← The Metabolic Classroom with Dr. Ben Bikman
The Metabolic Classroom with Dr. Ben Bikman
Stop Metabolic Inflammation at the Source: Your Gut
00:34:57
More Knowledge, Better Health
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Hi, it's Paige Desorbo from Giggly Squad. You ever stand in front of your closet and just say I have nothing to wear while you're literally surrounded by clothes? Because same so I started listing pieces. I'm over on Depop and honestly, it's been amazing. You can sell what you're done with and someone out there will love it. And the best part about it is there's no seller fee, so the money you make actually stays in your pocket, which feels very chic. It's also insanely easy. I listed something while watching TV and it sold before the episode even ended. So download the Depop app and list your first item today because your old outfit could be someone else's new favorite. Depop where taste recognizes taste Payment processing fees boosting fees still apply. For more info, visit depop.com hey, Ryan.
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Mic check1 2 are we recording? Hi, I'm Michelle Bernstein, an award winning chef, restaurateur and mom. I have a lot on my plate, including my psoriatic arthritis symptoms. That's why I was prescribed Cosentyx. It helps me move better.
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Cosentyx Secukenumab is prescribed for people 2 years of age and older with active psoriatic arthritis. Don't use if you're allergic to Cosentyx before starting, get checked for tuberculosis. An increased risk of infections and lowered ability to fight them may occur. Like tuberculosis or other serious bacterial, fungal or viral infections. Some were fatal. Tell your doctor if you have an infection or symptoms like fevers, sweatshirts, chills, muscle aches or cough, had a vaccine or planned to, or if inflammatory bowel disease symptoms develop or worsen, serious allergic reactions and severe eczema like skin reactions may occur. Learn more at 1-844-cosentix or cosentix.com Ask.
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Your rheumatologist about Cosentix.
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Welcome to the Metabolic Classroom Podcast. I'm Ben Bickman. Thanks for letting me be your guest professor for the next few minutes. Don't worry about any pop quizzes. I'm here to simply make the science of metabolism clear, practical and engaging before we get started. Just as a reminder, you can listen to both of my podcasts ad free by becoming an insider. Just go to Ben Bickman.com or click on the link at the top of the show. Notes welcome back to the Metabolic Classroom. I'm Ben Bickman, biomedical scientist and professor of Cell biology. The topic for today's mini lecture is one that connects your gut health directly to metabolic problems. Lipopolysaccharide, or lps. This molecule, produced by bacteria in your intestines, can trigger inflammation throughout your entire body when it escapes into your bloodstream. Understanding how LPS gets out of your gut and what you can do to stop it is crucial for preventing insulin resistance, fatty liver disease, and the chronic inflammation that precedes it. Let's start with the basics. LPS is a large molecule found in the outer membrane of gram negative bacteria. These bacteria naturally live in your intestines by the trillions. Under normal circumstances, LPS stays safely contained within your gut. But when your intestinal barrier becomes compromised, a condition often called leaky gut, LPS can cross into your bloodstream. Once LPS enters circulation, it triggers a powerful immune response. Your immune cells recognize LPS as a foreign invader and release inflammatory molecules called cytokines. This creates what we call in the biz metabolic endotoxemia, a state of chronic low grade inflammation that disrupts insulin signaling and promotes the other problems that I mentioned. Now, when I use the term low grade, that's a very deliberate term because it might not be that your body's reaching a point of inflammation that would be clinically red flagged, but it's still higher than it ought to be. So the intestine and its lining is very important here, and no surprise, it is a remarkably sophisticated structure. The intestinal lining is designed to allow some things to come in, but not everything. So it's designed to absorb nutrients while keeping harmful substances out. And think about the sheer number of harmful substances there could be yucky, bad, toxic things. And whatever you may be drinking or eating, the barrier itself consists of a single layer of epithelial cells. And these epithelial cells are connected by specialized structures called tight junctions. But to truly understand how LPS escapes from your gut into your bloodstream, you need to understand the two fundamental different pathways by which molecules can cross this gut barrier. It's helpful to think of your intestinal lining as a brick wall where the epithelial cells are the bricks, and the tight junctions between these cells are the mortar between these bricks. Molecules can cross this barrier, this brick wall, in two different ways. It can either move through the cells or between the cells. The transcellular pathway is the route through the cells themselves. This is how your body absorbs things like nutrients. When you eat protein, for example, it's broken down into amino