"Why do I have food intolerances?

Food intolerances are growing and more and more people are unable to eat FODMAPs-containing foods, histamine-containing foods, nightshades, legumes, fructose-containing foods and numerous others, sometimes reduced to consuming only a handful of "safe" foods. 

Why is this happening, something that was virtually unknown only a generation or two ago? Much of it is due to the excessive proliferation of Proteobacteria species in your gut. But it's not just about food intolerances, as these intolerances are just the tip of the iceberg. 

Transcript

Why Intolerances Are Suddenly Common

William Davis, MD 0:00

You may have noticed that many modern people have developed all sorts of intolerances to various foods. It could be an intolerance to FODMAPS, so-called fermentable oligosaccharides, monosaccharides, disaccharides, and polyols, essentially fibers and sugars. Could be to nightshades like eggplant and tomatoes, it could be to histamine-containing foods, especially cheese and wine, that either contain histamine or trigger release of histamine and leave you with hives or asthma or other odd feelings. It could be to fructose, it could be to gluten or gliden, really, or it could be to any number of other foods. And of course, the actual estimates of the number of modern people who have these intolerances varies because the definitions don't all agree. The populations differ, location, geographic location differs, age group differs, but it's probably somewhere around a quarter of the population now, which is very odd when you consider that food intolerances were rare just two generations ago with our grandparents and your great-grandparents. So what is happening? Well, oddly, there's a kind of a growing appreciation that this is an overgrowth of specific kinds of bacteria in your gastrointestinal tract. It's coming from a variety of uh lines of evidence. A lot of it, oddly, comes from exploration of what goes on in people with cirrhosis, liver cirrhosis, fatty liver, nash, non-alcoholic steatohepatitis, that's the liver inflammation and dysfunction of the liver and damage that leads to cirrhosis. So those liver conditions are almost all associated with SIBO, that is, small intestinal bacterial overgrowth. So it's not unclear exactly why that happens. It could be a chicken or egg, chicken and egg type of phenomena, which came first, the liver disease or the SIBO. But it's clear that people who do have some measure of liver dysfunction have SIBO. It's a very high proportion of these people have SIBO. That is, fecal microbes. We say gram-negative proteobacteria. That is, these are largely fecal microbial species. Nor in the normal situation, you should have two, three, four, maybe as much as five percent of your colonic bacteria comprised of this group of microbes, gram-negative proteobacteria. I point that out that they're gram-negative, meaning they stain a certain way. When you apply a stain like a gram stain, it doesn't take up the last stain, the violet stain, and so they look red or pink. So we say they're gram-negative. Gram-positive organisms do take up the violet stain. They look blue or purple. But it's the gram-negative species that have a very specific construction of their cell wall that doesn't take up that last violet stain, but it also means that cell wall composition is different. And one of the most important things that sets apart the composition of that gram-negative cell wall is the ingredient or the component called lipopolysaccharide or lipopolysaccharide endotoxin. Now, there's a very solid model of what happens when this LPS endotoxin gets into your bloodstream. It's called sepsis. So let's say you had a bladder infection and you ignored it, you had some burning, and your urine smelled funny, but you took some mannow sugar, you took some cranberry juice, and you're hoping it goes away. Well, it didn't go away, and in this case, it ascended to your kidneys, that's called pylonephritis. Now you're having fevers and back pain and starting to feel real sick. And sometimes the microbe, let's say it's E. coli, which is the most common cause of bladder infections, pylonephritis. Let's say that E. coli enters your bloodstream. That's sepsis, in this case, gram-negative sepsis. Now you get sick very sick very quickly for a lot of reasons, but one of the reasons is that E. coli releases its lipopolysaccharide endotoxin because the microbe dies and releases its toxin. So people who have higher levels of LPS endotoxemia tend to die or develop very serious consequences, such as respiratory failure. We call it ARDS, acute respiratory distress syndrome. Those people are intubated and put on a mechanical ventilator, or develop kidney dysfunction, sometimes even going on dialysis. You lose control of blood pressure, you can go into shock. And so medications, sometimes even devices, are inserted to support