 We really need to rein in these metabolic markers that are fundamentally important for disease resistance for longevity and overall health. All right. Let's dive right in about your exciting new research in drop acid. All right. You're a neurologist. Why did you decide to hone in on uric acid of all things? Well, you're a cardiologist. And what do we share, you and I? We share the idea that metabolic problems are at the heart of the diseases that you are most interested in, those of the heart, and diseases of the brain, the area that I specialize in as well. So that disturbed metabolism becomes a big player. It relates to coronary artery disease. It dramatically relates to risk for Alzheimer's disease, for a disease for which there is no pharmaceutical treatment. So my interest for many, many years and years too has been to look at what's available to help people regain their metabolic health. And these days to kind of offset the metabolic mayhem that is so pervasive, looking at obesity rates, diabetes rates, hypertension rates, problems with this lipidemia, elevated triglycerides. These are all metabolic issues. Sure, they're bad for the heart, but they are so bad for the brain as well. And that's why I'm interested. And that's why, you know, I even wrote Grain Brain now a decade ago talking about stopping the sugar because it's threatening to your brain. Well, we now have a new tool to look at and it is not your grandfather's uric acid. You know, you and I in medical school learned about uric acid and something called gout where people who ate rich food would get a painful problem in their toes and would be unable to walk. This is not your grandfather's gout related uric acid. We now know with two decades of really intense research globally that uric acid is not just a happenstance. It's a central mechanism that is worsening those very metabolic issues that we need to reign in. Matter of fact, an interesting article was written back in 2016 and it was entitled Uric Acid in Metabolic Syndrome from Innocent Bystander to Central Player. So this is a new tool for all of us, for you and me and certainly for all of your viewers today. You know, it's not the end all, but it's a powerful new tool in the toolbox and that is bringing your uric acid first identifying where it is and then bringing it under control. So why do you think like you, I've been interested in uric acid for years because of, you know, fructose metabolism and we're going to get into that. But why do you think that this has been missed by the medical field for so long? Well, it's not for lack of information. You know, as well as I do, as it relates to heart disease, for example, that the messaging was taken off of sugar and fructose in particular and that for years it was all about dietary fat and cholesterol. We know how that all played out and why. So I think we were sort of let off the scent, you know, taken off the trail about carbohydrates, refined carbohydrates, specifically fructose. And the second event that related to fructose not getting in the spotlight and therefore uric acid, which is what fructose is metabolized into is because we've known that fructose doesn't require insulin, doesn't acutely involve insulin in its metabolism. So the whole focus was on glucose and glucose metabolism and insulin functionality and then insulin resistance. So we were sort of led to believe that fructose was the safer sugar. Nothing could be further from the truth. And it's heart wrenching that that messaging took place for such a long period of time. The idea that fructose and its downstream metabolite, which is uric acid specifically, is an issue well beyond gout was written about just very recently. That's 1898 by a Dr. Alexander Hague publishing a book about all of these other aspects of uric acid. In 1898 being related, uric acid being related to headaches and mood issues and a variety of other non-gout related disorders. But it really took researchers about the last two decades led by somebody here in United States, Dr. Richard Johnson actually interviewed him just yesterday to really bring to light this notion that here is a central player. It's not just about understanding your blood sugar, where that is moment to moment, which we have the technology to do. But it's all about fructose, not just the fructose that you eat. And we'll talk about that a little bit later on. But this primary metabolite of fructose consumption, which is uric acid, which for more than 99% of our time on this planet, the production of uric acid from fructose was a life-saving survival mechanism, especially during times of food scarcity. Fructose, which was very rare, would allow our bodies to make more fat, increase blood sugar production by making us insulin resistant, even raising our blood pressure as a hedge against dehydration. And for an awful long time, for hundreds of thousands of years, that was a survival mechanism. We didn't have fructose much. These days, of course, fructose consumption has gone through the roof. We eat now more than 1,000% increased fructose consumption going from 1970 to 1990. The average American, it's consuming 55 pounds of sugar a year. And so we are constantly stimulating this survival mechanism that's telling our bodies, prepare for winter, prepare for food scarcity, make fat, store fat, lock it up, make more glucose to power the brain, raise the blood pressure, because you might not be able to find water. So this is what we call an evolutionary environmental mismatch. That's our task. Our task is to first identify that, and then do everything we can to rein in this uric acid production, which is the danger signal to our entire physiology to get ready for winter. Yeah, interesting. With my first book, years ago, Dr. Gundry's Diet Evolution, I had a whole part that great apes only gain weight during fruit