysbiosis ratios, we're going to look at keystone species, short chain fatty acid producers. And then. Again, what separates because of the technology, which we'll get into the functional analysis, sacrolytic fermentation, proteolytic fermentation, hormones and neurotransmitters, as well as vitamin biosynthesis. So when you open up the test, you're going to get a report summary. This is a high level overview, you know, 50,000 foot view as far as what the test is going to tell you.
And for those of you who've done this test, I personally don't spend too much time, but this is a nice page when you're working with your patients because it gives kind of just that snapshot. So it gives an overview of the general health, strength, and resiliency, and that's something we could term this microbiome index. And that takes into account your alpha, beta, resistome, and pathobiome. So again, it's just a snapshot of how healthy the microbiome is. We're going to get an at-a-glance, out-of-range keystone species and which functions are out-of-range.
And then also tells you your dysbiosis ratio is out-of-range. So we're going to go a little bit into depth into each of these sections. So the first section of the test is... focusing on diversity. This is what's known as alpha and beta diversity.
And again, this is the only functional stool test that looks at both alpha and beta. Most of the tests will look at components, but we are the only one that looks at both. And these are two very important markers. I could spend the rest of the time talking about alpha diversity. So alpha diversity, this is a quantity measure.
It's looking at richness and abundance of species within the microbiome. And this is really essential when it comes to having health. healthy micro-m.
We saw in that schematic before that as you start to lose diversity, we start to have more pathogens that become present. We start to lose strength in the intestinal barrier. So this is very important. And we know that this varies from person to person. Even in the research, you know, early microbiome research, they say, you know, we can have up to a thousand species.
This is not as true anymore, but we are looking for, you can see here, this is looking at the number of species that we are trying to get above that 250, because we know greater diversity is generally associated with greater health. And there's been studies that have looked at that. So we're also looking at, you know, diversity of species within the same individual. And so this.
marker here, what's known as the Shannon index. This is a measure of richness. So it's a little bit more of a sophisticated measurement than just the pure number of species that are present in a sample.
So it's looking at, you know, if you have 100 species, which is richer than someone who has five species, it's also taking into account the distribution. So are there two or three highly abundant species that's not evenly distributed? That will drive that number lower.
So in this case here, you can see this person just really doesn't have a lot. And there isn't a lot of richness among the species that this person has. So I like to call this person a desert, essentially. They don't have a lot going on there.
So beta diversity, right? This is a quality measure. So lower beta that someone has, of all the species someone has, they aren't containing the ones that are most represented in that healthy population.
So again, it's looking at the... quality of species. So this person has a desert and very poor quality of species. This is not a good test. So we've got work to do for this person.
Okay, so resistome. We get lots of questions about resistome. Resistome is basically microbes will compete with each other.
And they do this by producing natural antimicrobials and genes that create microbial resistance. And so a stronger and more diverse microbiome will be more resilient against gut damaging factors. So we are capturing around 1500 antibiotic resistant genes.
And again, the more antibiotic resistant genes to antibiotics and medications and foods is going to drive that score. This is comparing to a healthy reference population. And then when we look at, you know, who produces antibiotic resistant genes, we, like I said, are measuring a broader range that captures over 1500 antimicrobial genes. So broad range, we know these are mostly pathogens.
So we know this number is going to be affected, especially if you are exposed to lots of antibiotics, if you use lots of antibiotics. So again, this is a marker of resiliency. So again, that's what I just said, antibiotics, we would expect lower diversity, lower keystones, and that's going to drive that resiliency down.
So this is just an example. By knowing your resistome, if someone has a low resistome, so 5.51. We always say eight is great.
So anything above eight, we always like to see that's going to kind of give you a higher overall score. But what do we do, right? So part of learning this test, and as you go through this Biomeffects webinar series, we're going to learn clinical pearls and different things that we do when we see some of these out of range contexts or out of range sections.
So with a lower resistome, we want to look at decreasing exposure to antibiotics from diet or what's happening in our environment. We want to... obviously focus on increasing diversity and commensals to compete with those pathogens that we know produce antibiotic resistance. Something like if you're familiar with any of our products, things like HU58 is great because it produces 12 natural antibiotics. We also have something like Restore Flora that can be taken along with antibiotics to potentially decrease that loss of commensals and to help to maintain some of that diversity.
Okay, moving on to the pathobiome. I love this section because this is where we get a a good glimpse of, you know, those unfriendly neighbors. I always say, like, I kind of think of the microbiome as a neighborhood and you move into this house and all of a sudden you realize your neighbors are like the Stepford Wives. Those are like your pathogens.
We don't really want to next door to them. So this gives a good overview of, you know, who's there that we don't necessarily want there. But this is also the section that I encourage people to kind of stop and think, because when we see pathogens popping up, different pathogenic species, we do look at bacteria, protists, and fungi.
But this is the section where all of a sudden we see, oh, these are bad. We must kill. And this is, again, kind of that paradigm shift that we talk about of, well, what's happening within the rest of the microbiome?
