I call this discussion fatty liver. It's no mystery because if you talk to most doctors in the mainstream world, they'll tell you things like, "Well, you have fatty liver." We know this because your liver function tests, measures like A or ALT are higher, telling you that something is damaging your liver. Or they did an ultrasound of your liver or an MRI or a CAT scan and they showed fatty infiltration of the liver. And they typically say things like, "We don't know why this happens. It could be some unexplained virus. It could be something we're not aware of, maybe even genetically programmed, and we'll just watch you. Don't worry, we'll watch you." And as you go into cerosis and liver failure, we'll talk to you about a liver transplant. Now, let me tell you what that means. Cerosis is horrible. I've seen cerosis mostly from alcoholism where the liver becomes shrunken and dysfunctional and your abdomen expands becomes tense with fluid that's called acites. It has to be tapped with a needle and eventually a shunt put in to redirect that fluid into the venus system and that's a rapid path to death and liver failure. How about liver transplant? Liver transpl transplant is a catastrophic procedure. There's a huge amount of bleeding. Your post-operative course is very stormy. Maybe you bought yourself a few years completely reliant on imunosuppressive drugs and then you eventually die. So these are grotesely inadequate responses. But the simple truth is fatty liver is easy to get rid of. But I I'm going to tell you things that you might not hear from other sources. In fact, some people will say things like this. Well, take take milk thistle or other herbal preparations to treat the fatty liver. That is no better. If you had an eczema rash, say, and you came to me and I said, "Well, put a band-aid on it." You would say, "That's stupid." It doesn't get rid of the cause. to cause by the way almost always some bowel flora issue particularly SEO small intestinal fungal overgrowth or at least colonic overgrowth of fungi that often transplants itself to the skin and that's why a lot not all but a lot of eczeus rashes a lot of eczema responds to topical antifungals whether it's a dilute essential oil or uh lotin clot primosol they often respond to topical antifungal fungal agents, but so putting a band-aid on it while not addressing in this many cases the fungal overgrowth in your colon or small bowel and transplantation of that fungus fungus to your skin. Putting a band-aid on it's not going to do anything and that's what these herbal preparations are. So why do most mainstream doctors and many and some of the alternative health people say things like well there's nothing we can do. You might try to lose 10 pounds that might help somewhat. Translation: We have no pharmaceuticals or procedures to treat your fatty liver. They therefore resign you to a future of worsening liver necrosis, death of your liver, liver failure, cerosis, ascites, and then liver failure and liver transplant. If you even survive, if you are among the very few people who actually receive a liver, most die waiting for a liver. So, let's get to the nitty-gritty. How do you get rid of it? Now, first let me tell you how you get it. Why do why do I have to run through the science to tell you how you get it first? Because I'm going to tell you things that are so contrary to popular opinion offered by the vast majority of my colleagues, physicians, that if you don't understand why, and someone challenges you, your partner, your family, your co-workers, whoever says, "Oh, I don't think that's right." You say, "Well, here's my understanding of the rationale, the logic, the science behind it, and it makes better sense and it makes better outcome for you. If I just tell you what to do, and you don't know why, well, going to take it on faith." And I don't think that's a good idea. You want to know with good logic, rationale, and science, this is all scientifically based. It's not me making stuff up, okay? that it's you're more confident that you're going to get the outcome you want, which is absolute reversal to normal of fatty liver in a vast majority of instances. So there are three basic processes that lead to fatty liver. Now let's be clear, fatty liver means the infiltration of fat into your liver. It does not mean as many doctors think a fat accumulation in the liver from consuming fat. That is not true. Consuming butter and pork fat and hamburger and beef and other sources of oils do not add to fatty liver. So it's a misnomer. It is fat in the liver. Where did it come from? Three basic processes. The first one is liver or hpatic dnofol lipogenesis. And all that means is your liver is very good at taking carbohydrates and sugars and converting them to fats, namely triglycerides. Dooo, making something new, lipogenesis, making new fats. So the liver is very good at converting carbohydrates and sugars to triglycerides. Now among the most offensive carbohydrates, the