season. And my editor said, oh, don't be ridiculous. And I actually, there's an entire book that I have in my office strictly about great apes depending on eating fruit, which only happened once a year in the jungle to gain weight for the winter, whether that was a dry season or rainy season or cold season. And that was, and you go into that beautifully in your book, and it's nice to see somebody else saying, look, this was our survival mechanism that we inherited from our cousins, the great apes. And you're right. That's right. And if there's anything that could have happened to these primates that could have allowed them to make a little bit more fat, then they would have been selected for in terms of survival. And the difference was a mutation, a genetic mutation that took place about 14 million years ago. A genetic mutation where actually it was a series of mutations in the genes that code for an enzyme called uric case. That's the enzyme that breaks down uric acid. So they lost this function. They lost the ability to break down uric acid, and their uric acid levels went up. And that gave them a little bit of an advantage. It's not that they became obese. They just had a little bit of an advantage, a superpower having a little more body fat. All humans, every one of us has inherited that uric case mutation. Hence, the uric acid levels of humans are four to five times higher than that of other mammals. But let's be clear, this notion of making fat from fructose is seen in a lot of animals. How do you think the hummingbird survives these 1,000-mile epic journeys? There are times when the hummingbird has 40% of its body weight fat. And if you want a hummingbird in your backyard, what do you put out? You put out a bird feeder full of sugar, and it makes them fat. Whales, camels, for example. And the other interesting thing about it, and I mentioned it earlier, is that this body fat is a survival mechanism, not just for the energy store that it represents, but also because when we burn fat, we produce two things, carbon dioxide, which we exhale, and water, metabolic water. So storing extra body fat is a hedge against dehydration. I mentioned the camel. Camel can walk across the desert. They have a hump, and what's in that hump? It's not like there's a tank of water in there. It's fat, and that allows them to survive. Whales have so much blubber, because that's where they get their metabolic water, like the hummingbird, and like we do too. So when our bodies have a sense that we're becoming dehydrated, we make more fat. And how do we know when we're becoming dehydrated when our sodium level goes up? That's the relationship then between eating a lot of salty pretzels while you're watching the playoffs and getting fat. Your body thinks that it's dehydrated, and the hedge against dehydration is to make body fat because it's converted into water. Oh, it's so good to know. Now I know why I can put on a few pounds by eating those pretzels, which I never would do looking into the camera. I don't know if they're lectins and pretzels. Well, there's gluten in pretzels. And that's a lectin. I want to stop for a second to point out what many people still do not realize. You and I are kind of talking about fructose. And most people somehow don't equate table sugar with fructose. But you and I know that table sugar is sucrose, which is half glucose and half fructose. Can you elaborate on that? How did we miss that messaging? Not sure how we missed it, but the point is that in that 55 pounds of sugar that we're consuming a year, half of it, as you correctly state, is fructose. And that would be probably not so terrible if more than 60% of foods at the grocery store that carry a barcode didn't have added sweetener, and that added sweetener wasn't 50-50. It was much higher, is much higher in fructose, because it's derived from high fructose corn syrup that has as a minimum 55% fructose, but oftentimes even more. But your point is well taken that when we're eating table sugar, that's immediately broken down to fructose and glucose. And the body looks at them in a completely different manner. We tend to think, well, fructose, glucose, their sugar is pretty much handled the same way. Couldn't be more diametrically opposed. The absorption of fructose and its metabolism are very unique. The consumption of energy molecules in the metabolism of fructose, the fact that fructose acutely doesn't involve insulin, and the fact that fructose is then metabolized to uric acid really differentiated dramatically from glucose. So one of the main missions of drop acid is to identify the sources of fructose and two other things that raise uric acid. Purines, which are the breakdown products of DNA and RNA in certain foods, and also some forms of alcohol are known to increase uric acid. But by and large these days, it's this incredible signaling to our bodies to make ready for winter by making fat induced by our incredible consumption of fructose that is really at the center of the problem. I mentioned earlier that it's beyond the fructose that we consume, that we have within our bodies a mechanism that is also going to help us survive, called the polyol pathway, whereby we create fructose in our bodies even when we're not eating fructose. We convert glucose, blood sugar, into fructose, and what might stimulate that would be things like thinking we're dehydrated. So when serum sodium goes up, even though we're not eating fructose or we may be, our bodies take glucose and make fructose out of it because that's a surefire way to make more uric acid, to make more body fat, because that body fat can be water when our bodies think we are dehydrated. That is the relationship then between dietary sodium and obesity, dietary sodium and diabetes, for example. This activation of this polyol pathway, I'll tell you another