Jay Feldman 0:04
Welcome to episode 85 of the energy balance podcast, where we teach you how to live without constant hunger and cravings, fatigue, brain fog, poor sleep and other low energy symptoms by maximizing your cellular energy. I'm Jay Feldman. I'm a health coach and independent health researcher, and joining me again today is my good friend Mike Fave. Mike and I have been studying health and nutrition together for a long time now, and Mike also draws on his experiences from working within the healthcare industry. Today's episode is part two, the final part of our series discussing whether David Perlmutter and Rick Johnson are right about fructose and uric acid, and whether this means that we should be avoiding fructose. And as I mentioned in the last episode, this isn't personal toward either David Perlmutter or Rick Johnson. We're just discussing whether or not we agree in terms of their interpretation and view of fructose and uric acid. And with that in mind, throughout this series, we've been digging into the physiology and biochemistry surrounding this question and working to break it down into simpler terms so that it's easy to understand. And in today's episode in particular, we'll be focusing on whether we should be avoiding fructose containing foods due to their potential to increase uric acid. We'll be discussing whether the fact that we lack the uricase gene means that we shouldn't be consuming fructose containing foods. We'll be discussing the role of endotoxin and gut health in uric acid production and gout. We'll also be talking about which fructose sources are ideal for our metabolic health, and how to adjust fructose intake if someone is dealing with insulin resistance, non alcoholic, fatty liver disease or gout. This series has been inspired by a couple of listener questions. If you have any questions that you'd like us to answer on a future episode, feel free to send those in to Jay Feldman wellness.com that's Jay why at Jay Feldman wellness.com or leave those in the comments, if you're watching on YouTube, if you are new to the podcast, then after listening through today's episode, I'd highly recommend you go back and listen to episodes one through seven, where we took some time to build a foundation as far as the understanding of the bioenergetic view is concerned. To check out the show notes for today's episode, you can head over to Jay Feldman wellness.com/podcast where you can take a look at the studies and articles and anything else that we reference throughout today's episode. And if you are dealing with any low energy symptoms or chronic health issues, whether those are related to fructose and uric acid, maybe you're concerned about insulin resistance or gout or nanocolic fatty liver disease, cardiovascular disease, or any other chronic health issue, maybe autoimmune conditions. Maybe that's low energy symptoms like chronic cravings and hunger, low energy or fatigue, joint pain or other forms of chronic pain, weight gain, digestive symptoms, brain fog, poor sleep or insomnia, or hormonal imbalances, or any other low energy symptoms or chronic health issues that head over to Jay Feldman wellness.com/energy, where you can sign up for a free energy balance mini course, where I'll explain how these different symptoms and conditions are really caused by lack of energy, and I'll also walk you through the main things that you can do from a diet and lifestyle perspective to maximize your cellular energy and resolve these symptoms and conditions. So to sign up for that free energy balance mini course, head over to Jay Feldman wellness.com/energy, and with that, let's get started.

All right, so let's talk about the whole uricase situation, because that's kind of separate but important piece here to their argument. So the their argument is essentially that as humans, we don't have this enzyme your case, and they're us and our closely related apes don't have your case. And their argument is that the deletion of the uricase genes was something that allowed us to survive by increasing fat storage from fructose, and that, again, allowed us to survive in winters or in periods of famine, and because we have this uricase, we then can't handle a lot of fructose because it's just going to produce all this uric acid, and we can't convert that uric acid out to other things. And that's a major problem. It's very harmful. So for that reason, we have to be very careful with our fructose intake. That's essentially the arguments that's being that is being made. And there's a lot of problems with that argument, and I think some of the clearest ones will go, go through a bunch of them, but some of the clearest ones do come when we look at those ape relatives of ours. And again, these, these apes, you know, chimps and gorillas, and we'll talk through some some details here. They don't have your case, but they all eat very large amounts of fruit, and the ones that, and we'll talk about this. But the ones that tend to be the most intelligent and most advanced eat the most fruit. We'll talk about some details there. And they thrive in this high like on this high fruit diet, despite the fact that they don't have your case and they live extremely long. But they're very obese, right? And that's the last thing I was going to say, is they're massively obese. As you know, all wild apes are extremely obese, exactly. But as you're going to get, going to get at in a second, Mike, I'll let you describe it. But, but essentially, of course, we're not actually seeing obese apes. Naturally. They're very, very lean. The other piece here that I want to mention before we talk about some of the details there is this argument that maybe this helped us survive in the winter. You know, we needed to, like us apes, needed to gain fat so we can make it through the winter. Well, no other apes that humans live in climates with a real winter, like they all live in tropical climates where you have the food that they really need all year round, which is fruit there. And so they don't have real winters, at least the vast majority of them. Of course, there's some monkeys that do, but some of the monkeys do have the urica still. But of course, these apes are living in basically year round summer, and they're eating fruit year round and often as more than 50% of their diet, or at least in some of the most intelligent and longest lived ones. And yet, if, as Rick Johnson says, nature is trying to make us fat, and there's an evolutionary mismatch that we just lack. This, your case, Gene and so, you know, it just has to make us fat when we eat too much fructose. Why are these apes not obese? And Mike, I'll let you talk specifically about the bonobos and how not obese they are despite their very heavily, very highly fructose containing diet.

Mike 6:45
Yeah, so they have much more fructose than your average American. Who is, what is it? The 60% of the of the US is overweight, and then I think, like 30% or something like that is obese. So, like, the first thing we'll clear up here is, are these are these animals obese, or are they overweight? So what those so basically, this table comes from this study here, body composition and pan paniscus compared with sapiens, has implications for changes during human evolution, evolution. So pan peniscus Is the bonobos, and what we're comparing here is their body fat percentage. So female bonobos have a body fat percentage of around 3.6% male bonobos have a body fat percentage of around point 00, 5% so they're stage ready all year round. And then females humans, based in this study, they had an average body fat percent of 36% and then males were about 20% so these numbers, even for even for humans, maybe these are a little bit on the higher side, depending on the population you're looking at. But even so, I'd say these are probably close to I would say they're probably close to average, just considering some of the things that we talked about. But we have the overall The point being here is that the bonobos, which are the smartest and most frugivorous apes that that we know of, have very low body fat percentage, despite the fact that they lack your case and despite the fact that they eat. So I have another graph up here, and basically fluctuation and availability. So figure A is fluctuation availability of flowers, ripe fruit and young leaves, and then B is variation and intake of flowers, ripe fruit and young leaves. And basically, if you can see here. Let me see if I can, if I can make this a little bit larger. So essentially what you see here is this top bar. Here is fruit, ripe fruit. So between 60 to 100% of the Apes diet is fruit overall. So we basically have, like, pure frugivores, pretty much year round. This is year round. Yes, where's their winter?

Jay Feldman 9:09
Aren't they packing on all the pounds for winter?