your blood pressure. Because if your blood pressure is 50, you're going to die. So sepsis, where gram-negative microbes enter the bloodstream and release their endotoxin, serves as kind of an illustration, a laboratory to tell us what happens when endotoxin enters the bloodstream. Now, the levels of LPS endotoxemia in sepsis tend to be a hundredfold or greater than normal everyday life, right? But in the situation where you have either at least colonic dysbiosis, disruption of the of the microbiome composition of the colon, but more importantly, PSIBO, small intestinal bacterial overgrowth, there's about a two to four fold rise in endotoxin in the bloodstream. It's actually probably worse than that because the current assay to measure LPS endotoxin tends to underestimate because it's an antibody-driven test and it fails to identify all the different forms of LPS. But with the evidence as it exists, suggests that the blood level, when you draw blood, say from your arm, a venous blood draw, is 200 to 400% higher than normal. Not as high as sepsis, but still several fold higher. Now, here's an odd thing. Your gastrointestinal tract, the entire gastrointestinal tract, drains its venous blood into a specific part of your circulation called the portal venous system. So this is a system of veins in the abdomen that go directly to the liver. And so when there's LPS being released because of an overpopulation of fecal microbes in the colon and small intestine, that LPS endotoxin floods the portal vein to the liver, and your poor liver takes a beating. So this is a very important phenomenon in liver disease. But it's also an important phenomenon in food intolerances. And so one of the essential features of these food intolerances is that there's an overgrowth of those gram-negative fecal microbes. We say proteobacteria. To make it even more confusing, the microbiology community, the scientists, have recently reclassified proteobacteria as Psomomona dota. I don't make these things up. I'm sorry. I'm going to call it proteobacteria just because that's the most common term used. You'll also see it sometimes called enterobacteriacea, because that's a subcategory within the broad category, phylum, of proteobacteria. But let's, for the sake of simplicity, let's call it proteobacteria. Gram-negative proteobacteria, microbes like E. coli, Pseudomonas, Campylobacter, Citrobacter, Ciracea, Pseudomonas, many others that have this lipopolysagarin in their cell wall. So if you were, if you have a food intolerance, let's say you say you can't eat such things as uh tomatoes or fructose-containing foods like fruit because they make you sick, or you eat eggs and it gives you a headache and nausea and abdominal discomfort. So, how do you tell this is a food intolerance? Well, there's a number of easy ways. You could test hydrogen gas on the breath. There's a consumer device that can help you do this. Uh it's called the air device. I have no relationship with the with the company. I do know the inventor, Dr. Angus Short. He's a PhD engineer. Uh, this device, the original device from 2018, measures hydrogen gas. The newer one measures hydrogen gas and methane. These are gases that microbes can produce, but you cannot. So uh now there's a way to use these. You have to use timing after ingestion of something that causes release of those gases. So typically what we do is we follow a preparatory diet a day before, day of testing, you get a baseline level, and on these devices it's 0 to 10 for hydrogen gas. Maybe your level's low as it should be at the start, let's say 1.2. You consume something that feeds microbes. Let's say inulin powder is what I use. I don't use the laculose or the glucose I use in conventional testing because I think that's a mistake. It's the inulin that is more widely metabolizable by the species that cause dysbiosis and SIBO. So insulin is much broader, more broadly metabolizable, more likely to identify the presence of these unwanted microbes. So you get your baseline, then you consume that fiber, like inulin, typically to maybe two teaspoons in a in your coffee or something like that. And then you test every 30 to 45 minutes for the next 90 minutes or longer. If there's a rise of more than four units, so let's say next measure at 45 minutes is 9.8, a big rise, more than four units on the device, you have microbes living in the upper GI tract, stomach, duodenum, jejunum, maybe ilium. So it's all about timing. So think of these devices, think about hydrogen gas testing as a mapping device to help you decide where microbes are living. So that's one way to do it. Another way to do it would be stool testing. Drawbacks to stool testing. When you obtain a stool sample, how did you get it? Well, you got it from your bowel movement or the toilet paper. Well, that's a rectal sample, right? It's not a sample of stool from your ilium or jejunum or even