amalopectin A of wheat and grains. Yes. The food you've been told to load up on your diet that's part of fast food, restaurant food, being served bread at before your dinner. Uh the buns, hot dog buns, sandwiches, bagels, breakfast, all that stuff made with wheat and grains. The primary carbohydrate is amalopectin A. And the liver is very good at converting the amalopectin A of wheat and grains to triglycerides. Likewise, sugars, sucrose, glucose, and fructose. fructose especially bad. So the liver converts those carbohydrates and sugars to triglycerides. Now triglycerides cannot be released into the bloodstream directly because they're fats. If you release fats into the bloodstream directly, they will coalesce. Just like your salad dressing, when you have oil and vinegar, it separates, right? There's an aquous or vinegar and water containing phase. There's an oil phase. oil phase at the top of course because oils coales. If oils coalesed in your bloodstream, they would block various organs and you would die within probably minutes from all kinds of horrible things. And so your liver knows to package triglycerides into water soluble aquous soluble particles, lipoproteins, fat carrying proteins. by adding proteins and other components to the triglycerides. And they they're packaged as something called very low density lipoproteins. They're low density, very low density because they contain lots of fats. That's why in your salad dressing, what floats to the top? Not the water and vinegar, but the oils like your olive oil. Likewise here, when you package a lot of triglycerides into a lipoprotein particle, it's very low density. That's VLDLDL. That by the way is a direct cause for coronary disease. Not LDL cholesterol, not that nonsense, but VLDLDL particles, one of the major particles that leads to coronary disease. So you have these VLDLDL particles floating around, but that's not the part that leads to fatty liver. When your liver makes those triglycerides through liver denovalogenesis, not all triglycerides exit the liver as VLDLDL particles. A lot of those triglycerides stay in the liver and accumulate. Triglycerides are fats. Fats are triglycerides. So that accumulation of triglycerides in the liver leads to fatty deposition in the liver. Fatty liver. Okay. So when you have fatty liver, an increase in a fatty infiltration by some imaging method, you also have higher blood levels of triglycerides. So when you have a cholesterol panel and the doctor focuses only on LDL or total cholesterol but often ignores the trigly triglycerides they've ignored a very important biioarker for what's going on in your liver. So a typical triglyceride level would be something like 300 242 193 milligrams per deciliter. What's desirable? 60 milligrams per deciliter or less. Typically people in my programs doing these things have blood triglycerides levels on a cholesterol panel of between 45 and 60 milligrams per deciliter telling us that their liver is not making much in the way of triglycerides thereby very little or no VLDLDL particles and very little or no triglyceride accumulation in the liver adding to fatty liver. So that's hypatic or liver denovo lipogen genenesis. The second process that adds this effect is insulin resistance. And all that means is the organs of your body, the brain, muscle, liver don't properly respond to insulin. And when that happens, the pancreas recognizes this and massively overproduces insulin. So a person who is insulin sensitive responds to insulin their blood insulin level fasting is like zero or one or three microunits per liter. A person who is insulin resistant where their organs are not responding to insulin their levels are typically 40 90 microunits per liter. Not a little bit worse, not 10% worse, not 30% worse, but tenfold, 30fold, 100fold worse. When that happens, the liver responds by amping up its liver denovo lipogenesis. Okay, so insulin resistance and to a also a degree inflammation, which those two things go hand in hand. Insulin resistance and inflammation are two processes that often occur together. Those two things are the gas pedal on liver denovalogenesis making more triglycerides that accumulate in the liver as well as more higher triglyceride and VLDLDL blood levels. Another process that adds this effect is endotoxmia. Lipopolysaccharide endotoxmia. All that means the microbes in your colon fecal microbes live and die and release their components. Now some of those components are called endotoxin or lipop polysaccharide endotoxin. This is a component of their cell walls. So when those microbes die they release those toxic compounds into the bloodstream. Now here's the thing. The bloodstream drainage of the gastrointestinal tract goes right to the liver via a specialized portion of your venus system called the portal vein system. So when microbes die in the colon, they shed some of their toxic compounds, some of which get into the bloodstream, go directly to the liver and those breakdown products