Mike 9:12
I don't know what apes you're talking about, great apes or bonobos you're talking about. So essentially, they have a 60 to 100% fruit diet. When we break this down a little bit, they say in the study here essentially that the average daily caloric intake of female chimpanzees estimated in this study was, it was 2500 kilocalories. Was slightly greater, but comparable to estimates from previous study of kanyawara chimpanzees. So bonobos are essentially a class of chimpanzees, and I couldn't find specific information that was directly about bonobos diet. But so the next best thing was looking at chimps diet, because I want to see the macro breakdown and basically, kind of get an estimate of how much fructose that they were having. So we have a 60 to 100% Fruit diet, and the bonobos apes are pretty close to that. And essentially they have about 2500 kilocalories per day. So what did you see here? And then, of those kilocalories? So I have this table here, and essentially what you're seeing is that about 60% it's about a 60% carbohydrate diet with 1500 kilocalories of carbs from fruit based sugars. So if you convert that into grams, you have about 375, grams of carbs, with roughly half of that as fructose. Because the main fruits that they're eating are things like figs, which are like a one to one ratio of glucose to fructose. And then there's some other fruits that they had, some other fruits, I think they were like droop of the droop family. Then after that, when you look at fat, you have about 30% fat diet. And then the 10% what was left was available. Protein was 317, kilocalories came out to be about 10% of diet, which was about 80 grams of protein. So you're looking at, just to give an overall breakdown of the diet, but you're looking at about a mostly carbohydrate based diet, 60% carbohydrate, and about 187 grams, probably maybe a little bit less of fructose. So even if we were, even if we were half as much, we're still twice as much fructose as the average as the average person in the United States, which we established, the mean intake was 48 grams. So even if we have a margin of error of 50% based on my calculations, we're still at 90 something grams of or was it 93.5 grams of fructose for the apes and the body fat percentage, again, when we come down here, for the average human, male is 20% females 30% and then in the bonobos, it's point 5% and 3.6% and the bonobos actually have a higher intake of of fruits than chimpanzees do. So yeah, we're like the that whole idea that the lacking, the lack of uricase and consumption of fructose allowed us to hold on extra fat isn't really holding water in the other species that have this situation, for example, the great apes, including bonobos and chimpanzees, which have a larger intake of fructose than your average United States citizen and have significantly, Like multitude order, less body fat overall. And both groups lack the enzyme uricase.

Jay Feldman 12:26
And a couple other things is they are eating very dense fruit, like figs, which Rick Johnson actually mentioned in one of his interviews, those being incredibly dense and fructose and sugar, as in something that we should avoid. You know, they're like candy, and yet that's what they're thriving on. And again, if you want to make the argument that there's an evolutionary mismatch, and we were supposed to be eating this fruit that had very, very low sugar, and we could barely ever find it, and that's what we had evolved for, and that's what our genetic makeup is for, then how you explain these bonobos now that are eating very dense cart like very dense sugar based carbohydrate as a majority of their diet. And not only are they lean, but just for, like, just help conceptualize 0.005% body fat. So a lean male human who is maybe 10% you've got, you know, you can see at least the four pack there, like there's ABS showing which you even at like, 16% body fat, you'll normally, you know, still have, like, the top abs. So 10% is like relatively lean, that is 2000 times fatter than an average bonobo. A male human with 10% body fat is 2000 times fatter than a male bonobo. And if you have 20% body fat, which still is not like, it's not obese, it's just a little overweight, that would be 4000 times an average male bonobo.

Mike 13:41
Yeah. The other thing to put in perspective here, too is that the there were different types of fruits besides figs, and they they listed them as droops in here, and these fruits actually had a higher content of sugar than the figs. And I think that the from what they discussed here, there's increased feeding time for those fruits by the chimpanzees over the figs, because they were more sugars overall, so there was, like, a preference for energy dense fruits, yeah, yeah, yeah.

Jay Feldman 14:11
I mean, that's, that's it. Let's go home. I'm kidding, there's, there's more, but there's more so, but that's super important. We talked about this, the situation of intelligence, a good handful of times we've talked about in the past. But just to mention it a little bit like still very briefly, but just to mention it is that you do see in these apes that the ones that eat more fruit and have the digestive systems that are designed to eat more fruit with smaller, large intestines, so they're relying less on the fermentation of fibers to produce short chain fatty acids. The ones that are not like that, that have the larger small intestines, smaller large intestines, and have more fruit, have larger brains. And it's been shown in the research that the diet is what is allowing for the larger brain, as opposed to some other factor, like a lot of times, the social i. Sociality will be something that's that's pointed to, but there's good evidence that is actually the diet that is allowing for that, of course, because, and this is something we didn't talk about before, but because energy, which fructose and sugar and carbohydrates and fruit are an amazing source for, is what allows for greater intelligence and greater capacity, greater function, something we talk about all the time. That's why we focus from this view on that's why we're we focus on the bioenergetic view of health, and we've talked about various support for this, right in showing things like this that it allows for greater brain size. But also, there's the expensive tissue hypothesis, showing that less energy being used toward digestion allows for greater brain size as well. Both of those things kind of happening in parallel. We also, we've also talked about, like, the constrained model of energy expenditure. We've also talked again, about how energy is not the same as fat gain. So again, when you converting fructose and glucose and any other subs down to ATP, then that is not becoming fat. Excess energy is not the same as fat gain. And so again, I'm just going to cite or reference earlier podcast episodes of ours discussing that in more detail, because it would take us a little bit too far, similar to some of our tangents have already but yeah, just some things that I think are at least worth mentioning. But as far as things, I want to dig at least a little bit more into detail on really, the last point here, in terms of the urica situation, is how we as humans cope with higher levels of uric acid, and whether it's really coping or it's actually a benefit, and whether there's actually a reason for that that is not just genetic mismatch, where it was just a way for us to get fat, and now we don't need to get fat, so there's no use for it. And yeah, so we have and so the study I cited earlier showing the benefits of of your gas and in terms of its antioxidant effects, and not allowing for the like extensions, extensions in lifespan and reductions in cancer is an important piece here. I'm going to point to some other studies here as well. One thing I want to mention before we dig into these studies is just for reference, as humans, since we don't have uricase, we do have higher serum levels of uric acid as normal, healthy humans. It's still about five to 20 times higher than serum uric acid in most other mammals. So, and we'll get to this in a minute. I'll have an example where you have moderately elevated, like, what would be moderately elevated for us, levels of uric acid which doesn't cause any immediate harm. You know, long term can be an issue, but you create those same levels in rodents, and it will kill them, like more than half of them will die, and they'll have all sorts of kidney issues. And so again, kind of points to the fact that we're able to handle large amounts of uric acid. We have certain adaptations to that, and the uric acid itself is providing a benefit. It's providing a purpose, beyond just making us fat. And instead of just making us fat, of course, that's saying that facetiously.