Maybe they're not actually driving some of the problems. And maybe we need to think about how we can, you know, sort of crowd them out and change the environment to make our microbiome less conducive to pathogenic species. Now, that's not always the case.
And sometimes we have to look at the other portions of the test, look at what people are going through to determine if that's necessary. But what's happening in the environment and the microbiome that's allowing these pathogens to thrive and survive. So we want to take into account symptoms.
We want to look at the rest of the test to determine how aggressive we need to be or how aggressive, you know, or can our patients actually handle the type of therapy or treatment we're wanting to do. So I like this part of the test because it's going to give us a good insight into, well, who's there. But then as we look beyond, can our patients.
you know, even handle more aggressive treatments. And so, again, this is the section that I think challenge us the most, because our initial thought is going to be, well, we have to kill all the bad, but if we kill the bad, we also kill the good. And if we're already have a desert, do we want to keep a desert a desert that might continue to drive a lot of the symptoms and the issues that we're seeing.
So I like for everyone to kind of stop and pause and look. Our next section of the test goes through dysbiosis ratios. And we can tell a whole lot because when we look at our four main predominant phyla in the healthy population, which is from nicotines, bacteroidetes, proteobacteria, actinobacteria, this can really tell a lot of what's going on clinically in someone's health. And so we are striving for overall balance. And we know that an imbalanced ratio are clues for dysbiosis and inflammation and can even provide clues into.
what diet someone's on or how diet is driving changes in the microbiome, as well as changes in our digestion. So let's take a moment and talk a little bit about formicodies and bacteroidetes. So we know that these are the two most predominant phyla.
They make up about 90% of the microbiome. And they are, you can see here, they're really kind of one-to-one. Throughout the research, you'll see, you know, we always say bacteroidetes should take up the most real estate, but they are very, very close in that because We have, as much as there's pathogens in formicodies, there's also lots of really important keystone species. And so we really do want to see this in balance. When we have a low formicodies to bacteroidetes ratio, this generally is associated with a healthier metabolism, but it can also be a sign of digestion or a sign of inflammation.
It can also be clues into maybe digestive issues or maldigestion, malabsorption. Again, it's going to be a clue into dysbiosis and going to give us a little bit more insight into how we have to improve that, especially if someone has low diversity, right? Now, increased formicodies to bacteroidetes ratio, this is generally associated with unwanted weight gain or obesity, insulin sensitivity.
We usually see a little bit more metabolic conditions related to it. Also assigned towards increased inflammation. This is going to give clues into what's going on between the gut and the liver. as well as, you know, potentially clues into SIBO.
So we can see here that this person has a very high formic disease to back to wordies ratio, which we really don't want to see that. So I would be asking lots of questions about someone's diet. Are we eating, you know, lots of, you know, saturated fat, you know, standard American diet, high meat, I'm going to ask about someone's, you know, liver health, or is this someone who presents with like a non alcoholic fatty liver disease?
What type of inflammatory process is taking place? Now proteobacteria to actinobacteria. So proteobacteria, this is our most pathogenic file.
So this is where we have the most pathogens. And we also have lots of gram negative, which is our LPS containing bacteria. And as everyone knows here, LPS, if you've ever listened to any of our other webinars, right, this is really the villain and can be extremely inflammatory and highly immunogenic. This is a bacterial endotoxin, right? So it's on the cell walls, the outer cell walls of our gram negative bacteria.
And so when we see proteobacteria, again, it gives a little bit more insight into things like LPS and what could be driving leaky gut or hyperintestinal permeability. Actinobacteria, this is where we have lots of bifida. We have strong butyrate producers here.
Certain bacteria in this phylum are associated with even improved cognition, memory, even social skills. They produce a large amount of naturally derived antibiotics, as well as compounds that help to support a healthy balance of things like parasites and commensal fungus. And so when we look at the ratios, an elevated ratio can actually be linked to intestinal permeability, inflammation, dysbiosis, increased risk for chronic disease.
Because think about when there is a breakdown in that mucosal barrier and LPS, which we know drives inflammation. can drive immune activation and this can really extend beyond and we see LPS we see it present in certain disease states you know they've even found it you know in the brain and Alzheimer's patients so this can be giving us lots of clues into how the microbiome is driving symptoms and issues beyond the microbiome. Now, a low ratio, something we want to think about, can often be linked to digestive insufficiency because we contain lots of actinobacteria in our oral microbiome. So if we have a lot more that's showing up in our stool, it's telling us that bacteria is getting past a very key process, which is our stomach acid.
So if we have insufficient stomach acid, then we know that more oral microbes are going to show up in the stool and that... that can be clues into what's happening digestively with our patients. So again, this is going to help kind of guide a lot. We know that proteobacteria thrives on saturated fat. We know actinobacteria loves dietary fiber.
So again, it's going to help also look into your patient's diet and how we have to start to modify. Keystone species, we all love keystone species, because this is really the beneficial bacteria that only take up a very small portion of the microbiome, about one to 3% of the overall microbiome. Some studies show up to 5%, but there are most potent short chain fatty acid producers. So they just have this disproportionately large effect on both their habitat and the status of other microbial communities within the gut. So they really help to change the ecosystem.