interesting way that it's activated. It's activated by something called hypoxia, meaning not enough oxygen in the blood, and it doesn't have to be dramatic. A little bit of lowering of the blood oxygenation saturation will trigger this pathway and make more fructose in the body. Why is that important? Who gets hypoxic? Well, you don't have to climb K2 to get hypoxic. If you have sleep apnea, which is exceedingly common, you become hypoxic at night and you stimulate this pathway, which makes your body gain more weight, which does what? Makes your sleep apnea even worse. So it becomes a vicious cycle. You dramatically increase your risk for obesity, diabetes, and yes, sleep apnea is related to risk for Alzheimer's disease and coronary artery disease, for that matter as well. Now we have the mechanism. Now we understand how that happens. So there are interventions that become available to us at multiple places along the way, like a CPAP, of course, but also recognizing this connection to fructose formation and uric acid. All right. Now, you and I have been concentrating on fructose and sugar, but you did mention purine metabolism and you also mentioned alcohol sources. So let's go into that side of where uric acid comes from. So anything that feeds into the uric acid production we want to talk about. And interestingly, the metabolism of the three things that you just mentioned, the purines, the alcohol, and even the fructose are all enhanced in the presence of higher levels of uric acid. Think about that for just a moment. This is what we call a feed forward cycle. Normally, we have checks and balances in our body such that when things start happening then at the end of the line, there is somebody that happens that tends to turn it back down. This is just the opposite. This is a, this is uric acid raising the alarm saying we've got to keep this whole thing going because we're going to starve or we're going to become dehydrated. Now, alcohol is metabolized in exactly the same way as is fructose. It requires ATP. It depletes our bodies of energy. It challenges our mitochondria because of that energy depletion and forms uric acid. But there are variations in the type of alcohol that I think are very relevant. We know, for example, that at least as we look at what are called food frequency questionnaires, in other words, asking people what they eat, we find that women who drink wine have a slightly lower uric acid. Men, it's pretty much neutral. But beer tends to be a big, big player. Why? Because beer contains alcohol, but it's also very rich in purines because it's made from yeast. So you're getting two very powerful inputs into the production of uric acid. So that uric acid then is causing the body to make more fat. Now we fully understand what's behind the beer belly. The mechanism is that we're targeting the uric acid pathway twice. So the third input, purines are the breakdown products of DNA and RNA. So in that regard, certain, for example, organ meats, liver, kidney, a certain small fish like anchovies and sardines have higher levels of purines. So they, if a person has elevated uric acid, are things to consider to remove from the list, or simply eat less of. It turns out that as it relates to purines, about two-thirds of them are actually produced within your body. One-third come from food, two-thirds produced as you break down muscle fiber when you exercise, etc. So again, the big player is going to be fructose. So incredibly increased in our modern world. We used to say the standard American diet. Then we started to say, well, no, the Western diet because it kind of spread around the world. Now it's the global diet. This change in dietary patterns has become prevalent across the entire planet. And as such, we are seeing these metabolic issues exploding around the planet. And now we have a new tool. And that is measuring your uric acid and getting it under control. And that's something you can do at home. All right. So wait a minute. Do I go into my medicine cabinet and reach for my uric acid monitor? Or how do I check my uric acid? I know I check it on my patients three to four times a year. Here's how you check it. This is a home uric acid monitor. And I checked it yesterday and my level was 4.7, which is really good. So again, this is done with a little finger stick, much as we used to use for measuring our blood sugar. Now many people are using continuous glucose monitor. So we don't actually have to stick ourselves anymore. I'm actually wearing one right now. So using my smartphone, I'm able to determine my blood sugar right this minute as I'm talking to you. And some people may say that's a bit neurotic. And maybe it is. But you and I both know that keeping blood sugar under control and now keeping uric acid under control are really important tools that we have well before we get to the doctor's office. And she or he tells us, hey, you know, your blood sugar is starting to climb because we noted it was such and such a year ago. And now it's five points higher. I want to know long before my blood sugar is five points higher on one simple test. I'd like to know my blood sugar day in and day out and understand how it's affected by my foods, certainly, but also my sleeping patterns, my stress level, how much I'm exercising. We really need to to rein in these metabolic markers. They're fundamentally important for disease resistance for longevity and overall health. Speaking of uric acid levels, I use several different labs with my patients and I am shocked with the variability of what's a normal uric acid level depending on the lab I use. And quite frankly, that also corresponds to triglyceride levels as what quote is normal. I bet you you're going to tell me that we're way off on what a normal uric acid level should be. I'll give you two answers to that. I think that was a question. First of all, I don't care what people are defining as normal because normal is not good enough for Dr. Stephen Gundry's patients, nor is it good enough for mine. I don't want anybody to be normal because normal is average and average these days is terrible in my opinion. Only one in eight Americans is metabolically intact. 