Mike 18:02
An important extension of this too is that when you're looking in rodent models at the effects of uric acid for metabolic syndrome and different things like that, it's really important to take into consideration that humans have evolved to tolerate and have larger amounts of uric acid in their serum. And if you're trying to put it in some legitimate evolutionary context that makes sense of like with an underlying perspective that there's purpose to things, then you would then perhaps you understand that there may be a benefit to having those higher level levels of serum uric acid. So again, this is like this. The same thing going back to when we were discussing processing of fructose in human livers versus processing of fructose and refined carbohydrates and rat livers, where the studies are showing, oh, if you have, you know, X number of grams and and rats, you have all this de novo lipogenesis. But then when you convert that into humans, which technically evolved along the lineage of high fruit eating, which was what we see with the other great or what we see with great apes. What you wind up seeing is that, oh, de novo lipogenesis from sugars is actually quite low in our species. So it's very important to understand that context, especially when you're trying to make justifications around like having zero fructose diets because of DNL or or uric acid or whatever the deal is.

Jay Feldman 19:23
Yeah, yeah, absolutely. So to dig into a couple of these studies. First one is titled hyperuricemia and urate nephropathy and urate oxidase deficient mice. So they state to create a mouse model for hyperuricemia and gout. And to address the question of whether urate oxidase is essential in lower mammalian species, we've disrupted the urate oxidase gene in the mouse by homologous recombination in embryonic stem cells, unlike the human situation, urate oxidate urea oxidase deficiency in mice causes pronounced hyperuricemia and urea. Nephropathy, more than half of the mutant mice died before four weeks of age, indicating that your ADOX space is essential in mice. And the we'll get to the numbers here in a second, which are also demonstrative of this situation. But the other thing that they're kind of pointing out here is that we are fine, like we maintain our uric acid levels and everything without your ADOX space, and these other animals have to rely on your ADOX space. So we must have some pretty good mechanisms for for handling uric acid without your ADOX space, because all you have to do is remove that in other animals and other mammals, and their uric acid levels will shoot up. So this next part of the quote, or next quote, which is later on in the study, they state that the serum uric acid of the homozygous mutants reached 11.0 plus or minus 1.7 milligrams per 100 milliliters, which is 10 fold higher than that of wild type and heterozygous mice, and about twice the value found in normal humans. And so this was the level that was causing more than half of the mice to die before four weeks of age due to this nephropathy, this damage and disease of the kidneys. And this was happening. So first off, they reduce, you know, they take out your a doxidase, and you have a tenfold higher increase in uric acid levels. Again, in humans without URI oxidase, we're stable, so we have good ways to handle uric acid, again, just another reason why we shouldn't be so concerned about, I mean, every step of this process that we've discussed. But then they they mentioned that this is a level that is just twofold the normal value in humans, but this is a level of 11 milligrams per deciliter that is like you have, like people typically might have gout in that scenario, but they're walking around and they're fine. They're not dying, you know, like these mice are dying before four weeks of age. I think they said in the study was 65% of them did. And then, of course, the other ones are not just healthy and normal. And so while it's not ideal for us to have those values, we're obviously able to handle considerably higher values of serum uric acid compared to animals that do not have or that do have your atoxins, your case?

Mike 22:06
Yeah, I don't know. I mean, I don't have much to add there. My preface already is, you know, we're looking at organisms that have humans, specifically, that have the ability to tolerate higher amounts of uric acid. There's an undisclosed reason so far, with numerous theories about it. And then trying to make, adjust, make assessments from animals that require uric uric acid oxidase, or your URI case to function appropriately, and then, like make extensions to humans, is quite, I think, a risky or questionable proposition without taking into consideration those pretty drastic physiologic differences?

Jay Feldman 22:47
Yeah, 100% Yeah, it's because of these huge confounding factors. As you're saying. It's, it's really questionable whether we can just translate the research between the two. And when we look at the research in humans, as we've gone through quite a bit of it today, it's, it doesn't point in favor of this argument in terms of fructose and uric acid. Yeah. So this next study is talking a little bit more about the context, the evolutionary history and some potential reasoning for elevated levels of uric acid, and then also comparing it with mice as well. So this study is titled diabetes insipidus in urica deficient mice, a model for evaluating therapy with polyethylene glycol modified uricase. So they state that the uric acid creatinine ratio in the urine of uricase deficient mice ranges from 10 to over 30 on a weight basis, these mice excrete 20 to 40 fold more urate than do human subjects. So this is mice without your case, and they're having these massive loads of uric acid that they have to get rid of 20 to 40 fold as much. And then just it says after that, the mice in the situation develops severe defects and renal concentrating ability, resulting in an approximately six fold greater urine volume and a five fold greater fluid requirement compared with normal mice. They then go on to state that this nephrogenic diabetes insipidus leads to dehydration and death of nursing mice, but with adequate water replacement, high urine flow protects the adults from progressive renal damage, so they're able to get along, you know, for a little while without major kidney damage.

Mike 24:18
If they it all out in extremely large volumes.

Jay Feldman 24:21
Exactly, and that's and that becomes really relevant, because when we look at our kidney function versus animals like rodents, that's kind of our norm, and they talk about that as a way that we deal with higher levels of uric acid without any issue. So they then state that discussions, or later on, they state that discussions of uricase evolution have often speculated on advantages derived from the loss of the enzyme. So this is in Ozu and primates are saying that we must have benefited from losing it. And they say such as increased longevity resulting from radical scavenging ability of urate. A less anthropocentric. Anthropocentric view might consider the benefit of uricas to other species for which renal. Water Conservation has been an essential adaptation to seasonal drought or arid climates. The avoidance of uric acid precipitation and maximally concentrated urine would strongly favor the retention of your case. Its loss might lead to lethal nephropathy, as in your case, knockout mice. So what they're saying here is that in other like the vast majority of other species, water is a like a lack of water is a more relevant concern, and so they don't their urine is less, is more concentrated. Typically, they aren't urinating as much water. And so because of this, it actually benefits them to have the uricase to already get rid of the uric acid, because they can't do it through their kidneys effectively, because it would cause this kidney damage. But they then describe why apes and humans might not have that same issue, which allowed us to then cope with higher levels that have other benefits. So they state that, in contrast, ancestors of New World monkeys, hominoid apes and humans in which the ureadox stage gene mutations became fixed may have lived in rainforests with abundant water maintenance of relatively dilute urine may have been better tolerated and favored as an adaptation to environmental toxins, as well as to the loss of hurricanes. Other protective mechanisms might have been in place or selected subsequently, such as efficient proximal tubular reabsorption to limit the excess of uric acid to collecting ducts where maximal concentration and acidification occur, or shorter renal papillae to limit distal water reabsorption. I'll finish this quote in a second. Then decipher the reduced ability of the neonatal kidney. Oh, this is an important part. So they then state that the reduced ability of the neonatal or neotinal kidney to concentrate and acidify urine may protect human infants from uric acid nephropathy at a time when urate clearance is considerably higher than that in adults. So what they're pointing at here is that we can handle higher levels of uric acid in the serum and get rid of it effectively, as long as there's enough water coming in and if, instead of this being the product of a situation where we were in famine and winter and and drought and whatever else that we remove like that, we lost our your case capacity instead, maybe it was a situation where we had adequate water so we could actually handle elevated levels of uric acid without it being an issue Due to a concentration issue leading to precipitation, which is what leads to the like uric acid crystals in Gallup. And so they're saying that this could have been why we are able to have much higher levels of uric acid. And so again, I there, we've kind of talked about a few different angles here, but they definitely don't land on the situation where uric acid is there? Or yeah, uric acid is there in higher amounts in order to increase fat gain. You know, we have discussions of increased antioxidant capacity, of of other benefits, like being able to excrete more toxins in the kidneys and other adaptations here. But none of this is suggesting that this is a bad thing, but rather, actually a good thing. It's not an evolutionary mismatch, but rather, we've developed this situation because it's something that supported us, increased our complex, our complexity and our function, and therefore continued on.