They essentially create an environment that's unfriendly to pathogens and they create an environment that allows for good microbiome. microbes to thrive. So a lot of us will see this section and say, Oh, no, this person doesn't have bifidobacterium adolescentis. So, again, kind of in some of that traditional thought process, we think, Oh, well, then I need to add bifidobacterium.
And, and, again, you know, this is kind of that paradigm shift of, if we just focus on microbes in isolation, we don't think of the microbiome as a whole. And this can actually help kind of guide some of our probiotic supplementation recommendations. I always like to talk about kind of the idea behind when we take probiotics, it's this idea of are you a tourist or a colonizer? And we know that our traditional probiotics like bifidobacteria and lactobacillus, that they're not necessarily changing the habitat of that community of microbes, that they're having very specific effects, whether it's immunomodulatory effects or neuromodulatory effects. And so it's not that we don't want to take those because we want to achieve those effects, but we also want to think about what's needed.
to come in and actually change and prime the environment that allows for all of these keystones to grow. So again, it can just give us a little bit more specifics into how we have to actually recondition and reseed the microbial environment. So just pointing out, I just want to highlight a few here just because we love talking about keystones and they're fun.
I love Oxalobacter. I think this is a cool keystone species. We know that bacteria can actually break down oxalates in the pollen and that can...
therefore reduce the risk of potentially forming calcium oxalate kidney stones. So people who suffer from repeated unexplained, you know, kidney stones, they're observed to have a low potential for oxalate degradation in their microbiome compared to those non stone formers. So if you don't suffer from kidney stones, your gut microbiome's potential to create oxalate that's not necessarily a concern. So I love this. We don't we don't see it detected that often.
But this can also help sort of guide the diet. If someone doesn't have any oxalo back there and they are forming kidney stones, and this is where you may have to monitor the diet. This is where we want to start working on reconditioning. But if someone doesn't have this present, then maybe we want them to consume more oxalo containing foods so that those microbes can consume them and help to build the growth of that community. Acromantia is another favorite, favorite keystone that is talked about all the time.
It's such an important keystone species. It's probably all of our favorites. It's a mucin loving, right?
acromantia muciniphila. And so essentially, it eats and degrades the mucus layer while simultaneously working to rebuild it. And we need that mucus turner, but that's essentially a part of a very healthy gut. So if we're lacking this microbe, right, this is going to be a sign of poor intestinal barrier health. But I want to point out here, because in this case, this one's higher than what is generally part of the healthy range that we see.
And this is why balance is so important because like everything in the Goldilocks world and beyond, you know, to not too hot, not too cold. So there are some studies that have been done that have found that there was a study that came out in 2023 that looked at an overabundance of acromantia actually led to a thinning of the intestinal mucus layer. So degrading that mucus layer too rapidly.
And that allowed for more harmful bacteria and bacterial byproducts to directly, you know, to disrupt those tight junctions, right, and to get to those. to get to the epithelium. So again, it really comes down to balance. One thing you'll see in a biome effects test as well is you're going to get kind of a breakdown. This is the page that I like to use with patients a lot because it just showed kind of a nice depiction of how we essentially want to achieve balance, right?
Who's taking up the most real estate versus who should be there. So we have our predominant phyla in our healthy sample. And again, we want everything to kind of be in that nice, working towards that green column so that we have microbial competition.
We know that when microbes are out of balance, right, this is essentially dysbiosis. And as we've discussed, you know, dysbiosis is rooted in so many of our conditions. But some clinical pearls. So the less abundant phyla, this can actually give lots of great insight into what could be driving some of our symptoms.
So our urethra, our periota. These are methane producers, so constipation, slow motility. Synergisticities, this often correlates with oral dysbiosis, gingivitis. So if we're seeing lots of oral microbes, again, this can be a sign of insufficient stomach acid for digestion. Ascomycota, this is where yeast, fungi, and mold live.
So if this is elevated and corroborating with symptoms and what's going on, this might lead to further testing to see if there's mold toxicity or yeast overgrowth. So we have Fusobacter. Bacteria, very inflammatory.
We'll often see this when we talk about microbial patterns, which we'll learn in our upcoming Biome Effects webinars. This one can be associated with inflammation and especially with irritable bowel disease and colorectal cancer. Candidatus, this is also found in the oral microbiome.
So if we see that elevated, it can be related to periodontal disease. But again, elevated oral microbes in the stool, that's a sign of poor digestion. We also go into the family section. This is more specific.
So when we talk about taxonomic hierarchy, this is getting more specific than the phyla. So we'll be able to see which families are out of range. And when they are, it's not necessarily a bad thing. But knowing these families can actually provide further clues and insights into those clinical and microbial patterns.
And again, that's what you'll learn as you continue through this series. But families are more specific. So it's not to challenge us on whether or not we can say these big words, but it's really just to give further insight.
Okay, so Getting now into the functional analysis, this is really what separates this test from other tests. And so the functional analysis is the section that mines for samples for genes that are known to contribute to the production of metabolically important functions. And so the previous sections really focused on taxonomy. So who is in the gut? And then this section isn't looking at taxonomy.