acids. These amino acids will bind to specific transporters on the surface of the cell, and then these transporters will actively move the amino acids. It will pull them in through the cell and then release them on the backside, getting into the bloodstream. This is a very selective process. The intestinal cells will decide what gets through and what doesn't. Imagine it's like bouncers standing at the entrance of a club. They're deciding who can come in and who can't. The same principle applies to things like sugars or fats or vitamins and minerals. Each has specific transport proteins that recognize and move these molecules across the cell membrane. Again, no surprise. The transcellular transport is tightly regulated. You want your body and these cells to be able to control what can cross and how much can cross at any given time. It's the designed pathway for absorbing the things that we need. The paracellular pathway is the route between the cells, and it's through these tight junctions that will seal the spaces where the cells meet. That's the. That's the mortar in that, with the metaphor of it being like a brick wall under normal, healthy conditions, the tight junct, highly selective barrier, they do allow some things to pass, like water and very small ions, although it's in very small amounts, but they will block any large molecules, certainly bacteria and bacterial products like lps. But here's where the problem begins. When your tight junctions are damaged or their proteins are disrupted that are keeping them locked together, the paracellular pathway becomes pathologically permeable. The spaces between the cells will widen. Now, large molecules that should never enter your bloodstream, including lps, including even some undigested food proteins and bacterial fragments, can leak through. This is the essence of leaky gut. To understand how the barrier breaks down, I think it's helpful to know what holds it together. Again, we're talking about the mortar between the bricks. Tight junctions are very complex structures made of several protein components. And I'm going to mention the main ones that have been shown to be relevant in research. So the first one is something called Zonula occludens 1 or just Z01. I'll refer to it as that this is what's called a scaffold protein that will anchor the tight junctions to the cell's internal skeleton. Think of it as the framework that keeps everything in place. When Z01 is reduced or mislocalized, meaning it's not found in the right spot, the entire tight junction structure will suddenly become unstable. So what's binding the cells together starts to kind of fray apart. Another one is occludin. Occludin is a transmembrane protein that spans across the cell membrane and interacts with occludin on an adjacent cell. So this is almost like the hooks and loops of, like, Velcro helping lock things together. And research has shown that when occluding is phosphorylated or altered at specific sites. This can certainly happen with things like oxidative stress and inflammation. It will detach from the Z01 molecule I just mentioned, and then the seal between the cells, the mortar, starts to fragment. And then one other part that's important in this process is claudins. Clawdins are a family of proteins that determine the selectivity of the tight junction. So different clawdin types have different properties. Some clottins will form barriers that tighten the junction. Others form selective pores that will allow specific ions to get through the mortar. That tight junction, the specific combination of claudins expressed in, in the intestinal cells will determine how permeable the gut barrier is. And of course, when these proteins are all functioning properly, your gut barrier is functioning properly, it's strong, and it is, most importantly, selective nutrients cross via the regulated transcellular pathway. Remember, that's going through the cell while the paracellular, meaning between the cells, that pathway will remain very, very tightly controlled. But through dietary factors, intestinal inflammation, other things we'll get to in a moment, that paracellular pathway will open up inappropriately. Now that you understand the structural proteins that hold the tight junctions together, you need to know about the signaling molecule that tells them to come apart, and that is zonulin. Zonulin is the only known physiological modulator of tight junctions that we've described, that has been described and identified so far. Think of it as a master switch that controls how permeable your intestinal barrier becomes. When zonulin is released by your intestinal cells, it will trigger a cascade of events that causes the tight junction proteins to disassemble, and the spaces between them will start to widen. So the mortar is crumbling and the bricks are being pushed further apart. The mechanism is elegant, but of course it's problematic when it is dysregulated. Zonulin can bind to receptors on the surface of these intestinal cells and the binding will activate a series of proteins. You know this activation cascade and ultimately causing Z01 to detach from an anchoring position. Simultaneously, you have other molecules, like actin filaments within the cell that will reorganize and polymerize. But the combination of this is that the cells will contract and pull apart, allowing the junctions to be much wider. Under normal circumstances, you