Mike 28:11
Yeah, and the research basically says, I have a quote here from the study says the majority of cases of elevated serum uric acid result from impaired renal excretion, possibly because of intra individual differences in function of the urine. You are a T transporter, urate transporter. So most issues of and you can see most of the issues around the uric acid situation isn't necessarily an overproduction. So they talk about situations of overproduction, and in those situations, as productions can be increased by several mechanisms, including rare enzymatic defects, states of high cell turnover and alcohol ingestion, partly because of purines contained in alcoholic strength and alcoholic drinks. So the the main areas that have been linked with the high with causing or being the etiology behind the increased uric acid, or states where you have a destruction of cells, right? You have a so perhaps, like a cachexic state of cancer, where you have this massive adjustment, or massive cellular turnover, death and and growth, etc, etc, causing phosphate depletion, increased serum, phosphate, etc, etc, etc. And then also states of alcoholism, where you have the increased production due to alcohol. And then also issues, specifically with the kidney, where the kidney is causing a lack of excretion. So, and it said in most cases, it's LA, it's a issue with the excretion less so the production. So that's another thing to keep in mind, right? Because you have a situation, okay, so fruit. So even if fructose does increase your serum urate, if your kidney is able to excrete it, is it still a problem? That's the other, the other question to keep in mind. And they talk about pathological states as well, and they talk about in state, in in states that. Have, like, kidney issues or whatnot, where there's a buildup of uric acid, there's actually an increased secretion of uric acid in the urine. So the kidneys have a degree of flexibility with compensation. But interestingly, a large proportion of uric acid is actually reabsorbed in the kidney. So I think, like something like 10 to 12% is what's excreted. So that's another interesting piece of the puzzle. Is it's the body is maintaining uric acid at a certain level. So yeah, just some interesting pieces to consider in the overall picture of elevated serum uric acid. And they even talk about one of the quotes that I pulled out from this study is that is argued that elevated ceremonial gas, and those are cardiovascular disease, may simply reflect the presence of other risk factors, such as hypertension or diabetes, diuretic treatment, impaired renal function, atherosclerosis itself or increased oxidative stress, and they also, therefore the association may simply reflect impaired renal function, and the associative associate oxidative stress and cardiovascular risk, while most studies have adequately adjusted for renal impairment and cannot be excluded, that raised uric acid concentrations reflect or contribute to subclinical levels of renal impairment, which contribute to the association in as yet undefined ways. So the the problem with the the epidemiologic evidence, and the evidence for the increased race serum uric acid levels in people with diabetes, heart disease and etc, is that a lot in a lot of these states, they may have some subclinical renal impairment, because the kidneys are the major excreters of uric acid. And then in that situation, it's hard to say is this person? Is this person having all these negative effects because the uric acid is actually negative? Or are they having, do they have this, again, this overlying pathology that's leading to this elevation in uric acid? And then is that, if you're in like, super physiologic concentrations of uric acid, does that? Then we know that that then adds to the problem. But what is the initial cause? Is the initial cause the state overall? And if so, then like would addressing the state lower the uric acid, and then what is causing that initial state overall? So those The question is always going to come back to that context, what is going on in the initial state? And I mean, that's what now, I guess the the next argument here is, like, if you're gonna like is fructose, which we kind of discussed already, is that causing the initial state? And it seems unlikely. I mean, unless you're going to start doing, you know, 219 grams per day.

Jay Feldman 32:37
On its own, in an excess of the rest of your diet...

Mike 32:40
Yes, in a caloric excess, um, or would something like fructose from fruit be an actual causative or problematic component here? Because essentially, where this comes in, in the bioenergetic perspective, or the perspective that we we come from fruit, and fruit juice is seen as an important food source. So where does that? So, where does this all fit in with that? And we're, I guess this, the last piece to kind of get together here is essentially that it seems to be like, largely a non issue with fruit, especially considering all of these, the the elements of the argument that we've built beforehand.

Jay Feldman 33:18
Yeah, and juice and dried fruit, all of it, you know, concentrated. Well, yeah, let's get into it. So in that practical sense, and even just to give them their like so to describe their view that they describe on fruit, basically it's that and on fructose as a whole, which, as you were kind of getting at, everything you were describing was so much more than fructose. So much greater context, so much more going on here that is not driven by fructose, so much dysfunction that's not driven by fructose. Yet their focus is on fructose, and their view is that we need to avoid it. But they do say that it's okay to get it in moderate amounts in certain fruits, especially the ones that have particularly lower amounts of fructose. And they say, you know, it's okay to have a couple apples and some berries and no banana and whatever like it's okay to have some fruit. And there's a few reasons why they say it's okay. One is because they do acknowledge that it's packaged with glucose, but also that it's packaged with fiber, and so there's gonna be slower absorption, also that there's bioflavonoids and polyphenols in there that can help to inhibit xanthine oxidase, and then lastly, that there's vitamin C and that the Vitamin C helps to excrete your gas at the kidney.

Mike 34:30
Yep, those are the three main ones.

Jay Feldman 34:33
Yeah. And so that's their kind of general view. But otherwise, like outside of that context, fructose is the problem and is driving these states. And you know, one of the we kind of pointed this out when it comes to the situation with the bonobos, but it's interesting that they're saying that like fruit is okay, yet their whole argument for the idea of having your. Case is that it was supposed to allow for fat gain, but the only thing that would have been available during that time is not sodas and candy and whatever else they're saying is the problem. But the fruit that they're actually saying is okay. So they're saying there's this evolutionary mismatch that would have that, you know, back then we needed the fat gain, but now you won't get fat gain from fruit. The fruit's okay. It won't cause fat gain, but that's why we had your case get removed in the first place, was to allow for fat gain. And they kind of, like, they're kind of half they try to get around it by just saying that it's wouldn't have been a lot of fat gain, right? They aren't, they wouldn't have been obese. They just would have gained a little bit of fat that would have allowed them to get through a famine, which, I mean, I don't know, like, an extra pound of fat is not going to help you get that much more through a famine than anyone else, but, but also, the entire argument for people nowadays in terms of like dieting and weight gain, is that it's a small amount of fat that's added on a cumulatively, accumulative view, over time. It's not no one is saying that you're gaining a pound a day. Like, it's always been that small amounts of fat gain contribute to large amounts of fat gain contribute to obesity. And so if they're saying, like, are they saying that eating fruit now is okay because it would only cause a little bit of fat gain, like, it would have back then, yeah, it's okay to eat that year round, and that's not going to make us fat. Like, there's a there's there's some, I don't know. There's some pieces here that aren't lining up, and so that's one of them. And there's a another piece of evidence that I want to mention, but I don't know if there's anything you want to say first.