It's literally measuring the genes that are present. from all the microbes whose job it is to code for all of these specific functions like sacrolytic fermentation. This is where we measure butyrate, propionate, acetate, and lactate.
These are obviously short chain fatty acids. These are the byproduct of carbohydrate fermentation. And so it's essentially telling us how well our body is using dietary fiber or whether or not we're intaking it.
So again, we're going to kind of go into the nitty gritty of it, but it's not measuring those end products, which we'll talk about. proteolytic fermentation, polyamines, phenols, ammonia. We also look at hormones and neurotransmitters, GABA, glutathione, histamine, indolemine, strobilone, as well as vitamin biosynthesis, because we do know that our certain microbes have the ability to create endogenous B vitamins, vitamin K2.
So something we can really take away from this section in consideration, I love this section because it really gives us so much more. You can have beautiful neighborhood and you're like, wow, I love all those houses. This is exactly where I live.
And then all of a sudden you find out that your neighbor's not really functioning the way you want them to do. They're not really the neighbor that we envisioned having. So considerations, if functions are high or low, is we don't have those fermenters there. So we don't have the microbes there that are necessary to ferment our dietary fibers or to ferment our proteins and peptides. So why aren't they there?
What dysbiosis risk factors? Are we exposed to what chronic conditions are taking place? What have we been doing prior to leading up to this test that could have impacted the microbiome? We're also going to give us insight into the diet. Who are we feeding and who are we not feeding?
So we'll talk about that as we go through each section a little bit more. But if I see someone has really low short-chain fatty acid production, well, I'm going to ask them, well, is this person not consuming our dietary fiber-resistant starches? And if they are, then why aren't those microbes performing those? those jobs.
Well, maybe it has to do with digestion, right? Insufficient stomach acid or digestive enzyme production. So knowing how well our microbes are carrying out these functions really helps to provide this insight. So sacrolytic fermentation, this is measuring the bacteria who are known to produce short chain fatty acids, you know, are all the ones there that need to be there that are making butyrate and making propionate.
And you'll see that it's represented in a bell curve. And your sample abundance and percentile is where we fall within that curve. So I generally will look at the sample percentile. for a lot of these, but it is also important to note the abundance within the healthy range that some people. But we have colors there to kind of make it easy and to kind of use the eye and say, oh yeah, you're within that healthy range.
So again, these are not the end products, but the genes that turn on and off to promote short chain fatty acid production. We're going to talk a little bit in the next slide about the difference between stool short chain fatty acid production and looking at the genes, which I'll just go right to it now. So a lot of people will ask me, well, how does this differ?
When we're looking at stool short-chain fatty acids, it's called metabolic limits. And it's a different depiction, really. And it's not always as accurate as it is because it's more indirect. And it gives you a more somewhat limited picture of the complex interactions. And they don't actually tell us about the utilization of short-chain fatty acids.
So stool short-chain fatty acids, we know that location of short-chain fatty acid absorption occurs in the colon prior to reaching the rectum. So stool measurements may not represent the total short chain fatty acid production or absorption that's happening in the gut. So, you know, for example, if we see high butyrate on a stool short chain fatty acid on a stool test, it's actually telling us that something's potentially going on. You know, it's not necessarily being used by our enterocytes.
And, you know, it's not acting as a signaling molecule, right, to our neuropods that lead to us supporting the vagus nerve. because we know that dysbiosis and things can weaken the vagus nerve. There's been research to even show that high butyrate in stool can be related to obesity.
And it actually makes sense, right, because it plays a role in blood sugar. But it's telling us that it's just not being utilized. So again, it's not giving us that full depiction. We know that stool short-chain fatty acids can vary depending on the diet, the gut microbial composition, right, transit time even.
So that single stool sample may not reflect the ongoing dynamics of total short-chain fatty acid production. And it provides information on just the end product fermentation, and it doesn't provide insight into those specific microbial communities and their functions. So moving on to proteolytic fermentation, I apologize, but I probably will go over just a little bit, but I'm getting through it. We're almost done. So we know that our gut microbiota can also metabolize amino acids into specific microbial metabolites.
While there are some benefits to these microbial metabolites, many of them in large quantities will be related to more inflammation and become toxic to the body. So we know that proteins and peptides that escape digestion are metabolized via our gut microbiota. And shifts in proteolytic fermentation alter that relative abundance of the microbial species in the gut.
So we can see a reduction in keystone species. And we're going to see a greater production of metabolic byproducts. And this can really kind of give us a sign of, you know, someone's diet and how well our microbes are utilizing what's coming through the diet.
So one of the first proteolytic byproducts that we're going to talk about, we're not going to go through all of them today, but I'm just going to highlight a few. So ammonia production, we know that elevated ammonia can be toxic to the gut. It can be toxic to the liver. And this is because ammonia secreted by bacteria.
It doesn't just. stay in the lumen. It can potentially reach out and put more of a strain, especially when there's a dysfunctional gut barrier.
