Microbial Enzymes and Metabolites Walkthrough - Tiny Health Gut Health Test

Hi, my name is Emily Cerda. I'm a microbiome specialist here with Tiny Health. Um, today we're going to talk about the microbial enzymes and metabolites portion of your patient results. So here we have the main patient page. I'm going to go into see all metrics, and I'm going to click on the last checkbox for the microbial enzymes and metabolites section. Here in the microbial enzymes and metabolites, we are really looking at, um, things that are present in the microbiome and microbiome's ability to function based on the genes that we're finding there. So in the first section, we're going to look at histamine-producing species. This individual does have some histamine producers in their gut. Um, we are looking at the species specifically, so we can see, um, the reference range here and where we would like— we would like there not to be any. So below our sensitivity level of 0.005% is where we would love this to be. And, you know, people are sensitive at all different ranges. So I would really check in on your patient presentation when it comes to this metric in particular. But this is indicating that histamine-producing species are in the gut. So it's— it may not just be the food that they're taking in. There is actually taxa in the microbiome that is creating histamine on its own. So if we look down, within this metric to see, like, I want to know who that is. And here we can see the species in the sample. There is a bit of Citrobacter jungae in there, and you can always click this dropdown arrow to read a little bit more about it. A common question is, where did this come from? It may just thrive in this environment if there's a lot of other disruption in the gut. But you can always click in again in the metrics to learn more about it if you have questions questions about, gosh, I can't quite remember what histamine symptoms might look like, we're going to list these for you here. So don't feel, don't feel bad clicking into anything to get a little refresher. You will also get the action items on the side here. Now, the obvious action is that we want to try to rebalance the microbiome so that the Citrobacter isn't in there. And whether that includes that, that includes looking at the disruptive microbiome section because the disruptive pathogens are where the Citrobacter would be. So, if I go out, I'm going to do this real quick. Here's the Citrobacter yongei. If I go out to results, see all metrics, and we want to look at the disruptive microbes, here we can see a list. We can see there's quite a bit of disruption here. Here is that Citrobacter. And if I scroll down, there's that yanggei. There's another one in there as well, but that's where that's coming from. So you can use that to really give yourself a picture of the disruption and to figure out how you're going to get rid of this and look at the greater microbiome, the greater picture of the microbiome. I go back to the— stay on topic. So microbial enzymes and metabolites, we are looking— we're calling out those histamine producers. And it's interesting to note, you notice that there was two types of Citrobacter in this individual sample. Only one of those species was a histamine producer. I hear that with Klebsiella a lot too. People will have Klebsiella overgrowth, but it may be a species of Klebsiella that is not a histamine producer. So, um, that's where you can really look in here and see if that's contributing factor, uh, if your patient is exhibiting histamine symptoms. So further down, um, we have complex compound breakdown, and here we have beta-glucuronidase capacity. So if you've seen some of the other, um, walkthroughs that I've done, capacity in our test means that you are looking at the functional genes in the microbiome. So each of these microbes, they can carry a gene, a few genes, a number of genes. Um, but if they don't have the genes to execute a specific function, then that microbiome is not able. To do that function. So here we're looking at the microbiome's ability to produce beta-glucuronidase. This individual has a beautiful result. Um, we'll see this low, we'll see this high. It can relate to beneficial bacteria, dysbiosis, if there's like deficiency of beneficial bacteria, or if there's an overgrowth of disruptive pathogens. It can also relate to fiber intake. And, you know, are we feeding, are we creating an a good environment and feeding prebiotic foods to our microbes so that they are robust, um, in population. So this is beta-glucuronidase capacity. We know you can read all about glucuronidation and how beta-glucuronidase kind of undoes that glucuronidation, um, so that we're not really detoxing like medications, um, hormones,, toxins efficiently, and instead the beta-glucuronidase will undo that, and then we're recycling those things. So, um, a lot of people who work with hormone health really wanna check in on this. Now again, this is capacity, so this is the microbiome's input to the way beta-glucuronidase may be used. Um, in our PRO test, we do have beta-glucuronidase activity as well, and that is the amount of enzyme that is physically coming out in stool. So it's a difference between what is your, your microbiome's ability to make this versus what is physically coming out in stool in the PROTEST. Um, and I do talk about that in depth in the PROMARKERS video. Okay. Next metric down are microbial GABA capacity. So again, we're in the microbiome in this test. Um, and that's in the large intestine, in the colon. Now, most of the GABA is created in the brain, um, so the body is creating this GABA. And I don't have a picture here based on this test of what that looks like, so we're only looking at the microbiome's input to GABA creation. And it's important to underline here that this can have an influence on things like anxiety, um, and definitely immune health, a number of things. But that the GABA produced in the microbiome, it does not actually cross the blood-brain barrier to get into the brain. So we, we have two different things going on. We have what the brain's doing, and then we have what the microbiome is doing. Now, in GABA production, this individual has a great result. Again, you can click, click to learn all about this. It's going to tell you about GABA. It will tell you that, um, yeah, like there's a study suggesting the amount of GABA in your gut may impact how well your brain manages stress and anxiety. Again, that GABA isn't crossing the blood-brain barrier, so it's not a direct contributor, but there may be a link there somehow. We're still learning so much. So you can always click in and learn more about these. And in these metrics, you can also see species in your sample. And this species in your sample, whenever you see the word capacity where we're looking at those functional genes. When you see species in your sample, these species are associated with this metric. So Escherichia, for example, um, that's— it's not a good guy. This is like