88% of American adults have at least one of the markers of metabolic syndrome. So I've given up on normal. Typically, the lab will tell you that the normal level for uric acid is seven milligrams per deciliter. And that number, number one, it's way too high. But number two, that number was derived from the observation that anything above seven is when uric acid begins to crystallize in the blood, hence setting the stage for gout. We're beyond that. We now recognize that uric acid is hugely relevant as it relates to metabolic issues. So we're targeting 5.5 as being maximum and anything below 5.5 then being not in the normal range, but in what we call the optimal range. That's what Dr. Gundry's patients want to know about. That's what anyone I work with I think deserves. I think we all deserve what's best, not just what is average for crying out loud. So we've gotten away from that. And as it relates to metabolic issues, a very interesting study was published back in 2009 looking at 90,000 individuals, 42,000 men, 48,000 women followed them for eight years. And what they found was that people having a uric acid higher than seven had a 16% increase risk of what is called all-cause mortality, in other words, dying from anything. They had a 38% increase risk of cardiovascular death, basically dying of a heart attack, a 35% increase risk of dying of a stroke. And what was even more interesting to me anyhow was that for every point increase above seven, every point was associated with a further 8% to 13% increase risk for all-cause mortality. So this uric acid really becomes important to recognize, especially in light of the research in which interventional trials lower uric acid and we see immediate improvements in various metabolic markers in humans. So we know that intervening and lowering uric acid really is important to consider, especially in people who are inching up and having higher and higher levels of uric acid. What do you say, I know what I say, what do you say when you point a uric acid level of 6.5 to your patient and they say, yes, but doctor, this is in the green and why do I want it lower? Do you hand them the book? Yeah, I hand them the book because they were told by their other doctor or by the laboratory that they're in the green. And I typically say, well, people tend to be down on what they're not up on because it wouldn't be the first time somebody, another doctor would criticize me for putting a patient, for example, on a low carbohydrate diet and adding in more fat or telling a person, hey, why don't you try gluten-free and maybe it'll help your headaches? I've been criticized over the years for things like that and I'm hoping that it continues because the day that people stop criticizing or challenging you and me is the day we have to hang it up because we're then just simply parroting the status quo. Status quo Ronald Reagan said is Latin for the mess we're in. People say, well, what you're talking about is really outside the box. That's not my goal. My goal is to make the box bigger so that more and more healthcare providers recognize what we're talking about. And interestingly, I was on a national morning show two years ago now, a network morning show, and they said, it was the revision of grain grain, the five-year anniversary. And they held it up. They said, we spoke to, no, they said, Dr. So-and-so is quoted as saying that your book is nonsense. And I said, you know, that's when it came out. That's exactly what he said. Now he's using that book in his Ivy League University Alzheimer's Prevention Program. So, you know, it does take some time for this stuff to rise to the top. And I'll be the first to say that, you know, some of the things that I think are interesting may not bear fruit moving forward, but it's good to look at what's where the hard bench research is happening and then extrapolate that and bring it to the public awareness. I don't really have to do that so much with uric acid because there's such robust data around the world that is looking at it. And, you know, in Japan, for example, lowering uric acid is a treatment that's being offered for hypertension, for high blood pressure. They're treating high blood pressure with drugs, and we could do better than that, but with drugs to lower the uric acid and getting good results. We know that how the drugs for gout work is by inhibiting a particular enzyme's antinoxidase, that'll be on the quiz, that lowers the production of uric acid. We can target that enzyme with quercetin, with luteolin, and you can buy those at the health food store or eat foods that have a lot of bioflavonoids in them, like onions, for example, and help to bring down your uric acid. So there's a lot of things that we can do to make this happen. And you know what? It happens very quickly. One study out of Britain looked at 22 young men with mild elevations of uric acid, put them on 500 milligrams of quercetin a day, and two weeks later, no dietary change. Two weeks later, their uric acid levels had already fallen by 8%. So there may be a time for a drug. I'm not advocating that or for or against, but there's so much we can do with food and other lifestyle interventions to bring it down where it belongs. So that was going to be my next segue. So why don't you and I take allopurinol, low-dose allopurinol, and put every one of our patients on low-dose allopurinol? Why not? It's cheap. It's free. The reason is that it's not risk-free being a pharmaceutical. It's a very, very safe medication. There