So we know it puts a strain on those detoxification pathways. And they've even shown that excessive production of ammonia via our microbiota can actually contribute to more increased, to increased levels of ammonia in the blood. And we know that ammonia production occurs when there's an overgrowth of ammonia producers with excessive dietary protein intake. So especially glutamine.
And we know then that there's also a potential when there's liver or kidney dysfunction. So like I had previously mentioned, you know, shifts occur when there's an overgrowth of those ammonia producers, and then there's more protein. So if we have this elevation of ammonia, then again, when we looked at considerations of high or low, is it because we're not digesting protein? Or is it because we have a lot of those producers there?
Is it both? But I always like to talk about glutamine because we use glutamine. A lot of us use glutamine. when it comes to gut supplementation and as a gut healing supplement.
But glutamine, we have to take into account because it can actually feed our ammonia producers, which can actually drive greater ammonia production. So we know glutamine is involved in the conversion of ammonia into urea in the liver. So with high ammonia, the body can actually struggle to handle the excess glutamine.
So supplementing can exacerbate that process. And we know that's secreted by many different inflammatory groups like our clostridium. Hydrogen sulfide production. So this occurs when sulfate reducing bacteria or hydrogen sulfide producers.
convert dietary sulfur and taurine to hydrogen sulfide. And it is another, obviously, byproduct of proteolytic fermentation. But at low levels, it's protective to the gut. That's why it's always important to understand balance, that having some of these is not necessarily a bad thing. And it can be protective to the gut barrier.
And this is why we say not all gas is bad gas. So a little question for people, you can put it in the chat if you want, but does anyone know what is considered a normal amount of times that we can pass gas in the day? I would have this conversation multiple times with my patients because many of them would say, I don't want to have any gas.
But does anyone know what the normal number is? 25, someone said. So I don't know, you know, again, how they really gauge this, but I was always told and read everywhere from, you know, 14, 14 to 20 times a day is actually normal. Many of my patients would say not on it. But so again, at low levels, we know that hydrogen sulfide is important.
It's a signaling molecule, right? It plays a role in mitochondrial health. So again, too much can lead to disruptions in ATP synthesis and can cause a breakdown of the mucosal layer, promoting inflammation.
We can often see it associated with things like irritable bowel disease. And it's often associated with a high protein, low fiber. So increasing consumption of our...
resistant starches, fructooliocasaparates can actually help to reduce it. We know it's produced by species of proteobacteria, vermicades, phyla, salmonella, desulfovibrio, bilophila. So methane, methane is another one we'd love to talk about. It's another marker of proteolytic fermentation.
It's produced through the reduction of carbon dioxide and hydrogen. So we do detect it in healthy populations, but too much of it can slow intestinal transit, affect gut motility. It can block the conversion of acetate to butyrate. So because we know that methanogens can consume acetate, it can potentially lead to impairment in gut-brain access.
We know it can produce some more of those byproducts and can lead to worsening inflammation. So methanogens prefer more neutral intestinal pH to thrive. There's even been studies to show that it can contribute to weight gain by slowing that intestinal transit by impairing that motility. And then it can actually increase that floor uptake from foods in the digestive tract.
So we oftentimes see constipation floating. And just as a reminder, you are karyotophyllum and that's elevated, then we want to also corroborate that with methane production. Histamine production.
So histamine is a big one, right? I feel like if I say the word histamine, our sirens go off. And, you know, but again.
small amounts of histamine. It's a bioactive amine. It gets a bad rap, but it's not all fat.
And we know that we need it to function as part of our body and part of some necessary systems. But we do have histamine that's produced in the gut and it can elicit an immune response in other areas of the body. So histamine can enter the bloodstream when there's a weakened gut barrier.
So we know common symptoms of histamine intolerance or overload or things like urticaria, chronic hives, swelling, oral allergy syndrome. So reflux, right, angioedema, these are all very common symptoms. So dysbiosis can drive certain bacteria to cause the release of histamine.
And this is often due to destabilization of our mast cells. So we need histamine production to be balanced with histamine breakdown. And if not, this will lead to mast cell degranulation and essentially higher histamine levels in turn.
We know these are produced by certain microbes. Very high proteobacteria pathogens like E. coli, Klebsiella, Clostridium perfingens, Citrobacter, these are all going to be histamine producers. GABA.
So I love talking about GABA. I think we all know the importance of GABA. And we know that glutamate is metabolized by certain gut bacteria to produce GABA, which is a very important neurotransmitter that blocks specific signals to the central nervous system.
So it essentially slows down brainwaves to elicit that calming effect. effect on the brain and improve mood and sleep. It's produced by a lot of our bacteroides. So B. fragilis, bacteroides, E.
bacterium, our bifidobacterium, even certain lactobacillus species can produce GABA. But it's important to understand that GABA produced in the gut doesn't actually cross the blood-brain barrier. And it may actually act locally on the enteric nervous system or more on the vagus nerve. And like we mentioned, the vagus nerve can be weakened when there's dysbiosis, when there's a dysfunctional gut barrier. So it's more often related to modulating intestinal motility and inflammation.