the ascending or transverse colon. Because you're getting it after you evacuate that stool, it's a rectal sample. Well, the rectal microbiome is different. If you go back into your colon, into the anus, rectum, sigmoid colon, descending colon, transverse, we're going backwards, transverse colon, ascending colon, cecum, ilium. Every step of the way, microbiome composition shifts, changes. So we have to accept that a rectal sample is not necessarily fully representative of the composition of microbes all throughout the GI tract. But we can still try to get a sense. So what you look for in stool testing, rectal stool testing, is an overabundance of proteobacteria, or could be listed as enterobacteriacea, or could be listed as species like E. coli, Pseudomonas, all those uh species I mentioned. You do want, I think the best platform for testing is a company called Tiny Health. It's a silly name, I know, but they do full DNA sequencing as opposed to some of the other methods where you don't get as much detail. When you get full DNA sequencing, you get a as broad and complete an assessment of the microbes present in your rectal sample as possible. And what you look for is an overabundance of proteobacteria or the species within proteobacteria, and that the report should tell you that. You'll see, for instance, you have too much E. coli or too much salmonella or too much serratia, too much Pseudomonas. That would be an indication. A typical number would be 10% of your entire gastrointestinal microme is composed of these gram-negative proteobacteria. It could be even higher, it could be 15%, 20%. And that's often accompanied by abdominal pain, diarrhea, as well as food intolerance, and often accompanied by other phenomena, because when you have this situation, the overgrowth of proteobacteria in the colon, and even worse, in the small intestine, when you leak that lipopolysaccharide, the LPS endotoxin, into the bloodstream, it has effects all throughout the body. So while you might be experiencing food intolerances, it's not uncommon to also be experiencing depression or anxiety from effects on the brain, even suicidal thoughts, disruption of sleep, nightmares, skin effects, eczema, psoriasis, rosacea, joint and muscle effects, weak muscles, muscular pain, joint pain, uh fibromyalgia, heart issues, recurrent atrial fibrillation, worsening of congestive heart failure, rupture of caronary plaque, heart attack, sudden cardiac death. So and virtually every organ of the body can be affected by this LPS endotoxemia. But the perceived effect for a lot of people is these are these food intolerances. Now, I make the distinction between colonic dysbiosis and SIBO, small intestinal bacterial overgrowth, because we know that it's a small intestine that is, by design, very permeable. That's where you absorb nutrients, vitamins, minerals, amino acids, fatty acids. But the small intestine is also poorly protected from fecal microbes. So when we have the invasion of those fecal microbes, those gram-negative proteobacteria, into the small intestine. The small intestine is permeable to begin with, the presence of those fecal microbes increases the inflammation of the small intestinal wall and increases its permeability. And so you have this flood of endotoxin first to the portal vein and then something gets through into the systemic, the broader circulation, and that's how you get those body-wide effects on the brain, skin, heart, and elsewhere. So look at food intolerances as your indicator that you've got an overgrowth of fecal microbes, of proteobacteria. Now, what do you do about that? Now, the solution I use, this is how I do it. So not everybody does this because they haven't thought this through. The conventional solution, well, sadly, the conventional solution is tell you you're nuts, right? Or there's not a problem, or did you consult Dr. Google or some other stupid answer like that? But my colleagues who do understand these issues will give you a prescription for xyfaxin or rifaxin. That's the antibiotic that tends to kill those microbes with about 60% efficacy. So even the best they have in conventional health care does not work very well. And it costs you about$1,200, typically not covered by insurance because it's off label, because the FDS does not recognize SIBO as a real condition. And so Xyfaxin would be the solution. But I'm going to tell you, let's think about that. So here's a little mental exercise that I've used over the years. What if you took a commercial probiotic off the shelf? Commercial probiotics are pretty much just haphazard collections of microbes. What if you took a high potency, multi-species probiotic? Does it get rid of the SIBO? Does it fully correct the colonic dysbiosis? Typically, no. It might have some benefit. Many people actually have symptoms from that probiotic, and because that's from something called D-lactic acidosis. So