Mike 36:33
No, I mean, I was just going to talk more about the specific fruit piece. I don't think the argue. I think the whole evolutionary context that has been tried to be created around fructose and then fat gain through uric acid. It's like de novo lipogenesis arguments failed. So like, let's try with uric acid now. And I, first of all, in real life, we don't, we're not seeing this, right? Like, we're not, I'm not seeing people get obese with fruit. I don't think you're seeing people get obese with fruit I'm not getting obese with fruit or fruit juice, or any of these things. And if like...

Jay Feldman 37:08
Fruitarians, like, if there's ever a group of people who is, who is, like, not dealing with fat gain, it's fruitarians.

Mike 37:15
Yeah, and they have a large amount well. And the other thing too is you're like, you're looking at an obesity epidemic inside the United States and Western countries overall, and you're not seeing massive fructose intakes like if we're looking at a mean fructose intake of 48 grams per day, we're comparing that to other animals that lack your case, who are eating at with a 50% margin of error on calculations, twice that number of fructose and they're 1000 times leaner, more than 1000 times leaner. The average weight for men, I think, was 20 body fat percentage was 20% like that. The whole argument, this whole evolutionary context for it is just not lining up like it doesn't. It doesn't seem to make much sense. And then then like to then you start looking at studies like, Okay, well, fruit isn't causing gout and fruits not causing metabolic syndrome. And it's actually, there's a lot of there's a lot of intervention studies, even in rats and mice, where, like giving pineapple juice and pears or blocks the development of metabolic syndrome in the high fat, high fructose, whatever feeding studies that they're doing. So it's like you're seeing these opposite situations with fruit, with fruit juice, and then you're trying to, like, create this evolutionary argument that we lost your case to put on body fat through fructose, but the only access to fructose we would have had would have been fruit, but fruit has inverse associations with body fat, gain, obesity, metabolic syndrome, etc. It's like it that doesn't make any sense. There's like, the pieces, the Ducks aren't in order there. Um, now and then, even in modern examples, you're seeing that the ducks aren't in order. As far as, like, fructose or sugar intake being the nail in the coffin for metabolic diseases that you're not you don't even have correlation in epidemiologic data. That is, that is like, strongly created, like, creating these ridiculously startling associations. And then even when you get into the associations, like, Okay, now when we look at causal studies and we do overfeeding with sugars, fructose, et cetera, it's like, okay, de novo lipogenesis, less than 1% so it's like, where's this obesity epidemic coming from with metabolic syndrome, from fructose the and then the other thing is, even beyond that, if we're going to put this into like the the populations of people that actually look at or listen to this information, who, who you know, care about their health, in any capacities, you're not seeing a bunch of paleo people or carnivores or vegans or plant based or any of these groups of people, regardless of their differences, going out and being like, Yeah, I'm gonna get me that 32 ounce Slurpee so I can get all of my my massive fructose bolus, and I'm gonna drink it in five minutes. That's not what you're seeing. It's like, the question is, oh, can I Is it okay if I have, you know, three oranges, or is it okay if I have, like, two, two kiwis? In a banana, like, is that going to be too much fructose in one dose? And it's like we're not even seeing like, if you look in fruit study, the studies with whole fruit and things like that, you're not even seeing increases in risks of gout and even in fruit juice. The in a study listed by one of the researchers who one of the names on the study, I think, was, uh, Dr Richard Johnson, right? So he was, he was listed on the study the he wasn't the lead author, though. And they discussed that out of all the fruit juices, only orange juice had been associated with gout. And they looked at Apple, they looked at grape, they looked at there's a couple, there's a series of juices there. And even then, when you look at the studies with orange juice in other areas, there's inverse associations with those things. So like the fruit, that the evolutionary perspective of it is quite shaky. And then when you start to get to fruit, it like, really just falls apart. And again, neither of us are sitting here and saying, You know what, go out and have that Slurpee, 32 ounces each meal. But when we're talking about, like, moving making decisions for your health, we're talking about, okay, having fruit as your carb source, having fruit juice as your carb source. And have been having fructose through those things, not being a problem and actually being healthy, considering all the other there are benefits to fructose, as we discussed, as you discussed in the the hepatic cell studies, but then also when you look at blood sugar regulation, and when you look at if you have a normal functioning metabolism, and then even beyond the fructose component, if you're looking at the beneficial components of fruit, you're seeing a whole bunch of beneficial effects. Who's to say that taking in the fruit or taking in fruit juice, and the compounds and components that are present in the fruit and fruit juice doesn't help to fix that block down the respiratory chain, or down the metabolic chain that allows fructose to be oxidized fully through and avoid the depletion of ATP, of ATP, and then subsequent production of uric acid through that pathway. So that's, there's so many questions there, and there's, there's like, clearly, I mean, there's not even questions like, there's clear answers there. Looking at this and saying, like, look, this really isn't a non issue overall. This isn't the smoking gun that we're looking for. But, yeah, taking in large doses of granulated sugar or free specific, more specifically, having large doses of free fructose and rapid boluses probably isn't ideal from a health perspective. But everybody already knew that. Like, this isn't new information. We didn't need a whole book on that.

Jay Feldman 42:23
Yeah, don't inject fructose. Don't take 20 grams of fructose and think that it's going to be healthy. And yes, we're not, like, we've never been suggesting that people go out and eat Slurpees, right? Or drink Slurpees is, like, a good thing. But as you're saying, also, like, not to diminish the difference here, like, we're also not saying, like, yeah, it's okay to eat an apple or two and, like, maybe a banana. Like, we're talking about getting large amounts of carbohydrates from fruit, large amounts of fructose, oh, you know, well, over 100 grams a day, potentially, again, in the right context. And that is very different from what they're saying. They're not saying that that's okay, like that. I don't want to, I don't want the default response to be like, Oh, well, they never said fruit was bad, and that's not really the case. And we're also talking fruit juice and everything, not really not being bad, not being a driver of this, is it this situation? So yeah, I want to make sure that that's there's...

Mike 43:18
Large amounts of fruit. We're talking large amounts of sugar intake from fruit on a regular basis. Like, I don't know, what do I personally do? Maybe, like, three or 400 grams of sugar a day, and I'm still waiting for the obesity to come. I'm still waiting now. N equals one doesn't mean anything, you know. But we also have groups of populations, as you mentioned, for example, fruitarians who are eating ridiculous amounts of fruit and large amounts of sugar and having largely carbohydrate based diets based around fruit specifically, and them also not being obese or develop or putting on body fat and large amounts of body fat, you're actually seeing them having a hard time meaning nor maintaining normal weights.