But acetate, which is a precursor to GABA, can cross the blood-brain barrier and be incorporated into that GABA-cobalic cycle. So low levels when detected on a stool test. We want to check in with our patients on depression, anxiety, behavior, how well are they coping with stress, and we can offer modifications there.
High-fat diets may reduce GABA levels in the brain, so we want to look at the diet, how much fat's in the diet, again, to help to improve some of the symptoms we're seeing. Indol, so Indol is a byproduct of microbial degradation. And I'm going to move through this because I know I'm running out of time, so I want to get to the technology aspect. So this is important. We need balance.
And this is related to tryptophan metabolism. And so this plays a huge role in different ways tryptophan metabolize and producing kynurenine, which can become neurotoxic. So again, very important aspect in looking at this level and reassessing it back to what's going on along the gut-brain axis and symptoms that our patients may be experiencing. The astrobilome.
So the astrobilome is a 60-droughter of bacteria that can recycle or decompose. conjugate inactive estrogens or reabsorption for reabsorption. And so essentially, if we have an elevation, this can be due to having impaired gut and can be related to having high estrogen levels in the blood.
So it can contribute to estrogen dominant symptoms. So the estrobilin is going to help determine whether or not we need to do further testing to corroborate, but it can also give insight into other supplements you may be adding. Do we need to help to support that? you know, estrogen levels, or do we need to use certain supplements to help to, while we're reconditioning the microbiome, things like calcium d-glucrate and sulforaphane. So low estrobil, and we know it can often be related to hot flashes.
So again, it's going to help kind of determine that clinical judgment and where do we go next when providing deeper insight and interventions for our patients. Finally, the vitamin production. So this is so important because we know that Our microbes produce very specific vitamins. And I always love looking at vitamin K2, especially because it is produced predominantly endogenously. So most Americans don't eat foods high in K2.
But this is not a measurement of sufficiency or deficiency. It's the measurement of bacteria that produce these vitamins. So if these vitamins are low, then we want to look at diet and supplementation to minimize that disparity. Okay, finally, I'm going to go through this.
Just a few more slides. We want to talk about the technology because what makes this different? And it's because of something known as whole genome sequencing. So just to kind of give a little bit of a background, most traditional stool tests are using something called 16S. And all of our bacteria have the 16S RNA gene.
This was created a very, very long time ago, actually almost 40 years ago. So I always say think about technology and like our cell phones. So this came out around the time of the cell phone.
Think of how much our cell phones have advanced. So the same 16S that was being used back then is being used now. So what is 16S?
So 16S, all bacteria have this gene. And so when we look at this gene, it contains what's known as nine variable regions. And these variable regions serve as fingerprints for particular species, and it helps us identify who they are. When we're using 16S, we are only using one or two hypervariable regions that get amplified using PCR because...
it's small amounts of DNA. So you're only able to, they're only taking a snapshot. And so that means that we're really only able to get accuracy to the genus level.
And that's important because that can be the difference between say a commensal and a pathogen. And so when we look at some of the limitations with 16S, it's really only a few pieces to the puzzle. You can't get the functional profiling of that because you're only taking a snapshot picture of it.
So it's just like cutting up a picture and putting a few pieces. You're not necessarily getting down to that strain, that species and that strain level. 16S has about a 14.7% specificity and a 90.8% sensitivity at that species level.
So with that, you can't identify viruses, fungi, protists, only bacterial identification only. So I'm just going to skip through this. You guys will all get it. But this is just going through a little bit of a snapshot of what culturing and... microscopy, you know, and some limitations with them.
But what I want to really kind of focus on is giving a little bit more of a visual between the 16S and what's whole genome sequencing or shotgun sequencing. So on the right here, this is whole genome sequencing, which includes the entire genome, right? Genome means the complete set of genes or genetic material that's present in the organism versus 16S is just one gene.
So you can see here, we're taking out that one gene. And we're amplifying it using PCR, where we're only focusing on one or two of those hyper variable regions. So it's only really possible to get that taxonomic profiling. You miss out on the functional profiling because you're not sequencing the entire gene. So it's a much more whole genome sequencing.
You get a much more grand view of the microbiome because you can do both. So again, taxonomic characterization plus genomic functional utilizing whole genome sequencing. So taxonomic, who is there? like Bifidobacterium longum. This is a GABA producer, but genomics identifies the gene or pathway with a specific function, not a microbe.
What are they doing there? So GABA production is the genes or pathway which result in GABA production, regardless of the microbes they originate from. So with whole genome sequencing, you're getting that end-to-end sequencing.
It's the complete puzzle. You're able to accurately identify the species and the strain level, and you can identify bacteria, fungi, and protists using whole genome sequencing. So just a couple more slides, and then I'll get to the end. But I just want to highlight, because this is a big question we get, is when do we use a functional microbiome analysis?
Because it is a different test. So clinical microbiology or parasitology, stool chemistry tests are oftentimes limited to those with GI symptoms and conditions, whereas a functional microbiome analysis, we're looking at not just someone who has GI symptoms and conditions, but how is the microbiome impacting beyond? Has anyone who's experienced dysbiosis risk factors, who do we think has leaky gut?