you're supposed to have L-lactic acid, not D-lactic acid. Well, when you have D-lactic acidosis, you have confusion, uh, mind fog, brain fog. That's because those proteobacteria are converting those fibers and sugars to D-lactic acid. And that's the source of D-lactic acidosis that makes you feel sick. So, but let's say you took a commercial probiotic because you think you have SIBO as a cause for your food intolerances, and will it all these things go away? Typically not. So let's ask some different questions. You're going to get microbes that colonize the small intestine. That's where SIBO occurs, as well as the colon. Most probiotic species don't do that. They don't colonize a small intestine. They only colonize the colon at best. Let's also choose microbial species and strains that are known to produce bacteriocins. These are nothing more than natural antibiotics that are known to kill those gram-negative proteobacteria. I've chosen three. Now maybe over time it just gets better and better, but right now I'm using Lactobacillus rotori that produces routerin, which is a very potent antibacterial against gram-negative proteobacteria. So lactobacillus rotori, lactobacillus gastrone, and bacillus subtillus. Bacillus subtellus, by the way, especially helpful. I DNA sequenced our strain I have, and it has seven, has genes for seven different bacteriacins. So we take those three and we cultivate them as something that looks and smells like yogurt. It's not yogurt. You can't buy it in the store. Stuff in the store is something completely different. This is just a uh fermented dairy using microbes sourced from humans. So I call them human ferments, but we cultivate them in a specific way. In the beginning, I did this, we cultivated all three together, but it's become clear, it's probably not the best way because I think subtleties eventually takes over. It's got some survival advantages. So the best way, it's more hassle, but we cultivate each one separately. The roteri gasterite, you those two you can cultivate together because they grow under similar conditions. So either separately or together, roteri gasterite, 100 degrees Fahrenheit or around human body temperature, 37 degrees Celsius, for 36 hours. We want them to double around 12 times, and we get, if individually fermented, about 300 billion. So this is a way to increase microbial accounts dramatically for added benefit, for greater hope for benefit. So rhodorite, gastrite, either individually or together, human body temperature, 36 hours. The subtlety ferments faster, reproduces faster, and we can go for 24 hours at 90 degrees Fahrenheit. So you do need a device, a sous-vide, a yogurt maker, uh, an instant pot with a yogurt setting that you can vary the temperature and timing. And then we consume maybe a quarter cup or so each of those every day for a minimum of four weeks. And so far, that has proven to be unexpectedly effective in eradicating food intolerances, normalizing breath hydrogen gas, and getting rid of some of the other phenomena that we can blame on colonic dysbiosis, SIBO, and endotoxemia. Now, how confident do you have to be? Well, if the solution, if the solution was something like surgically remove your small intestine, you better be damn confident that's necessary, right? What if the solution is something that looks and smells like yogurt that you make in the comfort of your kitchen at modest cost, very little cost. Well, you don't have to be quite so confident. And what if there's not side effects but side benefits? Because those three microbes, especially the rotori, and some degree the gastroe, have other benefits on skin, muscle, reproductive health, hormones. And so you make this thing, and it's tasty. You may have to sweeten it a little bit with a non-nutritive sweetener like stevia or monk fruit or allulose and add some blueberries or strawberries, whatever. And you can enjoy it minimum four weeks. And so far, that has now we will do a formal clinical trial. Uh my budget is not like farm. I don't have billions of dollars to spend, so we have to pace ourselves in doing clinical trials one by one. We just completed a large clinical trial that I'll be reporting in coming months. We haven't published it yet, so I can't tell the details. But that once that's completed, that will generate probably three different uh research papers. Then we'll proceed to this next one and some others to validate this idea. But in the meantime, you don't have to wait for the validation because the solution uh is so benign, so beneficial for so many reasons. So if you want the full details on how to get where to source these microbes, all that sort of see my super gut book, see my thousands of blog posts on my William DavisMD.com. If you want support, I always uh invite you to join my conversations, two way Zoom conversations on my inner circle.dr Davis Infinite Health dot com.