can have this being part of a defensive mechanism. When your small intestine is exposed to certain bacteria, zonulin release will cause a temporary increase in permeability, essentially flushing out the microorganisms as part of your innate immune system response. This is zonulin working as intended, a quick opening and closing of the barrier to deal with a threat within the intestines. The problem arises when zonulin release becomes chronic or excessive. Research has identified two primary triggers for zonulin secretion, bacterial exposure and gluten. But importantly, dysbiosis is imbalanced Gut microbiome, specifically with an overgrowth of gram negative bacteria. Remember, gram negative bacteria are those that have lps. This can cause a persistent zonulin elevation. These bacteria continuously stimulate zonulin release, creating a chronically permeable gut barrier. And there's relevant human evidence on this. Studies examining patients with type 2 diabetes or inflammatory bowel disease, or rheumatoid arthritis, and even cardiovascular disease consistently show elevated serum zonulin levels alongside elevated LPS levels. The correlation is striking. When zonulin is up, intestinal permeability is compromised and endotoxemia follows. Or this, and then the chronic inflammation. What makes zonulin particularly important for metabolic health is that it connects gut barrier dysfunction to systemic diseases. Elevated zonulin levels can predict the transition from asymptomatic autoimmunity to active inflammatory disease. And in the context of metabolic syndrome, zonulin elevation may be one of the earliest detectable signs that your gut barrier is failing and that you have some metabolic endotoxemia beginning. The therapeutic implication is there, and I think it's clear any strategy that will reduce zonulin signaling will help maintain barrier integrity. Prevent LPS from getting in. Now, why even talk about lps? LPS is a large molecule. It is far too big to cross through the healthy gut tight junctions via the paracellular route. And it doesn't have transporters to cross transcellularly. Under normal conditions, LPS will stay safely contained in the gut. But when tight junction proteins like Z01 or occludin and claudins or are disrupted, that paracellular space will widen. Now, LPS can leak between the cells entering that space and getting into your bloodstream. Once it is in circulation, LPS triggers the inflammatory cascade that we discussed earlier. This is one of the reasons why maintaining a tight junction is so important. So what makes the barrier breakdown? There are a handful of variables here, and I want to focus on the ones that I believe are most relevant when it comes to dietary factors, because there are several. And let's examine the two that I believe are the most significant. Fructose and omega 6 fats. Fructose consumption has of course, increased dramatically with the widespread use of sugars and high fructose corn syrups. Research demonstrates that high fructose intake directly compromises intestinal barrier function and increases LPS movement into the blood through multiple mechanisms. Preclinical studies show that oral administration of fructose exacerbates problems in the liver. And that is a relevant marker because the liver is directly downstream of the intestines. So if things are leaking through the liver, leaking through the gut wall, if things are leaking through the gut, the liver is the first one who has to see that it's kind of the front line of what's coming in from the gut. The mechanism here involves reduced expression of z01, that is the critical tight junction protein that I mentioned earlier. This then allows the translocation of LPS through the portal vein and directly into the liver. This gut derived LPS then promotes inflammation and even fibrotic or scarring changes within the hepatic tissue or the liver. This interaction between fructose stress and the gut barrier is particularly concerning. Research demonstrates that high fructose combined with restraint stress. So in an animal model, upsetting the animal and making it stressed can increase this disrupted barrier even faster than normal. So this ends up being a wicked combination of stress plus fructose, which, if we're being honest with ourselves, is, is a pretty common occurrence within human daily living as well. Now let's move on to the fats. The ratio is what's important here. The ratio of omega 6 to omega 3 fatty acids in your diet profoundly affects your gut barrier. Modern western diets contain excessive omega 6 fatty acids, primarily things like vegetable oils or so called vegetable oils, but they're seed oils, corn oil, soybean oil, sunflower oil. This creates an inflammatory environment in your intestines. Diets enriched with omega 6 polyunsaturated fatty acids dramatically alter gut microbiota composition. In a mouse model where they were fed high omega 6 diets, researchers observed significant enrichment of a family of bacteria that includes many gram negative or LPS producing species. This we could call is a type of microbial dysbiosis and no surprise in these animal models it was associated with a heavy degree of colitis, so inflammation of the gut and increased susceptibility to normal bacterial infections. Remarkably, fish oil supplementation or omega 3 attenuated these negative effects. The addition of omega 3 fatty acids reversed the omega 6 induced