are a very small subset of individuals who have a specific genetic predisposition to having a really bad negative reaction. And I would say back to you if why not start with a nutritional supplement that we know is safe, that is something in our food. But I do know of a physician, for example, who is treating himself with allopurinol to lower his uric acid, and has never had gout, but is lowering on the basis of understanding how uric acid threatens metabolic health. Yeah. And quite frankly, I will use allopurinol, low-dose allopurinol with some of my recalcitant patients, particularly in my patients who have declining kidney function. And I am so impressed. And maybe you could talk about that. You and I are not all that interested in kidneys. But uric acid is pretty nasty to renal function. And I've noticed in my own practice, if I can get uric acid levels down in these individuals, and they're usually quite high, that we can not only stabilize EGFR, the filtering ability of kidneys, but really start to see it improve. You know, I would say over the years, your lead-in statement that you say you and I really aren't interested in the kidney. And early on in my career, I was interested in the brain pretty much exclusively. And then began to become interested in the gut of all things. And from there, of course, the liver. And we can't leave the kidney out. I mean, the kidney as it relates to metabolism is playing a huge role, especially with this new understanding of how uric acid affects the kidney, how fructose is metabolized in the kidney as well as the liver. And this whole notion that, well, uric acid is a threat to the kidney because we thought maybe it's forming crystals in the kidney, that's not what happens. It's actually inducing inflammation that is amplifying an autoimmune reaction in the kidney against something called heat shock protein, which then ultimately helps manifest hypertension. And beyond that, that uric acid in and of itself away from the kidney participates in amplifying higher blood pressure because uric acid inhibits the activity of something called nitric oxide. We need nitric oxide for our blood vessels to be able to relax. That's what it does. Well, it actually does two things. I'll cover the other thing in just a moment. But when our blood vessels cannot relax, blood pressure is going to go up. It's the reason that when a person's having an angina attack, they pop a nitro, sublingual nitro to help dilate their coronary arteries. Well, this happens throughout the body. And we need to keep our blood vessels the ability to keep blood supply to our vital organs, of course. So there are multiple mechanisms by which uric acid is a real player here. Why might that have been a selective advantage? Of course, if we're dehydrated, our blood pressure is falling and falling, and finally we cannot send blood to our vital organs, we're going to need ways of increasing the blood pressure in order to survive. That's not the way it is these days. We're not generally getting dehydrated, although it's been demonstrated that patients who are obese tend to drink less water. Hence, their sodium levels are higher. Hence, they're stimulating this fructose production leading to uric acid day in and day out. So as we look at these incredibly pervasive metabolic problems now through this mechanistic lens of uric acid and fructose, man, it really is just a new and exciting way of participating in this research. And it really allows us to take a step back and also ask the question, how was this beneficial back in the day? How was this horrible thing that we all talk about called insulin resistance? Why was it a good thing? Well, it was a good thing for our ancestors because becoming insulin resistant allowed them to make enough blood sugar so they could power their brains so they could find food and not become food. They wouldn't be eaten by other animals. We need to power our high card. Our high card is our big brain. We're not the fastest animal. We're not going to outrun a cheetah. We're not the strongest one. We're not going to beat a bear or a gorilla in an arm wrestling competition. But we have a big brain and we can think our way out of a lot of problems and we've got to power that brain. Hence, becoming insulin resistant in certain contexts is a good thing. The hummingbird is profoundly insulin resistant prior to making these epic flights, storing body fat. 40% that I mentioned earlier, its body weight is fat so it can make water. It becomes insulin resistant so it can power itself with glucose. So it's all really contextual of our current times as evolutionary environmental mismatch with the time of our paleolithic ancestors and certainly our primate ancestors as you mentioned earlier. One other thing that you and I have both arrived at and neither of us probably would have believed it years ago, the gut and the microbiome. Where does uric acid fit in the microbiome picture? Uric acid elevation specifically selects in the gut bacteria for the predominance of inflammatory or inflammation related types of bacteria. So it's changing the array of organisms such that various types of bacteria that are more inclined to disrupt the gut lining and lead to hyperpermeable or gut leakiness or leaky bowel if you will. That increases inflammation. That's what uric acid does. A lot of the downstream effects of inflammation of uric acid elevation deal with inflammation because again, what is the context? Inflammation for our primate and paleolithic ancestors was an advantage because it helped them deal with various types of infection, bacterial infection, parasitic infection, etc. So it changes the gut bacteria. It directly enhances gut permeability. And interestingly, now there is published research showing that in patients who have a disease that is characterized by a very high