Jay Feldman 43:59
So just and for other reasons, but yeah, for other reasons as well, of course. And also, I mean, n equals one matters a lot, right? I mean, for each person listening, it is an N equals one, and that's what matters probably the most to them, or unless they're trying to help someone else, which maybe it's an N equals one for that other person. But yeah. I mean, what else is there, right? Like, and I know the point that you're getting at. But also, when we include each other and the people we work with and all the other people who are using this approach, it's a much larger n sample size as well as whatnot. That's true, but even that beside the point. So there was one thing you touched on earlier, which was talking about the low amount of de novo lipogenesis from fructose. I wanted to just mention one other detail there, which is that in fatty liver disease, that 60% of the fat in the fatty liver is coming from our own fat stores that are, you know, through lipolysis. So again, fructose is not the primary contributor there, either. And we talked through that extensively in in that fatty liver series. But just, again, some numbers that just very clearly. Highlight and kind of silence that that opposing concept, that it is fructose. And in those studies, they've shown that only about 25% of the fat in fatty liver is coming from de novo lipogenesis. And again, that's in the context of dysfunction.

Mike 45:15
Where you can't, you can't oxidize the substrate, so you have to your the liver has to convert it into fat and again, right? This again, as always, con that context is so important, like, you're talking about a completely deranged metabolic situation versus somebody who doesn't have a metabolic situation, like, what? When you put different substrate and you have, like, if I, if you put, if your engine is broken, and you put gasoline in it, it's still not going to run. Well, you still are going to have problems. So the question is always, what's going on with the engine? What's going on in the cell with the mitochondria? How is glycolysis The how is the electron transport chain working, etc? And the study that you posted directly talks about those specific things like it. So besides adding fructose or the glyceraldehyde or dihydroxyacetone, etc, into the into the medium. They also added in things like methylene blue and created an electron acceptor, etc, and fix some of those problems. And then you saw a regeneration of ATP and a lack of reductive stress. So there's like...

Jay Feldman 46:19
That was in the like hepatocyte injury study,

Mike 46:22
Yeah, exactly the hypoxia study,

Jay Feldman 46:24
Yeah, yeah, that fructose rescued ATP production and everything, yeah. But So speaking of that context, and again, kind of bringing it back to is fructose the cause here and all that, there was one more study I wanted to mention that was actually something that was brought up by Rick Johnson in an interview where he was he mentioned that you can do a like from fecal microbial transplants, where you're transplanting the microbiome from one person to another, and when they do this from a healthy person to someone with gout, it improves their symptoms, like their symptoms get better, and their serum uric acid goes down, and it's like, well, that's interesting, because we didn't, you know, you didn't change any behavior there as far as changing their fructose intake. And so if you look at that study, it actually is pretty telling when we talk about, you know, that kind of larger context. So I'm going to pull up a quote right here. So the study is titled, effects of washed microbiota transplantation on serum uric acid levels, symptoms and intestinal barrier function in patients with acute and recurrent gout a pilot study. And so the quote here they state that the levels of Dao, D lactic acid and endotoxin were higher in patients. This is gout patients than in healthy donors. After the washed microbiota transplantation treatment, the levels of Dao and endotoxin decreased. And they say that the washed microbiota transplantation is effective for reducing serum or gas levels and improving gout symptoms in patients with gout, and contributes to improve their impaired intestinal barrier function. So again, this is no change in fructose intake. All they're doing is improving the gut health side, and one of the things that they specifically mentioned is reducing endotoxin and it improves their this, their serum uric acid, and improves their symptoms. And we talked a lot in that fatty liver series about how much of an impact endotoxin has is in inhibiting mitochondrial respiration, driving de novo lipogenesis, driving oxidative stress. And of course, in this in this case, it would be one of those things that drives uric acid production, and so again, talking about that larger context, and having nothing to do with whether you're having too much fruit juice or not, is something like endotoxin, and that's why we talk about those kinds of things all the time. And I'm sure you would see similar things if you're looking at PUFA intake and and all sorts of other factors that affect mitochondrial respiration.

Mike 48:38
Well, and we've seen this with obesity. We saw this with alcoholic liver disease. Every time you lower endotoxin in these situations, or you change the microbiome to produce less endotoxin, overall, you see a decrease in obesity, a decrease in metabolic syndrome. It's like, let's talk about a real smoking gun. It's endotoxin. It's not uric acid. And again, the mechanism here is it's not necessarily direct, right? It's urine, the endotoxin is impairing mitochondrial function at the liver, and then it's leading to an impaired like in those situations with gout, and leading perhaps to an increased production of uric acid, or an impaired ability to clear uric acid, perhaps at the kidney. There's multiple mechanisms that you can have going on there, as well as delactic acid being a metabolic problem as well. So again, yeah, the gut situation is a huge one. Now here's an interesting hypothesis. Perhaps the refined food, which makes up the 70, the other 70% of the refined sugar consumption in the United States is leading to intestinal dysbiosis, and that intestinal dysbiosis with subsequent production of endotoxin is driving these metabolic states. And it's not necessarily the refined sugars, inherently in and of themselves, but perhaps, if you have a dysbiotic intestine, and then you dump a bunch of refined sugars or free form. Fructose in there? Well, now you have endotoxin production. Now you have more disruption of the intestinal barrier. Now your liver is taxed. Now you have hepatic, hepatically, hepatic insulin resistance. Now you have fatty liver from because of the endotoxin situation, etc. It's like, maybe that's driving the situation. And it's not just, you know, fructose, like when you look in the in the germ free mice studies with alcohol, they don't develop cirrhosis. When they're the germ free mice exposed to alcohol aren't developing cirrhosis. They're not developing the same level of body fatness and obesity and metabolic syndrome on germ free mice. Why is that? Well, endotoxin, I think, is a huge driver, and we've seen that pretty consistently. So there's, like, there's so many different angles to look at it, besides just fructose, ATP, depletion, Xanthe and oxidase, uric acid. And then uric acid is, is just like this terrible compound. It's like no and every step of that process, there's question. There's a questionable context there that's being that's being described to create this picture. It's like, okay, well, how, how much fructose do we actually need to drive ATP depletion? What state is required for lower doses, or for the doses of fructose to drive the ATP depletion? In the beginning is that, how is the fructose being administered? Are you getting it in the vein? Are you getting it large boluses, orally that aren't getting absorbed, or is it going to be after that? It's like, how much, how much ATP is actually depleted, how much uric acid is even being created, and is that even a problem? And then you know what, where's where else you're getting your fructose from? Is it coming from fruit? Is it coming with all these other compounds? So it's like, every step of that hypothesis has questionable con that has context that need to be questioned. And when you start questioning that context overall, you start to break down the argument. And it's just like, this is, this is a this is a non issue, particularly if we're like in the context. So let's put our context together in a context of a diet that has adequate amounts of fruit and fruit juice as your carbohydrates, and you're eating adequate amounts of protein, you're covering your vitamins and minerals. It seems very unlikely that the fructose driven uric acid pathway is going to be this problem, especially other thing as well as if you're on, like, a eu caloric diet, you're not eating in like, 35% excess of your calories, which may cause problems overall, regardless, depending on, especially depending on the metabolic state that you're coming from. Are we talking about diabetics and obese people? Are we talking about normal people? Are we talking about athletes like this? All changes the situation.

