The Inflammatory Signal That Your Bloodwork Missed

Añadido: 2026-05-18

[00:00:00]Right now, as you're sitting there, bacteria may be leaking into your bloodstream. And this is not in a metaphorical way, but I'm talking about in a measurable, peer-reviewed, and this is happening to most people kind of way.

[00:00:14]By the end of this video, you'll be able to understand the mechanism behind this, what are the downstream effects of it, and why it may be causing some of your issues that you've been trying to fix for the longest time. Okay, so what most people don't talk about is that the barrier between your gut, which hosts hundreds of trillions of bacteria and microbes, and the bloodstream, which feeds into all of the other organs and tissues throughout your body, the barrier between those two things is only one cell thick, a single cell.

[00:00:50]Okay, a single epithelial cell. So, this layer between the gut, the inside of the gut, and the circulation, the bloodstream, is about only 25 micrometers thick.

[00:01:03]Okay? That's about a 40th of a millimeter. It's thinner than a sheet of paper. When most people think of the gut, they picture a thick rubber tube, um like that of a bike tube, but it's more like some wet tissue paper. That's what it's more like. When the lining holds together, you're fine, but when it doesn't, it starts letting things cross that shouldn't be in the bloodstream, and shouldn't be floating around your body, and that's when issues can arise. So, the cells of the gut lining have these kind of gates that hold them together, or hold them shut, and these are called tight junction proteins. They're made of the proteins occludin, claudin, and ZO-1. You can think of them like zippers, which open and close to regulate the traffic from the gut to the bloodstream.

[00:01:58]Um most of the time things that cross the gut lining are regulated by the cells themselves and the transporters within the cells.

[00:02:09]So, things enter the epithelial uh lining first, those cells, and cross those cells to get into the bloodstream, released by those cells again into the bloodstream from the gut.

[00:02:22]But, when zonulin is chronically elevated, the tight junction proteins can get destroyed, and that will just let undigested food through, bacterial fragments, things you do not want in your bloodstream, which will cause immune responses and different >> [snorts] >> different downstream effects throughout the body systemically, okay?

[00:02:43]In this case, what's getting through is fragments uh fragments of gram-negative bacteria, >> [snorts] >> and these fragments are called lipopolysaccharide or LPS or endotoxin.

[00:02:56]And these are fragments of the outer wall of the bacteria you can see here.

[00:03:01]These are these things here.

[00:03:03]Right here.

[00:03:04]Right here. These are LPS, and these bacteria shed these uh these endotoxins, and then they can cross the gut lining and then start to cause some issues. So, what happens first is that [snorts] it goes to the liver because everything from the gut has to go through the liver and be filtered, >> [snorts] >> and this can trigger Kupffer cell responses, okay?

[00:03:26]Um via the receptor TLR4.

[00:03:29]So, LPS or endotoxin binds to these receptors, okay? In the liver, and then what happens is these receptors trigger the Kupffer cells to release nuclear factor kappa beta one, okay?

[00:03:46]And this is the master inflammatory switch in the cell. So, this triggers different inflammatory cytokines to get released or to get secreted.

[00:03:55]Um such as tumor necrosis factor alpha, also interleukin 6 and interleukin 1 beta, okay?

[00:04:04]So, these are inflammatory molecules, inflammatory cytokines, which go throughout the blood and cause inflammation. So, what happens when your gut barrier is permeable is the LPS, they get through the gut barrier, they trigger this inflammatory signaling, and the reason they do this is because usually if LPS is in your bloodstream, it's a sign that of a bacterial infection in your blood. Bacteria are not supposed to be in your blood, the blood is sterile. If bacteria get into the blood, this can cause some major [snorts] issues, okay? So, the body has an immune response to this LPS in the bloodstream because it thinks there's a bacterial infection.

[00:04:45]But, what really is happening is the LPS is leaking from the gut, it's binding [snorts] to these uh Kupffer cells in the liver, and that is secreting inflammatory cytokines.

[00:04:57]So, TNF alpha is going to be one of the main mechanisms or the main drivers of diet-driven insulin resistance, okay? Cuz it interferes with insulin signaling.