uric acid level called gout, that doing something called fecal microbial transplant. In other words, taking the fecal material from the colon of a person who's normal, doesn't have gout. Transplanting that into the colon of a person with gout dramatically reduces the number of gout attacks that they have. So there's a lot to learn. There are a lot more interesting connections that we will make moving forward. But uric acid wants to increase inflammation in our bodies by any number of mechanisms, by antagonizing insulin receptors, by increasing fructose production. Uric acid stimulates this pathway whereby we increase fructose production from glucose. What does that do? It increases inflammation in the body through what is called glycation, where sugar is bind to protein and then our immune system gets lit up and increases the production of these chemicals called cytokines, interestingly. And cytokines is a word that a lot of people are talking about now because in COVID, people who have a very bad outcome experience an overproduction of these inflammation mediators called cytokines. It's been called the cytokine storm. And interestingly, we know that uric acid dramatically increases cytokines and new research that has recently been published a collaborative study from China and Chile looking at about 1,800 hospitalizations found that risk of being put in the ICU is increased about three fold if you have a high uric acid level on admission. Risk of being put on a ventilator is increased about 2.8 fold. And risk of death is similarly increased about two to three fold as well if you happen to have a high uric acid level when you come into the hospital. Uric acid increases risk for metabolic diseases, which we know are associated with bad COVID outcome, and uric acid dramatically increases the production of these inflammatory chemicals. So interesting to think about. People are talking about the cytokine storm, but I want to just mention a new term and throw it out there, and that is chronic inflammation or the cytokine drizzle. Not the cytokine storm, but this chronic drizzle, this chronic elevation of these inflammatory chemicals that you and I know are seen with coronary artery disease, type 2 diabetes, and certainly with Alzheimer's, chronic elevation of inflammatory chemicals, which we do see with elevated uric acid. So bottom line, we've got to do everything we can through multiple inputs to bring inflammation under control, keeping our blood sugars low. As you've made very clear, reducing our consumption of lectin containing foods because of the threat that that also poses to gut lining integrity. But also keeping uric acid in check is yet another powerful tool now in our toolbox. All right, a perfect segue. I want you to show us your love, LUV. What's the program to get this in check? LUV stands for lower uric values. So we've created dietary protocols and obviously recipes in the book that can help people lower their uric acid, A, by taking away those things that stimulate uric acid production. I mean, you won't find any added fructose, certainly to any of the recipes, but also focusing on alcohol, focusing on purines and certain high purine foods that are known to elevate uric acid. I mean, we've known that who got gout in the day was the disease of kings and the king of diseases. It'd be eating really rich meat, meat dishes with rich and organ meats, et cetera. The big issue is that we want to avoid free fructose. Does that mean we can't have fruit? Not in the least. It looks like some fruit consumption, though it does contain minimal amounts of fructose, fruit sugar, is good and is actually associated with lowering of uric values. Why might that be? The fiber in the whole fruit slows fructose absorption. The bioflavonoids target fructose metabolism by targeting the same enzyme that the drug you mentioned earlier, allopurinol targets, xanthinoxidase. And finally, fruit contains vitamin C that helps us excrete through the kidney uric acid, all good things for us. Interestingly, we humans, about 10 million, we weren't humans then, but our ancestors developed a mutation such that we don't make vitamin C and, therefore, we have to have it from exogenous sources. Why would that have been a good thing? Why would losing the ability to make an antioxidant be a good thing? Again, survival mechanism is oxidative damage to our energy-producing parts of the cell called the mitochondria. When we damage the mitochondria and they're less able to function, our bodies make more fat and our bodies use less energy. That's a survival mechanism. And interestingly, when fruit ripens and its fructose level is the highest, the vitamin C level is the lowest. Vitamin C levels taper off as fruit becomes ripe. So that was in the day a very powerful mechanism for survival. That low level of vitamin C would keep uric acid in the body. We want to let uric acid go, hence taking some vitamin C, eating fruit that has some vitamin C is a good thing. But it doesn't mean an apple a day keeps the doctor away. But five apples a day and the doctor, you will pay, meaning that you can overdo it. You can eat a lot of fruit. But a lot of it has to do with the rate at which the fructose is released in your body. Eating fruit doesn't suddenly bombard your body with fructose, but drinking fruit juice clearly does. Apple juice, orange juice. We all grew up thinking, oh gosh, big glass of OJ in the morning and you're going to get all your vitamin C and you'll have superpowers. Well, it turns out that that's a powerful way to suddenly challenge your liver with fructose and it activates all of these pathways for metabolic mayhem that we're talking about. Certainly, sodas, certainly the foods that contain fructose as an added sweetener, which the list is very, very deep indeed. And beyond that, we focus on high fiber to help