Jay Feldman 52:31
Yeah. But I also, just to clarify, I don't want to make it sound like it's overeating. That's the driver here, either, because the dysfunction, like the dysfunctional mitochondrial respiration, decrease ATP drives extra hunger, leptin resistance, that whole pathway. So it's not just that eating excess of calories is the problem either.

Mike 52:50
Well, 219 grams of fructose.

Jay Feldman 52:52
I'm not saying that that is ideal. I'm saying that in a real context, where someone is not forfeit an extra 215 grams of pure fructose, the overeating is not the problem. It's not the driver here, the fixing types of foods, all that should help if somebody is, quote, overeating. But again, that's all relative. And if you're going based on whatever calorie calculator and all that, I mean, there's so many issues there so but anyway, to wrap up here, I want to focus on the practical application kind of this last part that we've been talking about, talking around, give some practical suggestions and some thoughts on the specific types of foods, fruits, dried fruit juices, table sugar, high fructose corn syrup, things like that. So that people have some some takeaways here, maybe in contrast to the takeaways that are provided from the opposing view that we we've been discussing in terms of just avoid fructose, except very moderate amounts in fruit. And so what I would say, of course, as we're getting at, is fructose doesn't need to be avoided, and there are differences between fructose sources, right? So when we're getting the juice versus the whole fruit, we're missing out on the fiber. So it's going to be absorbed quicker, and that means you're going to get more fructose and glucose and sucrose all at once. It's still not the same as injecting it at all, but it's going to be faster than if you ate whole fruit. That's something to consider, depending on the context we'll discuss that dried fruit is the only thing that's being removed there is the water. So again, it's going to digest quicker. You'll see bigger blood sugar spikes and things like that. Again, fine, depending on the context, but between those three and all of them, you have the polyphenols, you have the nutrients, and you have a good balance of glucose and fructose when it comes to table sugar or high fructose corn syrup. Of course, when you have table sugar alone, it doesn't have fiber, doesn't have fiber, doesn't have polyphenols, doesn't have vitamins and minerals. So that can be an issue. It also can be absorbed very quickly. But if you were to combine it with those other things, then it should be better. And depending on the context, you might be fine with having some amount of table sugar. Again, we'll talk about those contexts in a second. Then when it comes to high fructose corn, soy. Syrup. This is one that even though there's a similar ratio of fructose to glucose as table sugar, there's still some issues with it when it comes to heavy metal toxicity, possibly some starchy components in there that aren't accounted for, maybe some digestive issues that might result there from like the syrup, part of the corn syrup, like, I don't know if anybody's ever had, like tapioca syrup or other syrups that they use to sweeten things, sometimes those can cause some digestive issues because there's non sugar carbohydrates that might be raw or not well cooked, not well digested, and so that can sometimes contribute to some issues. So high fructose corn syrup is not the same as table sugar. And then we also sweeteners like maple syrup and honey, which are going to have the beneficial polyphenols and some nutrients more maple syrup than honey, but they're, of course, not going to have the fiber and water content. So those will be, you know, larger concentrations of glucose and fructose that you'd be taking in when you have those. So you might want to pair it with other foods that would slow down the digestion and fiber and things. So that's kind of what I would say, is the overview of just like different fructose sources. Of course, you're getting some fructose in like other vegetable type, you know, fruit vegetables like squashes and peppers and things. But the main source is really going to be from from actual fruits. In that context, the small amounts in those other you know from those other carbohydrates is small and in general, what I would say, and I'll let you go here after Mike, is that if you're healthy metabolically, and you're not dealing with insulin resistance, you're not dealing with fatty liver or anything like that, I really wouldn't worry about fructose intake from good sources, as long as you aren't Dealing with nutrient deficiencies and you're addressing the larger context. Larger context. I don't think fruit juice is going to be an issue. I don't think dried fruit is going to be an issue. Again, assuming you're digesting everything, well, all of that, it's ripe. There's not like other toxic components in there. And I think generally, those people you know are fine with some table sugar as well, maybe even moderate amounts, decent amounts of table sugar. But I think there's certain contexts where, again, you want to make sure that you're not driving nutrient deficiencies there. I think it's better to be getting more sugar from other sources, whether it's maple syrup or fruit juice or fruit as opposed to sugar, because of the nutrients and polyphenols. But the sugar, on its own, like the sugar itself, isn't the problem there. It would be the lack of other things. I would still, you know, even if someone's healthy in general, lean away from high fructose corn syrup. But then the other situation is, if someone's dealing with glucose metabolism, struggles, insulin resistance, non alcoholic, fatty liver disease, gout, anything along those lines. I would be a little bit more careful when it comes to fructose. I still wouldn't avoid it, but I would titrate up slowly. I would favor slower digesting sources like whole fruits, as opposed to juices or honey or something like that. And I would definitely pay attention to how you're tolerating them and how you're responding. I think that's a huge, huge component, something we talk about all the time is our response to the foods that we're taking in being a really great indicator for how we're responding, right? And so like how our bodies are doing, if it's actually supporting us health wise. So I would pay attention to those things and how you're responding, but I've seen severe non alcoholic fatty liver disease improve without any concern of avoiding fruit juice, or, you know, I shouldn't even say that, with the inclusion, the intentional inclusion, of more fruit juice and more whole fruit and starches as well, and even some sugar sources too. And so I don't think that those things have to be avoided, especially if there are other issues that are really drying driving those processes, which there are. But especially if those things are being addressed, you might not really have to worry about the fructose at all. But in the interim, I have seen situations where it's helpful to kind of, again, go slower favor the full. Like whole fruit form that's going to digest slower has all the components. And the other piece here too is there's a difference between having a fructose source in the context of a meal versus on its own. Again, if you're healthy, metabolically, and you have some whole fruit as it's a snack on its own, I think that should be fine. Maybe even juice on its own should be fine. But if not, you might need to worry a little bit more about pairing that with protein and fat to help slow digestion a little bit further. So those are all considerations I would have if you're if you have a reason to be concerned about fructose intake, which again, is not because of the fructose driving the issue, or rather due to other factors driving the issue. And again, I would lean toward trying to slow the amount of earning, concentration of fructose you're getting in that case, but still getting as much as you can in that context, because of how supportive it is in terms of carbohydrates in general, but also some unique factors that have to do with fructose itself.

Mike 59:37
Yeah. I mean, another thing to keep in mind here, a pretty big one is vitamin C, which is also discussed by, I think, Rick Johnson and Dr Rick Johnson and Dr Perlmutter, is that vitamin C can drastically decrease serum uric acid. So I have a quote here. So here we say studies have shown that supplementing vitamin C at five. 100 milligrams per day for two months can significantly reduce serum uric acid concentrations in patients with hyperuricemia. Moreover, moreover, studies have concluded that the incident incidence rate of gout decreases by 45% with an increasing increase in vitamin C intake. Fruits such as, I don't know, I'm proud, jujubes, guavas, kiwi fruit, strawberries and oranges are rich in vitamin C, so just getting you having adequate vitamin C in the diet, the best source is obviously going to be fruit. Is a great way to go. And then other specific fruits that are known to be helpful with gout are actually, I think black cherries have specific plant compounds that are quite helpful for gout.