like endotoxin are very toxic to the liver and they worsen insulin resistance and inflammation and turn up liver denoval lipogenesis. Now the situation gets even worse if those fecal microbes that are supposed to be confined to the colon have ascended into the 24 ft of small intestine the douadinum jigunum and illium. Now, the small intestine is very permeable by design because that's where you're supposed to absorb vitamins, minerals, amino acids, fatty acids, and it's illequipped to deal with invading fecal microbes that have ascended from the colon. Now, while the colon has denser populations of microbes, the small intestine is longer. The com is about four to five feet long while the small bowel the entire length of the small bowel is 24 feet long. And so when fecal microbes have come to colonize infest the 24 ft of small intestine they live only for a few hours at a time. When they die they shed those toxic compounds again such as lipopolysaccharide endotoxin into the bloodstream especially since the small intestine is very permeable. Now you have a even worse flood of lipopolysaccharide endotoxin emptying into the portal system portal vein system to the liver once again amping up increasing liver denovo lipogenesis and causing triglyceride accumulation in the liver. Okay. So we have these three processes. We have liver denovo lipogenesis made worse by insulin resistance made even worse by lipopolyaccharide endotoxmia. What do we do about it? It sounds awfully complicated, right? It's actually very simple. One, stop eating foods that feed your liver with carbohydrates. The most effective way I know of, eliminate all wheat, grains, and sugars, doing the opposite of what many of what many dietary guidelines tell you to do. We never limit fat because it's not fat. Fat is produced by liver, but fat does not cause fat accumulation in the liver. So, we're going to not restrict calories. We're not going to restrict fat fat intake whether it's saturated fat or polyunsaturated whatever we're not going to restrict fat intake but we are going to eliminate the sources of amalopectin a and sugars sucrose fructose glucose so that the liver no longer is engaging in dnoval lipogenesis going to correct insulin resistance and help make your organs insulin responsive just that dietary change alone because one of the other things you do when you eliminate wheat and grains is you no longer have that rise in blood glucose from the amalopectin A nor from those sugars and so insulin resistance starts to recede. Now you can accelerate that process by restoring nutrients largely lost because of the quirks of modern life. We restore magnesium, iodine, omega-3 fatty acids and vitamin D. Those four basic things when put together turn down insulin resistance and thereby liver denovo lipogenesis. Another thing we do we address the dispiosis or more commonly the SIBO in your small intestine that's causing a flood of endotoxin to go to your liver and amplify liver denovo lipogenesis and insulin resistance. How do you do that? Well, there's a number of different ways to do it. The way we've been doing it in my programs is to engage in something called SIBO yogurt. And all that is, it's three microbial species. It's it's a it's a strain of Lactobacillus rotary, a strain of Lactobacillus geride, and most recently the most recent recipe, basillus subtilus. Why are those three microbes? Well, those three microbes are unique in that they tend to colonize or in the case of subtilus, germinate. It's a spore in the small intestine where SIBO occurs. They'll also go to the colon. So it it also addresses colonic dispiosis. So those three microbes unique in that they take up residence in the small intestine where they produce what are called bacteriains. Bacteriains are natural antibiotics that kill kill the species of SIBO. So if your SIBO your small intestinal bacterial overgrowth is dominated or your colonic dispiosis is dominated say by E.coli coli or klebsella or campalobacttor or sudamonus or other species like stafllocus strepox or enrooccus. The mix of bacteriains you get from those small bowel and colon colonizing species kill those microbes reducing their populations and it leads to a reduction in endotoxmia draining into the portal venus system. So there you have it. That basic approach has worked incredibly well for us. We don't have to treat the fatty liver. We don't have to wait for you to have cerosis and a liver transplant. We simply address the underlying causes that does not involve use of any pharmaceuticals. Now, if these kinds of unique conversations interest you and you want to explore it further, I invite you to join to look at all my other materials in this YouTube channel or in my defiant health podcast, my thousands of posts on my wdavmd.com blog, my super gut book, of course, uh or if you'd like some handholding or some camaraderie and guidance, join my membership website, which is uh inner circle.drdavis Dr. Davis, infinitehealth.com