dysbiosis, reducing LPS containing populations and improving overall microbial balance. However, the research revealed an interesting complexity. While fish oil improved the microbiota and reduced colitis, it simultaneously impaired LPS activity, which in some contexts changes it changed the overall ability of LPS to move in and act or harm the body. One other line of research in animals finds that when they could genetically modify mice to make its own so the animals could make their own Omega 3s so it was no longer essential in the diet, they were making it all the time. What they found is that that was sufficient by changing to change the omega 6 to omega 3 ratio and it was enough to totally oppose the effects of endotoxemia. And what's important is that they were able to get that ratio of omega 6 to omega 3 to about a 1 to 1 as opposed to in normal human diet typically about 15 or 20 to 1 where we're eating about 15 to 20 times more omega 6 than omega 3. It's not overall feasible in a human diet to get it to one to one, but it is certainly feasible to get it closer to like a 3 to 1 of omega 6 to omega 3. And there's human evidence to suggest that could be sufficient.
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Hi, it's Paige Desorbo from Giggly Squad. You ever stand in front of your closet and just say I have nothing to wear while you're literally surrounded by clothes? Because same so I started listing pieces I'm over on Depop and honestly it's been amazing. You can sell what you're done with and someone out there will love it. And the best part about it is there's no seller fee, so the money you make actually stays in your pocket, which feels very chic. It's also insanely easy. I listed something while watching TV and it sold before the episode even ended. So download the Depop app and list your first item today because your old outfit could be someone else's new favorite. Depop where taste recognizes taste Payment processing fees boosting fees still apply. For more info, visit depop.com.
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All right, now let's get back to the metabolic consequences here, because this is an area that I can speak to with some authority, having published some papers on this topic. When LPS enters the bloodstream, it doesn't just cause local intestinal inflammation, but it can trigger systemic metabolic problems. First, LPS will bind to receptors called toll like receptor 4 toll like a toll booth TLR4. This is on immune cells and many other tissues throughout the body. When TLR4 is activated, it in turn activates inflammatory signaling pathways, which will ultimately result in a massive ramping up of the production of pro inflammatory cytokines like C Reactive protein or tnf? Alpha. Now I should note here, as I alluded to that my research has focused on this. Some colleagues and I discovered that TLR4 activation can drive ceramide biosynthesis. And as you know by now, probably ceramides are a type of lipid or fat within the cell. They're part of the sphingolipid pathway that can directly cause insulin resistance. Importantly, not all fats can disrupt the insulin pathway. Ceramides is the one that does it more than any other. So we identified again that when TLR4 is activated, it promotes the accumulation of ceramides, and then ceramides in turn disrupt the insulin pathway. And then of course, LPS will turn on TLR4 dramatically. Now another one. Second, the chronic inflammation directly interferes with insulin signaling. When inflammatory pathways are active, they phosphorylate insulin receptor substrate 1 or IRS1 at a wrong site. So basically insulin would be coming and trying to activate the receptor. And yet the internal inflammatory signals have disrupted that signal from getting turned on. And then a third mechanism here is that when LPS reaches your liver, it can promote fat accumulation and inflammatory changes in the liver. Remember, the liver is on the front line of this. It receives blood directly from your intestines through the portal vein. And when that blood contains elevated lps, your liver will become inflamed and Fat accumulates in the liver cells and over time, you can progress through this standard protocol of, or the standard progression of, starting with fatty liver disease and moving all the way to cirrhosis and even potentially liver cancer or carcinoma. Okay, now all of this has been a kind of terrifying story so far in the mini lesson, so let's get to the good news. You can adopt habits to strengthen your intestinal barrier and reduce LPS translocation. Let me walk you through just a few evidence based strategies. Okay, one, and this is a favorite molecule for me to discuss, or not a molecule, but a food stuff, apple cider vinegar. Apple cider vinegar has gained attention in recent years because there's a lot of research to support its beneficial effects on cardiometabolic health, perhaps in part because of its effects on the gut. Preclinical studies demonstrate that apple cider vinegar supplementation significantly modulates the intestinal microbiome in ways that can be healthy. The research shows impressive results. In one particular study, apple cider vinegar reduced weight gain by over 26% while also decreasing serum markers of liver injury. So the liver was healthier and they were gaining less weight. But the mechanism is what matters here. Apple cider vinegar works primarily