And we want to know what's happening in their overall health. So again, thinking about that gut organ access. So fertility issues and autoimmunity and liver issues and metabolic conditions, right?
So we're gaining a better understanding of the microbiome impact. It can provide insight into clinical direction, your next course of action. If someone doesn't have an elevated strobiloma, they're not showing signs of detoxification issues or hormone issues.
Do we need to do a Dutch test? It might not be necessary. You may be able to go right into reconditioning the microbiome. It's going to give us clues into can the patient's microbiome withstand a more aggressive treatment? Are there any additional tests that we need to do while initiating a protocol?
So functional microbiome analysis, again, it's not about diagnosing conditions based on a single marker or specific microbes, but it is about gaining that valuable insight into the overall microbial ecosystem. And it's providing that roadmap to restore balance and resiliency. And lastly, I'll just kind of show you that there are resources available.
Aside from our webinars, you do have a report recommendations. We have an interpretation guide as well. And these can provide, you know, a little bit more detail into nutrition, lifestyle, supplement recommendations for each marker on the test. So everyone can, you know, get a copy of that. But we also have, you know, again, as we start to learn bio-effects, and I challenge you to use this tool, you know, differently, to use it as a way to...
guide and gain better understanding of the microbiome and how it's impacting our health and beyond. You do get the report recommendations, interpretation guide. Every test comes with a 60 minute consult. There's also 30 minute consults that are available for quick questions.
Clinical interpretation emails are received after registering the kit. We're doing these webinars and our webinars are going to go deeper into those microbial patterns. So I just kind of touched on ammonia and histamine, but we're going to start to learn about how someone with, say, SIBO or someone with reflux or H. pylori, what would we expect to see on a functional microbiome analysis?
And you also have access to us at the clinical team for deeper questions. So I'll just go, again, just kind of put this up here so you can see. It is the first functional microbiome analysis.
And again, it's utilizing whole genome sequencing. So it's a different test for a different purpose. And again, it's going to...
guide that insight into not just what's happening within the microbiome, but how that could potentially be impacting beyond. So with that, I just want to give you guys a few moments to see that we do have lots of upcoming education. And I think this Biome Effects series pairs so incredibly well with our foundational series.
That's the first webinar of every month where we really just take everyone through the digestive tract, the microbiome, what happens when there's changes in the microbiome, and how do we start to restore that balance. you know, things in the diet, what can we do about it, but it does reflect nicely. Because we talked a lot about biomeffects, our second biomeffects webinar is going to be focused on.
And that's February 21. It's looking at clinical patterns. What are clinical patterns? What are microbial patterns?
What do we expect to see with some common patterns like leaky gut? And how can we use that to guide our clinical judgment? So with that, I want to say Thank you.
I know I sped through some of the end, but I want to make sure I respect everyone's time. It does say 59 minutes. So I'm still good. I'll take a few moments to answer questions.
But just so everyone knows, you are going to get a coupon code. We'll put it in the chat today. for 10% off your entire cart plus free shipping.
So please utilize that. That's great. We have now on our team some devoted BiomeFX reps. And so happy to get anyone connected with your BiomeFX rep if you want to learn more, if you have more questions.
But hopefully this kind of just got everyone's, piqued everyone's interest into learning more. And I really do think that this test is one way to just drive more of that microbiome knowledge and how to use that information to help us clinically. Okay, so if everyone can hold on, I'll answer some of the questions.
It looks like some have been answered. I might not get to everyone, so I apologize. Are there specific microbiome tests you recommend depending on what issues we're looking for? So it depends.
You know, I will say for me clinically, and I'm speaking as a clinician, I love biome effects because it kind of sets an overview, right? Like I may have someone come to us and let's be The truth is too, right? Patients coming to us in the functional world, oftentimes they've seen a lot of other practitioners.
So there's already been a lot of other tests done. So for me, it's a nice way to kind of take a step back and say, okay, what's happening within your foundation? And do we need to do other tests?
So I love biome effects as a way to sort of set the stage of really saying, can we get started on reconditioning and fixing up and patching those holes in your microbiome? Or do we need to do a SIBO breath test? Do we need to do hormone testing? Do we need to do mycotoxin testing?
So I kind of use this as really my sort of foundational microbiome test. I mean, yes, if we are someone's acutely ill, we may have to do, you know, more acute ova and parasite testing, you know, there's lots of other options out there. Does this test provide digestion and inflammation markers too? So it doesn't. And we're going to talk a lot about that actually in our next BiomeFX webinar.
So I don't want to give away all the secrets. But I think personally, you know, we we love I love digestive markers too, but sometimes I use those and I'm speaking just from personal experience. Sometimes I use those as a crutch, like I'll see secretory IgA or I'll see some markers and I'm like, oh, they're low, but it takes me away from wondering, well, why are they low? What's happening in the microbiome that's driving a low secretory IgA or an elevated spray? What's going on?