[00:05:07]Um interleukin 6 is one of the main drivers of metabolic dysfunction because it creates chronic low-grade inflammation. And interleukin 1 beta actually crosses the blood-brain barrier and can cause neuroinflammation. And these are the reasons why someone with a permeable gut, someone with LPS seeping into the bloodstream, are going to have symptoms like brain fog, low mood, motivation crashes, per- persistent fatigue or chronic fatigue, and random aches or pains and stiffness in the joints.

[00:05:45]Okay? Because of this chronic low-grade So, this is a big mechanism on how the gut permeability can affect your mental clarity and your mental function and how you function day-to-day. So, the reason that doctors usually miss this and why their tests um you know, are not satisfactory to detect this and treat it is because the test for the usual test for inflammation, what they do routinely, is a C-reactive protein test. And chronic low-grade inflammation, like what is caused by LPS seeping into the bottom binding to TLR TLR TLR 4 on copper cells in the liver is going to fly under the radar of the CP CRP threshold, the C-reactive protein threshold. C-reactive protein tests were designed to detect acute inflammation, acute rises in inflammation, for things like infection, Okay.

[00:06:46]Um an actual like disease. Okay.

[00:06:51]Not for things like chronic low-grade inflammation. So, now that we know the mechanism we need to know what is actually causing this, what is actually driving this. And there are four things that are most common in a modern lifestyle which are driving this. Okay. The first one going to be industrial food. So, firstly emulsifiers like polysorbate 80 and carboxymethylcellulose, like the emulsifiers in ice cream, salad dressings, etc. These strip the mucus lining and that mucus layer is the gut's second barrier which physically separates bacteria from the gut lining.

[00:07:23]When you strip this, the bacteria come into contact directly with the epithelial cells and the LPS can cross the barrier much easier. And then we have preservatives such as uh sodium benzoate, sodium nitrate. These are literally antibiotics that made they're designed to kill bacteria. That's what they're there for because bacteria is what um shortens the shelf life of different foods. That's why they're put in these foods to increase the shelf life because they kill the bacteria, stop it from proliferating.

[00:07:59]So, when you eat these preservatives, these are having the same antimicrobial effects within your gut microbiome.

[00:08:05]And it's killing off bacteria, it's irritating bacteria, and it's doing this also to gram-negative bacteria which make them shed more LPS which puts your gut micro puts your gut lining at more risk of >> [snorts] >> um you know, seep of that of those endotoxins seeping through the gut lining, okay? Then we have all types of plant foods from leafy greens, tubers grains, nuts, legumes, etc. These contain compounds that are literal toxins, okay? Things like polyphenols, lectins, glucosinolates, oxalates okay? There are far more than that, but these, first of all, they disrupt the microbiome specifically polyphenols and tannins these um these target gram-negative bacteria which creates more lipopolysaccharide shedding. And then lectins bind to the glycoproteins on the gut lining and the glycocalyx and cause these tight junction proteins to open.

[00:09:16]They interfere with different uh cellular signaling pathways which cause these uh proteins to get destroyed and open, cause the gates to open.

[00:09:25]And then we have oxalates. Now oxalates themselves for example, oxalic acid doesn't cause issues in itself to the gut lining, but oxalic acid has high prevalence to binding with calcium and then causing uh and then creating oxalates, which are these shards. It's literal crystal crystallized shards, which abrade physically abrade the gut lining. Physically abrade the epithelial surface, okay?

[00:10:01]And if you think about the gut lining as a roll of wet tissue paper, which is one ply thick, if you have all of these molecular crystals abrading it, that's going to not be something that you want to keep things from leaking out into the bloodstream from the gut.

[00:10:20]That's not something you're going to want. Now, our third biggest driver is alcohol, and this is not in order. I would say, honestly, alcohol is the worst. Alcohol directly creates acute spikes in lipopolysaccharide.

[00:10:34]This is because of how it disrupts the microbiome. It also directly damages the tight junctions and proteins, okay? So, it lets that LPS through between the epithelial cells, the enterocytes, okay? And then, number four is going to be chronic stress. So, when your cortisol levels, which is a stress response hormone, is chronically elevated, this thins the mucus lining of the gut and allows bacteria to come in contact with the cells themselves, the epithelial cells, and then this therefore increases the permeability of the gut lining. Now, these are the main four drivers, but there are a lot of things working in the background, which can contribute to these same issues and this same low-grade inflammation. So, if you want this applied to you, then you can apply to work one-on-one with me in the description.