in this case by remodeling gut microbiota composition. The research demonstrates that it increases beneficial bacteria, among them Ekkermansia, which is a keystone microbiome species known for enhancing mucus production and supporting barrier integrity. The mechanism, it goes even a little further where apple cider vinegar also contains pectin, which is a prebiotic fiber from apples. So this is where it becomes relevant with apple cider vinegar. So you're getting some of the prebiotic fiber, the pectin in there as well, and then pectin acts like a prebiotic. And I'll speak more on that topic in just a moment. Now, before we get to that, let's discuss probiotics. Not all probiotics are created equal. And of course, when I say probiotic, I mean when you're actually taking bacteria, you're orally consuming bacteria in the hopes that it's going to get through the acidic environment of the stomach and get to your intestines to help populate or to put in place a healthier population of bacteria. The key is choosing strains that have specific mechanisms for strengthening tight junctions and reducing LPS translocation and thereby in the process protecting against intestinal inflammation. One particularly well researched approach involves spore forming probiotics, especially Bacillus subtilis. Unlike traditional probiotics like Lactobacillus or Bifidobacterium strains, which are kind of sensitive to stomach acid and often won't survive the journey through your digestive tract. Spore forming probiotics exist in a dormant protective state. Think of them as seeds. They can withstand the harsh conditions, in this case of the stomach, and remain viable until they reach your intestines, where they germinate and become metabolically active. Research on Bacillus subtilis has demonstrated impressive effects on both gut barrier function and metabolic endotoxemia. A 2017 clinical trial examined apparently healthy individuals who experienced dramatic increases in blood endotoxin levels after meals, a clear sign of compromised gut barrier function. So they'd have people eat a meal and then measure the degree to which LPS had invaded into their bloodstream. After 30 days of supplementation with a Bacillus subtilis species, the participants in the study experienced a 42% reduction in post meal endotoxin levels. This is not a marginal improvement. This represents pretty substantial restoration of gut barrier integrity. The same study also showed reductions in triglycerides and inflammatory markers, demonstrating that improved gut barrier function has very expected downstream metabolic effects. In vitro research examining, examining this species, the Bacillus subtilis effects on barrier function, reveals more benefits here where they found that they had enhanced improvements in the expression of the tight junction proteins that we discussed earlier, so Z01, occludin and some claudins. And so the benefits of the Bacillus subtilis are myriads. Now, beyond the structural support that the Bacillus subtilis can provide, we also see some significant reductions in inflammatory signaling where many pro inflammatory cytokines like TNF alpha has been shown to go down significantly by about half in just a few weeks in human volunteers that are being studied. And this matters because the inflammatory cytokines are part of the vicious cycle that can happen here. When LPS enters your bloodstream, it triggers release of TNF alpha and other inflammatory molecules. These cytokines then damage the tight junctions, creating more permeability, which allows more LPs through which in turn triggers more inflammation. By suppressing the inflammatory response. Kind of at its origins, the Bacillus subtilis helps break the cycle. That's something we want to have happen. All right, now let's get to some practical recommendations for probiotic. Especially with probiotic supplements, you want to focus on supplements that will enhance the gut barrier function. And I strongly recommend looking for some that contain Bacillus subtilis. I mentioned some of the human evidence and you want to focus on just getting a few billion, what's called C fee cfu. Those are the the units, these functional units when it comes to probiotics. So a few billion, if you can get to that point, the evidence in humans finds that just a few weeks up to about eight weeks is sufficient to make a difference. All right, now that is you putting new bacteria in. What about feeding the good bacteria? Because in addition to adding the beneficial bacteria, you need to feed them. And this is where the prebiotics can become essential. Prebiotics are specialized molecules, mostly fibers that resist digestion in your upper GI tract, but feed the beneficial bacteria in your colon. Not all fibers are equally effective as prebiotics. Oligosaccharides are particularly interesting prebiotics. These are short chains of sugars that resist digestion in your upper GI tract but feed beneficial bacteria later on. Two of the most well researched types are fructooligosaccharides, often just abbreviated as fos, and xylooligosaccharides. Fos, which is generally derived from sources like chicory root or onions and garlic, has been extensively studied for its ability to increase Bifidobacterium populations. So those are healthy bacteria. We want them and more importantly, we can't often eat them. They're not typically going to act well to get through the stomach.