E. coli. E. flexneri, um, it's never a good guy. That's why it's red. It's a disruptive pathogen. Why would it be in there when GABA production is a good thing? Well, what this is saying is that Escherichia really flourishes in an environment where the genes for GABA production also are present. You can't really look at these species and say that, oh, well, we're making enough GABA because Streptococcus is there and Collencella is there. They're not all having a positive influence on this metric. They are just associated with the environment. In which this metric would be in a good place. So unlike that, bifido and akkermansia, those actually do have inputs into GABA production. And you'll see those are, those are beneficial. So that can be a little bit confusing. If you have questions, always reach out. It's definitely a little bit confusing even to be teaching it. So I understand if you need to reach out and ask about that, I'd love to clarify. So GABA production, this is very much linked to, um, Bifidobacterium levels, especially specific species of Bifidobacteria. There are some species of Bifidobacterium longum that can make GABA. It's also very linked to some Lactobacillus species. So there are some species of Lactobacillus reuteri that can make GABA as well. And so when this is low in our test, we'll often recommend fermented foods because we're trying to give the input of those Lactobacillus in the lactoferments. Um, and similarly, GABA breakdown. So we could be breaking GABA down faster than we're producing it, which is not a great situation. Again, we don't know what the brain's doing, but this is in the microbiome. Now, GABA breakdown, um, it can very much happen from things like Escherichia, Streptococcus. And if we scroll down, we see that both are in this sample. Um, so what usually this is all about, um, correcting disruption and also pushing toward those things that are GABA producers. So we want to kind of stop the breakdown by helping the disruptive pathogens, um, to exit the body, and then we also want to support the creation of GABA so we're not breaking it down faster than we're creating it. And that would be those ferments again. Okay. In the next section, um, we have bile acid production capacity. Now I'm going to do a separate video on this because I get a lot of questions about this and it's fairly complex. But just to give you a quick taste, um, basically the bile acids— these are, again, this is what the microbiome is doing You have what the biliary system is doing, and that's going to be more like questions around patient presentation. We can bring that into review when we're talking about your patient and your, your test results. But this is only what the microbiome is doing. So the microbiome can take some of the bile salts that are not recirculated in the enterohepatic circulation through the portal vein, can take some of those bile salts and it can unconjugate them. Or take them apart into free bile acids, and then it can also reconjugate them into secondary bile acids. For each of these metrics, um, again, this individual is doing pretty well. You can click in to learn more, to read all about it, to know what we know about unconjugated or UBAs, um, and that will give you a lot of information— there. Likewise, you can do the same thing with the secondary bile acids. Now, a lot of times I'm seeing these unconjugated bile acids are low. This is the genes for the unconjugated bile acids. So we don't have the genes to create the free bile acids because we don't have enough beneficial bacteria in our gut. So a lot of times I'm seeing this low because it's a deficiency. Of the beneficial bacteria. On the flip side, I see this high when there is a lot of— maybe there's a high-fat diet, or there's a lot of saturated fats in the diet, um, not a lot of omega-3s. So we're getting more of the saturated fats, maybe processed meats, things like that. So there's a lot of dietary shift that we do around the unconjugated and even the secondary bile acids. And the secondary bile acids, um, again, you can click in here, you can read about what we're measuring exactly. So you can see the different types, um, and what the health outcomes are. Now, interestingly, I always point this out, around 40% of adults and also 40% of children have no detectable genes for creating secondary bile acids within the microbiome. So they don't have these genes and that's normal. So you'll see the low end here is normal. Most of the health outcomes related to secondary bile acids are if you're making too many. And so if somebody is making too many, again, I'm checking in on that high-fat diet, saturated fats, processed meats, tons of red meat, low fiber situation. And in some cases, when both of these metrics are high, I'm thinking about lipid maldigestion and I'm wondering like, are we even breaking down lipids to use them very well? Or is there just kind of an influx of these? From those bile salts that really shouldn't be happening. Okay. Again, I will do another, another video on that one because it is pretty complex. And then the last part in this section is mitochondrial health support or urolithin-producing species. And urolithin, you might have heard of urolithin A. It's kind of out there as one of the new big supplements that are available. So the thing about urolithin is that we cannot eat foods containing urolithin. Instead, it's a postbiotic, or it's something that our microbiome has to create for us. At the same time, urolithin— there's a bunch of different types of urolithin, and they can come together to make different types. But one of them is urolithin A, and that's the most studied one. So here again, you can read about this. The benefits of Urolithin A or urolithins in general, you can see here: mitochondrial health, strong gut lining, reduced oxidative stress and inflammation, energy balance, muscle recovery. Um, so it's all really, really important things. Um, I see this, I see this low a lot when people are complaining about fatigue. Um, I, whenever I think about mitochondrial health, I just wanna check in. On this metric. Now, like I said, we can't eat urolithins. So what we do is we have to feed the microbes that create urolithins so that we're growing those populations and then they're performing for us. Feeding those microbes, um, is— we eat foods that contain ellagitannins and ellagic acid, um, and those are polyphenols. So think in terms of berries and walnuts, pomegranates, things like that to really boost these. Um, and down below you will see the species that we are looking at. So unlike, and remember this doesn't say capacity, we are looking at the actual species that can create urolithin in this metric. Okay, so that is the microbial enzymes and metabolites section. Um, I hope this has been helpful. I will make a second, uh, bioacid production capacity and I'll jump into that in more detail. Um, but otherwise, check out the other resources in our practitioner videos, and if you have any questions, let me know.