slow fructose release, also to nurture the gut bacteria and certain foods like onions, cruciferous vegetables, etc. that do contain these magic chemicals, these bioflavonoids that work to target uric acid production and really help us with excretion or reduce the formation of uric acid. And that's what that love diet is all about. Beyond that, getting uric acid under control is going to be certainly pushed along. If you take some quercetin, which you can buy online or go to the health food store, 500 milligrams a day, a Ludiolan, again, buy it online, 100 milligrams a day. Coffee is reasonable, helps with lowering uric acid, sodas, tea. In women at least, a glass of wine a day is not a bad thing associated with better brain health. Certainly, there is some discussion of cardiovascular advantage and we know that is at least associated with lower uric values, LUV, hence the love diet. Actually, there's a pretty good amount of quercetin in red wine as an example. I have some every day just to lower my uric acid. Well, it's because red wine contains the skins and it's those skins that are really the richest source then of these bioflavonoids. We don't get that in white wine. I try. I really do try, but I have really over the years become so intolerant of alcohol. We try. We want to do this thing where we drink a little wine in the evening, but I barely can get through a glass and I'm ready to hang it up. That's fine. There's other ways to get those benefits as you and I know. Oh, believe me. I hear you. All right. I got to let you go, but I think we've alluded to this all the time. You and I both continually challenge and research or look again at mainstream medical beliefs. I think that's why you and I have become good friends. Writing your new book, what discovery challenged your current beliefs the most? What challenged my current beliefs? I'd say, with all due respect, most of this research reinforced my beliefs about what we should do, but really shed a new light on why we do what we do. Yeah. For example, even back to grain brain 2013, the call there was cut the refined carbohydrates. We want to eat low glycemic index foods because we don't want to bump our blood sugar. Now we know through the new lens of fructose metabolism in uric acid production that one of the issues with this elevation of glucose is that it activates this pathway then to signal the body to make fructose as an alarm mechanism, making us insulin resistant and making us gain weight. Further, other things in our diets that we have talked about before in different contexts like lowering our sodium intake has been talked about because, well, yeah, it'll raise your blood pressure in many people, but when we look at dietary sodium and diabetes risk and obesity risk, I never understood how that could be. Now that we recognize that it stimulates the production of this alarm chemical that winter is coming, fructose making uric acid, oh my gosh, it really fills in a void for me because once you see this pathway, the biochemistry becomes clear, it's so satisfying, especially because we've been talking about this stuff for an awful long time. You have been, right? You've been talking about these good dietary recommendations. We know they were good dietary recommendations because the outcomes would be great when people would adopt them. Their various parameters would improve their blood sugar, their blood pressure, their serum lipids, et cetera, but we never really understood the mechanisms and now we've got that. And that is, it's very satisfying and it really takes away a lot of maybe uncomfortable mystery that we've been laboring through for many years. All right. So now we're dropping acid. What's next? I don't know what's next. I really don't know what's next. I'm going to be spending a lot of time, meaning years and years, with where I am right now on this whole understanding fructose metabolism, understanding the production of fructose in the body from the polyole pathway, what the effects of uric acid are, and there's still parts of that that need to be teased apart. For example, why is it that oxidative stress and damage to the mitochondria activates fat production? How does that work? Well, we know that there's a particular enzyme that's activated cis-aconitase that tends to make that happen, but that part needs to be further teased out and understood. I'm very fortunate that I've become friends with a really top-notch uric acid fructose researcher, University of Colorado, Dr. Richard Johnson, who's done so much incredible work in this area. And moving forward, we'll be working on projects together. He works on projects with researchers around the world. I actually dedicate a drop acid to him because of the incredible research he's been doing for the past two decades. What's next for me is a much, much deeper dive into this. And you know what? I don't know what else could come on the radar, but I'm always keeping an open mind. So there you go. Yeah. I think this was a nice shift for you. And I thoroughly enjoyed it, as you know. Well, and it's always a pleasure to catch up with you. And we'll talk offline. Now, before I let you go, we have an audience question, and you have not been prepped. So I'll let you go first, and then I'll go first from GS256 on Instagram. What if you don't manage to eat all your calories in six to eight hours every day? I'm a pretty small person and I feel too full and end up not eating enough calories in that window. What should I do? Well, first I would ask, why are we looking at calories? If this individual is metabolically healthy and not losing weight, then whatever he or she is doing is likely appropriate. There's a huge fixation on calories amongst people still because of this notion of calories in versus calories out has to do with weight loss. And we really realize now that