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XOS the Xylo oligosaccharides are derived from plant fibers like corn cobs and they offer similar benefits with potential better tolerability for some people. What makes these oligosaccharides special is their selectivity. They preferentially feed beneficial bacteria like Bifidobacterium while resisting the harmful by, well, resisting the digestion by harmful bacteria. So they're selectively feeding the good ones while starving the bad ones. When the bacteria will eat these prebiotics, this fermentation in the gut in turn produces short chain fatty acids, including acetate, propionate and butyrate. This leads us to the next point here, which is me discussing a little bit about the short chain fats, which I am fascinated by. First and foremost, I should note that apple cider vinegar is a short chain fat. So this is specifically acetic acid. That's the main molecule within the apple cider vinegar. That gives it its sour, tart flavor. But butyrate is another one that needs to be mentioned. It is the preferred fuel source for colonos sites. So these are the cells that line your colon and it plays a crucial role in maintaining barrier function. Research examining butyrate's effects on intestinal barrier function reveals that butyrate enhances the intestinal barrier by facilitating tight junction assembly. A study showed that butyrate treatment increased transepithelial electrical resistance in a dose dependent manner, which just indicates that butyrate was enhancing barrier function. Importantly, butyrate promoted the assembly of tight junction proteins at the cell cell junction, so literally bringing the cells closer together and sealing the barrier more effectively. Now the question is, how do you ensure adequate butyrate production? Well, the answer is dietary fiber. Your gut bacteria produce butyrate by fermenting fermentable fibers from vegetables, fruits and whole grains. But if you're worried about the source and food sources, this is where you can just get the prebiotics directly, like the FOS and the xos. Now you may be wondering, can't I just eat butyrate? You can. Butter, for instance, contains about 3 to 4% butyrate. It's actually where the butyrate gets its name from the Latin buterum, meaning butter. But the amount that your gut can produce by fermenting these prebiotics. Prebiotics will be much more than you can feasibly eat through butter. Although I'm certainly an advocate of butter, a great defender. All right, now let's synthesize all of this into some practical recommendations. First, reduce your fructose intake. Fructose will damage the intestinal barrier function and in a dose dependent manner. So the more you're eating, the more you are harming your guts. Second, try to balance the omega 6, the 2 omega 3 ratio. The easy way to do this, of course, is just don't consume foods with that have been prepared with refined seed oils. So when you look at the back of the label and you see that it's corn or soybean or sunflower oil, don't use it. Focus on saturated forms like, you know, tallow and lard and coconut oil, or monounsaturated like olive oil or even avocado oil. And then, of course, try to do what you can to get good Omega 3s, EPA and DHA either through just food like fish, or through good fish oil supplements. Third, get some apple cider vinegar. Research shows that apple cider vinegar modulates the gut microbiome composition in ways that will support metabolic health. So it's helping your gut have healthier bacteria. Particularly, it's going to be feeding and fueling the growth of Akkermansia, which is associated with enhanced mucus production and improving the integrity of the gut barrier. And the mechanisms with apple cider vinegar are even further, where as I noted, it also contains pectin, a prebiotic fiber that can feed the good beneficial bacteria. And then fourth, consider a comprehensive probiotic approach. So do what you can and look for strains that you can get, specifically Bacillus subtilis. You want spore forming, so that means it's going to be kind of locked up tight to get through the harsh environment of the stomach. And once it gets through, it can start to multiply and spread itself, spreading that bacteria through your intestine to help with normal immune function and get some good fiber. That would be the fifth thing here. Aim to get some good fiber sources. My role, my view on fiber is a little nuanced that the more a person is eating meat based or carnivore based diets, the less they may benefit from fiber. But the more you are eating carbs in your diet, the more you absolutely, I think, should