Jay Feldman 1:00:40
A lot of the tart cherries are I hadn't heard that about black cherries.

Mike 1:00:44
Or maybe it was tart, but the cherries overall have a beneficial effect because of some of their plant compounds on gout, specifically. So incorporating some of those, if you're dealing with gout or you're dealing with hyperusemia, having adequate amounts of vitamin C, there's some talk about adequate amounts of magnesium helping to prevent hyperuricemia, having adequate amounts of zinc, it has been shown to be associated with less get hyperuricemia, and then adequate amounts of copper can have a can actually inhibit antioxidase as well. So basically having a nutrient dense diet. And then, kind of, as you as you mentioned, if you are worried about, you know, fructose and fruits or whatnot, whole fruit would be the best way to prioritize first. And then, if you were doing fruit juice, something you can do is you combine some fruit juice with some with some of the dried fruits, and then you have the fiber with the juice as well. So if, instead of just having juice by itself, but having the fiber with the juice, can help the situation out pretty drastically by altering the rate at which fructose enters hepatic circulation, combining that with protein and fats as well, and like having an actual meal instead of just snacking all day long, can also alter the rate at which that fructose is hitting the liver because, again, it's a unit of time where large doses of fructose at a certain threshold per unit of time becomes a problem. And some of the studies, as we discussed, when they broke up the dosages over periods of time, they saw less issues. The other thing to keep in mind here is that a lot of these plant compounds, gallic acid, ellagic acid, chlorogenic acid, luteolin, quercetin, campferal catechin, epi catechin, hesperidin, norringen, nor engine hesperidin, anthocyanins, they all have functioning functions in inhibiting Xanthe oxidase and then increasing the excretion of uric acid at the kidney. So many of these different fruits. That includes, there's just a general list, mangoes, guavas. So mangoes also have magnaferin, which has a specific effect. But mangoes guavas, strawberries, all types of berries, apples, cherries, blueberries. What else do we have here? Bananas, grapes, lemons, oranges, grapefruits, limes, all of these pomegranates have beneficial effects overall, through the some of these specific compounds, and through their their content of vitamin C, and through the some of the vitamins and minerals to help deal with a with a hyper your Cemex situation. So overall, I think that fruits are generally helpful, and I would if you're having any issues with hypericemia, focusing on, perhaps adding some cherries into the diet, and then also having whole fruits, and if you're gonna have juice, combining that with maybe, like a dried fruit or a whole fruit, maybe having everything all together in a meal. And then we didn't really touch on protein sources, but you're the major purine protein sources is going to be really organ meats, shellfish and then, like yeast, but that wasn't really the main argument in their piece here. And I think protein, having adequate protein is more important than drastically limiting your protein intake overall, because you're worried about purines.

Jay Feldman 1:03:54
Yeah, and the nutrient density there in the organ meats, all that's going to heavily outweigh any uric acid concerns, but, yeah, I didn't want to, you know, I wanted to keep it centered on fructose, because diving into the other possible, you know, culprits for increasing uric acid would take a lot longer, yeah, so yeah, but I agree with what you're saying for sure. Yeah. And I would say also, if someone's dealing with gout, and likely the correlation there with kidney issues. I would also take a look back at our high blood pressure series discussing, you know, the context of high blood pressure. Obviously, they're having a big relationship, without having a tight relationship, with kidney function and also with uric acid. So I'd reference back to those episodes as well, talking about electrolytes and fat cell fat soluble vitamins and various other things to help improve a hypertensive situation that also don't involve reducing fructose.

Mike 1:04:53
Yeah, and other lasting piece is obviously clearing up the gut. So if you're having a lot of times, a lot of people that I've seen. With gout are usually guys, and it's usually guys who have pretty large bellies. And the large belly comment is not like to make fun of anybody, but to point out, usually a dysbiosis or an endotoxemia situation. So usually that large belly is a sign of inflammation, increased visceral fat, and then usually an endotoxemia that goes with the obesity and metabolic syndrome and impairment of liver function. So usually I see the combination of those, or I see it in patients who have kidney issues, and the kidney issues, again, is feature or product of metabolic syndrome. So a lot of these processes are driven by saying the like, similar etiologies. It's just how the individuals what the individual's predisposition is. And so fixing a lot of times gut is central in this. So fixing the gut in these situations, which can be accomplished by moving towards having adequate fruits and certain specific vegetables in your diet, getting adequate to your vitamins and minerals, having adequate amounts of protein, etc. And then maybe doing have putting in some interventions to try and alter the microbiome could be helpful in clearing up some of those issues. Overall.

Jay Feldman 1:06:09
Yeah, I'll link back to our episodes discussing, discussing gut health, digestion, ways to improve microbial balance, because, yeah, there's a lot to go into there. And as you're saying, overall, of course, these in general, being metabolic issues, endotoxin being a huge driver. There. We saw that with the fecal the fecal microbial microbiota transplantation study, very clearly, as far as how much of an effect that's having, obviously, in fatty liver. So yeah, and then, of course, I mean PUFA intake being another major one. But there's a whole, there's a ton of things that are involved in improving metabolic health and supporting energy production, and that's why we talk about that's why we have a podcast to talk through all those so I'll reference back to all the relevant episodes. But of course, if somebody is new here and they're dealing with gout and they're not sure where to start out, head back to Episode One and learn about the basics, foundations, things like how to support and optimize gut and digestion, blood sugar regulation, all that. Yep, awesome. All right, that's going to do it for this series discussing fructose and uric acid. If you did like it, please leave a like or comment if you're watching on YouTube and if you're listening elsewhere, please leave a review or five star rating on iTunes. All of those things really do a lot to help support the podcast, and are very much appreciated. If you do have any questions that you'd like us to answer on a future episode, feel free to send those in to Jay at Jay Feldman wellness.com that's j, A, y at Jay Feldman wellness.com or feel free to leave those in the comments. If you're watching on YouTube to check out these show notes for today's episode, you can head over to Jay Feldman wellness.com/podcast you can take a look at the studies and articles and anything else that we referenced throughout today's episode. And if you're dealing with any symptoms or conditions related to fructose and uric acid, maybe these are conditions that we've described throughout this series related to insulin resistance or diabetes, or maybe it's gout, heart disease or other metabolic issues. Or maybe you're dealing with various symptoms that are less tightly related to fructose and uric acid. Maybe it's chronic cravings and hunger, low energy or fatigue, chronic pain, weight gain, gut issues or digestive symptoms, brain fog, poor sleep, hormonal imbalances, or various other low energy symptoms. Then head over to Jay Feldman wellness.com/energy, where you can sign up for a free energy balance mini course, I'll explain how these different symptoms and conditions are really caused by lack of energy, and I'll also walk you through the main things that you can do from a diet and lifestyle perspective to maximize your cellular energy and resolve these symptoms and conditions. So to sign up for that free energy balance mini course, head over to Jay Feldman, wellness.com/energy, and with that, I'll see you in the next episode.