that just doesn't, you know, though it seems thermodynamically reasonable, it's not really how our physiology works. So I don't think there's really any need to be concerned about the number of calories a person is taking unless he or she is losing weight. Now, let's just suppose that's true. Then I would, if that person cannot tolerate more bulk of food per se, I would shift the food, the diet to one that provides then, if that person's really fixated on calories, higher calorie food, meaning more dietary fat, having more, you know, having twice the calories, gram per gram in comparison to protein and carbohydrates. So I would shift that. Also, if this person is involved in time restricted eating, I would say then bracket the meals. In other words, right at the first hour of eating, do some eating then, then allow whatever the time period is, six to eight hours, whatever that period is to add in at the very end of that, the second meal that is going to provide one would think adequate amounts of food. And finally, if there is early satiety, in other words, if anybody is suddenly noting that they just can't seem to eat the same amount of food in a, you know, all of a sudden it's happening to you as I can't even finish my dinner. That's the time to have a workup from a gastroenterologist because there are certain things that can happen in terms of the digestive tract that can limit the amount of food that a person's able to tolerate or even swallow for that matter. And I'd recommend considering going in that direction as well. Great answers. Yeah, I don't have a calorie count on any of my recipes in any of my books because I agree with you. The calorie and calorie out is wrong. It's just plain wrong. I personally, if I have somebody who can't gain weight and I talk about that in my upcoming book Unlocking the Keto Code, I put them on a fairly impressive dose of macadamia nuts. And it's very rare, speaking of fat, it's very rare that I can't get somebody to gain weight by having them eat macadamia nuts every day, a good quantity of macadamia nuts. And maybe offline I'll share a funny story on how I had a challenge. Actually, I'll do it right now. I had a woman who couldn't gain weight and this was in the winter about now. And as you may or may not know, I go on a one meal a day planned during the winter for six months. And so I usually lose about 10 to 15 pounds every year on purpose. And so I said, I'll tell you what, I'm going to go on a challenge. We're going to eat a cup of macadamia nuts a day for the next six weeks. We're going to weigh in today. I'll see you in six weeks. In six weeks? In six weeks, we'll do a weigh in. And she said, okay, you're on. So this is a time when I would normally lose weight. And I actually gained in six weeks, about 10 pounds. So and I'm proud. I say, yeah, see, it works. It's great. So she shows up and she's the same weight. And I go, what the heck? I said, I'm shocked. You're the first person this has happened to. She's, oh, I thought you were joking. I didn't believe you. I didn't do it. And I'm going, I just gained 10, 10 pounds to show you how well it works. And oh, well, it does work. I can personally attest to that. Yeah, you know, oftentimes people are going to, they want to gain weight for the wrong reason. You know, everybody around them is saying, Hey, what's wrong with this person? Are you losing weight? You know, you have some disease. What's happening? And I would say before anybody wants to jump into a program to actually gain weight, let's look at some metrics. And, you know, most of the time in my experience, people test out as being really in an ideal range. The problem is that everybody else is fat. And, and because of that, this person feels different, feels left out in our modern world. You know, here in America, now a third of adults are obese. And by 2030, which is in the distant future, right, eight years from now, that number is going to be 50% of American adults will not just be overweight, but obese, clinically obese. That said, you know, so we're skewing what looks to be normal, pretty much to the right side of that curve. And a lot of times people need to be encouraged that, Hey, you're in great shape. You know, we don't want people to become cacetic, obviously, and be, you know, just breaking down their body tissues for calories. But, you know, for almost the entire time of being on this planet, we're pretty lean individuals. I have my patients go watch a movie from the 1940s or 50s. And that's what normal looked like. And even the tourists in Mount Rushmore and North by Northwest, we're all skinny in the 1950s. And not anymore. So I just like, go watch a movie from the 40s and 50s. That's normal. And you're right. When we show them on a biometric scale, there's kind of smack dab in the middle of normal. And you're right, they're scared to death that they're too skinny. And they're normal. Yeah. I mean, at the moment, you put a pair of calipers on that person's tricep skin fold and tell them how much, you know, subcutaneous fat they have or calculate their BMI. And then you show them that, Hey, you're you're in the cat bird seat here. And, you know, the problem is again, comparison to others and people making comments, people make comments because they'd like this person to start to gain some weight. So they look more like they do. So that's very often an issue. Where do we find drop acid? Drop acid is, I have a copy right here, everywhere. It's local bookstores, online retailers, Amazon, Barnes and Noble. And if you know, the best place I think is just to go to drop acid book dot com. And then you can learn about it. I have my videos there linked my various blogs that I've been writing. And it's available everywhere. All right. All right, take care. Stay safe. And good to see you. Look David, take care. Thank you.