focus on deliberately including fiber in your diet. Now, how would you know if any of this is working? It's not really feasible for you to measure lps, so you just look at markers of inflammation and metabolic health. So insulin, track your insulin levels anytime you can. Of course, my general view is you want that insulin to be single digits, ideally below 7 micro units per mil. Also markers of inflammation like C reactive protein. It is so common now to have C reactive protein measured. Hopefully you're seeing levels below 1 milligram per liter. But even better would be 0.5, so half a milligram. But also pay attention to just how you Feel how bloated you are, how regular your bowel movements are, and if it's something you're concerned with, take create a symptom journal where you're documenting some of these effects. And there are a number of other metabolic markers like the liver enzymes, ALT and ast, triglycerides and glucose. Those all should be getting better, showing you that you're making improvements in the right direction. So in conclusion, I hope I've taught you that LPS driven metabolic endotoxemia represents a very important link between gut health metabolic disease. The research is remarkably consistent. Fructose damages your gut, omega 6 fatty acids will allow more LPS to get in and you have this metabolic endotoxemia that will drive a host of problems from the liver in the blood vessels and insulin resistance. The good news is that this process is really largely under your control just by changing your dietary habits and including some that you know to be good, like prebiotics and smart probiotics and the deliberate inclusion of apple cider vinegar. But what we do know, the science is clear. Your gut barrier is your metabolic gatekeeper. Keep it strong and you'll very likely keep metabolic and other problems at bay. Thanks for joining me today on the Metabolic Classroom. I hope you found this mini lecture helpful. Until next time, stay curious and stay healthy.
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Mic check 1, 2. Are we recording? Hi, I'm Michelle Bernstein, an award winning chef, restaurateur and mom. I have a lot on my plate, including my psoriatic arthritis symptoms. That's why I was prescribed Cosentix. It helps me move better.
- [40:03]
B
Cosentix Secukenumab is prescribed for people 2 years of age and older with active psoriatic arthritis. Don't use if you're allergic to Cosentyx. Before starting, get checked for tuberculosis. An increased risk of infections and lowered ability to fight them may occur. Like tuberculosis or other serious bacterial, fungal or viral infections, some were fatal. Tell your doctor if you have an infection or symptoms like fevers, sweats, chills, muscle aches or cough had a vaccine or planned to. Or if inflammatory bowel disease symptoms develop or worsen, serious allergic reactions and severe eczema like skin reactions may occur. Learn more at 1-844-cosentyx or cosentyx.com Ask.
- [40:40]
C
Your rheumatologist about Cosentyx.
- [40:45]
A
Hi, it's Paige Desorbo from Giggly Squad. You ever stand in front of your closet and just say I have nothing to wear while you're literally surrounded by clothes? Because same so I started listing pieces. I'm over on Depop and honestly, it's been amazing. You can sell what you're done with and someone out there will love it. And the best part about it is there's no seller fee, so the money you make actually stays in your pocket, which feels very chic. It's also insanely easy. I listed something while watching TV and it sold before the episode even ended. So download the Depop app and list your first item today because your old outfit could be someone else's new favorite. Depop where taste recognizes taste. Payment processing fees, boosting fees still apply. For more info, visit depop. Com Hi, it's Paige Desorbo from Giggly Squad. You ever stand in front of your closet and just say I have nothing to wear while you're literally surrounded by clothes? Because same so I started listing pieces. I'm over on Depop and honestly, it's been amazing. You can sell what you're done with and someone out there will love it. And the best part about it is there's no seller fee, so the money you make actually stays in your pocket, which feels very chic. It's also insanely easy. I listed something while watching TV and it sold before the episode even ended. So download the Depop app and list your first item today because your old outfit could be someone else's new favorite. Depop where taste recognizes taste. Payment processing fees, boosting fees still apply. For more info, visit depop.
- [42:16]
D
Com.