So sometimes I find that we can often make up our mind about what we're doing clinically with someone just based on those markers, but it's not something we currently provide on the test, maybe something down the road. that we do consider. So what, so what mold mycotoxins will this test look at?
So we look at kind of the larger phyla ascomycota, which is where molds live, but we're not looking at specific ones, you know, mold mycotoxins are obviously can be harder to test. So that's where if someone has elevated ascomycota and have obviously their symptoms align, and that's where you may need to do mycotoxin testing. And, and, but you may not need to do that if, if there aren't those signs in the microbiome. And that's why I say it's sometimes nice as a way to use this as sort of a foundation to figure out what other tests may be necessary.
Taking oil or oregano, or curcumin, berberine, which is the same recommendations for all three of this. Well, I'm not sure what that question is, but I think it's related to antimicrobials. So if you want to add into the chat what specifically we're asking, but again, I think there's different antimicrobials.
There's different ones out there, and some of them have other benefits. But I think ultimately, there's just a time and place to use antimicrobials. You know, again, I kind of speak from personal experience where I worked in the GI world. We have lots of SIBO, lots of really chronically ill patients, and I'd be taking them through antimicrobial or antibiotic regimens.
And, you know, they're just not getting better. Well, then all of a sudden, you know, I do a biome effects and I'd say, OK, wow, they have a desert. Like we're just we're almost perpetuating. a problem. So I think there's a time and place for antimicrobials.
We just have to see if their microbiome can actually handle and withstand that or are we actually making our problem worse. So maybe it becomes more about changing the environment to make the microbiome less friendly to those pathogens. How do we increase oxalobacter fermin genes? So lots of studies looking at just diet in general with keystone species. So that's one that there's been some studies to show that eating oxalates So if you don't have an oxalate sensitivity, that actually can help promote it because that bacteria prefer, right, that they like to eat oxalates to break down.
So that's one way. Also, Mediterranean diet's been studied quite often in overall keystone growth. So if acrobancy is too high, how do you gently weed it down? I see that every once in a while with science.
So again, it comes down to, well, why is it high? Is there inflammation? And so do we need to work on improving inflammation as well?
hole, which hopefully would help to just naturally start to restore that balance. Also, if formicides is high and bacillus is in the... would you not use spores?
No, no, because they're basically there. So the question is, if formicides is high, would we not use bacillus spores? Not necessarily, right?
Because if, I just like literally lost my train of thought. So there's different species within the bacillus, right? We know like for us, we use bacillus subtilis and bacillus coagulans.
And spores do an incredible job at really priming the environment to bring in a city to help crowd out those pathogens. So I wouldn't, I would look more at what's going on from an inflammatory standpoint. You know, is there digestive issues?
I would look at more of what in general is driving the formicidase violet to be too high in the first place. So, and again, looking at what else is going on in the test, but absolutely not because again, we've done studies to show the improvements that, you know, certain bacillus strains can have on improving the overall microbial landscape. Is Candidata staph bacteria related to receding guns?
I feel like I recently got that question. It may be. I haven't looked up any specific studies.
I know more of the studies I've seen with Candidata saccharobacteria is more with periodontal disease. I'm going to answer just one more question. And then, like I said, happy to get anyone connected to their BiomeFX rep. We're here to do that.
So if you do have more specific questions, please come to our next webinars. And we can also reach out to the rep and can get some of those questions back to us. Um, can any of your products help decrease the virulence?
Well, I'm not sure I understand that fully, but virulence factors, which are more toxigenic strains of certain bacteria. So it just depends on which ones, you know, someone has C diff present doesn't necessarily mean that they have a C diff infection because you would want to test for virulence factors. And again, if they have symptoms, but we do have, you know, certain strains that can absolutely help. Like for example, our Pylogard is a great strain that's.
been shown to form these co-aggregates around H. pylori and can help with H. pylori eradication. But we don't test for those virulent strains. They're a lot harder to test in stool in general.
Could this be a reason why some individuals cannot resolve SIBO? I absolutely think so. And I've taken that approach with my, what I call my sticky SIBOers, where we're throwing antimicrobials, where, you know, I'm alternating between, you know, Xifaxin and antimicrobials, and it's like, they just don't get better. Well, then all of a sudden I do a biome effects.
And it's because we're keeping a desert, a desert essentially. So I'll do one more question and then I'm going to leave you guys all today. And I really appreciate you taking the time. So how does this test compare to a more recent generation one of biome?
So if I can recall, I think biome is using mRNA technology. And mRNA is actually quite unstable. And so it's really not necessarily a good way to get a good depiction.
in someone's actual sample. So I think that's the technology that bio is using. But thank you guys so much. And I'm sorry, I didn't get to all the questions. I appreciate Alicia being on and helping answer through some of them.
But please join us for our next upcoming webinars. And like I said, please reach out to your, your rep, and we can get you connected with your, your botics reps. That way you can ask some more of these detailed questions. We'll make sure that we put the code.
in. And you will also get emailed the coupon code as well. So please be on the lookout for the email, you'll also get a recording and the slides. So with that, I appreciate everyone joining us today. And I hope you all have a really wonderful rest of your day.
Thank you.