Auto-transcribed and lightly edited for readability; speaker labels added by LIV3. Timestamps follow the published episode. The views expressed are the speakers' own. Individual experiences described in the conversation are anecdotal, are not typical results, and have not been evaluated by the FDA.

00:01 Welcome, and introducing Chris Mearns

00:01Burres:Hi, my name is Chris Burres. I'm a longevity expert and the chief scientist at a lab focused on a longevity molecule. My primary focus is to help people live longer and better lives with science. Make sure to subscribe and share so you and your friends can live longer and better, well, actually, so you and your friends can live beyond the norms.

00:23Burres:Hi, and welcome to the next episode of the Live Beyond the Norms health and longevity podcast. You know that fructose is bad. What if obesity, diabetes, cravings, fatigue, and even metabolic burnout are not separate diseases at all, but symptoms of one ancient survival program running nonstop inside the modern human body? Our next guest, Chris Mearns, is here to help us understand and unwind the ancient survival program that may be holding us back.

00:51Burres:A little bit about Chris, well, aside from a great name, Chris is a metabolic researcher and founder of Liv3 Health, where he studies how fructose metabolism impacts cellular energy, cravings, food, fat storage, insulin resistance, and long-term metabolic health. He recently published research that explores how fructose metabolism may contribute to insulin resistance and metabolic dysfunction, which is really the root driver of almost all chronic illnesses. His mission is to uncover and share the actual impact fructose has on metabolic dysfunction and therefore all chronic illness. Hopefully, we can help him with his mission in this interview today. Chris, thank you so much for joining us today.

01:34Mearns:Thank you so much for having me, Chris. It's great to be with you.

01:36 Growing up in Vancouver, with no health background

01:36Burres:All right, before we get to your area of expertise, I like to go back, I like to go much further back. What was it like growing up, little Chris? Where did you grow up? What were your parents like? And if there was some event or someone you could pinpoint as the reason you would ultimately become a metabolic researcher and health educator, who would that be?

01:53Mearns:That's an interesting question. I grew up around Vancouver in Canada. Great childhood, memories of just running around and playing and all that good stuff. Most of my career kind of took me a different way. I got into user research, user experience, marketing, stuff like that.

02:21Burres:Before we go there, so parents, were they in the health and wellness space? I know you've spent some of your career in marketing, entrepreneurship. What were their roles that they played in your childhood?

02:33Mearns:Yeah, no, I've got a nice family. I've got an older brother and parents. It was good that way. The way we ate as kids was what you'd see in the 80s, it was basically... what's the name of that famous cookbook that everyone would use?

03:00Burres:Betty Crocker, wasn't it?

03:01Mearns:Betty Crocker. Yeah, that kind of style stuff. Nothing too wild there. I have an indigenous background, so we'd enjoy some salmon that we would come across, but that was about as wild as our food would become. When I later got married, it was like I discovered cheese, it was like, oh, my mind was blown, there's more than just cheddar. It was a good childhood, but absolutely no real connection to health and wellness.

03:28Burres:How about school? How was school for you, easy? You had tough subjects? What did you excel at?

03:34Mearns:I think I was a pretty sharp kid. I did decently in school. Things came not too difficult, I would say, and I was happy about that.

03:50Mearns:I was super skinny as a kid, so I was like this spry little thing that could run. I think I took that for granted, because by the time I got married, I was 136 pounds soaking wet, if I remember right. I remember going to the gym at that point and asking, can I possibly gain a little weight somehow, because I don't want to look like a stick in my suit. I was happy that I had a fast metabolism, but I also kind of knew that was weird and that it probably wouldn't last. I had absolutely no concept of how these things worked. I think at that gym they basically made me a meal plan of eating more bacon and meat and stuff like that.

04:46Burres:I don't know why that sounds very particularly Canadian. You just eat more bacon.

04:51Mearns:Yeah, that's right. You got it.

04:53Burres:This is how we add muscle mass and potentially fat mass. You get out of high school and you study multimedia systems development. What was the path that you thought you were on going down at that time?

05:08 Career, agency ownership, and a slow decline

05:08Mearns:As a kid, I was into art and stuff like that. My dad was like, yeah, that's nice, but you're not going to get anywhere with that. He pushed me towards programming and things like that. I remember my very first job, even in college, I found myself going more and more down this path. It was like, okay, I'll do the programming stuff, the more analytical side, but I also wanted to keep the aesthetic and the creative side in mind. This was 2001, an interesting time, because those things were converging in a way, websites were becoming a thing where you could cross that bridge.

06:03Mearns:For the beginning of my career, I found myself more and more in that spot. I remember working at a major corporation on a UX team that was setting global standards for the way that things should work as far as like form.

06:18Burres:By that, UX is user experience, just for the audience.

06:22Mearns:Yeah. Meanwhile, I'm having conversations with the dev team that would be like, we can't build that. I'm like, yeah, I know you can't, here's a little snippet, you can build it. I found myself in this, I think that's probably what led me to this higher tendency of always looking at the bigger picture.

06:47Mearns:Eventually, that took me towards user research and those disciplines, where I just wanted to understand why things work the way they do and almost see the problem and the solution resolve at the same time. It was like, hey, this makes so much more sense, this is how things are supposed to work. That side of my brain just kept pulling on me and pulling on me. Eventually, that is basically what tripped me into this whole scene, where it was like, this higher solution kind of thing, like what are the actual problems that humans face, and is there a natural, ring-of-truth type solution that just becomes obvious out of it.

07:35Burres:We have something in common, we both have owned and operated digital marketing agencies. As you're owning it, which can be stressful, what's your health look like as you're going through this? You've started eating bacon at this point.

07:50Mearns:I didn't last that long, although I gained, I think, 20 pounds over the first year of being married. It's like changing in lifestyle, right? It's funny.

08:00Burres:What does your health look like as you're going through this business ownership journey?

08:07Mearns:Basically, after I got married, that lean thing kind of stopped. I think in the first few years of being married, in my early 20s or so, I gained probably 20 to 30 pounds, and not muscle, just kind of became sort of normal Chris. I didn't feel great, but I also didn't feel terrible. I think we ate okay. My wife comes from a health and wellness background, ironically, her family goes back decades in this area with supplements and stuff like that. Their family actually probably pushed it more on me, but on the other hand, the way that we ate was high calorie, it was all whole food, but not necessarily in any way restricted.

09:09Mearns:My health kind of just got a little sluggish as time went on. The stress from work started to build up, and my sleep wasn't as awesome as it used to be. My gut health didn't feel as awesome as it used to be, all that kind of thing. Any time I would try to exercise, I would find muscle tension that limited me.

09:38Mearns:So I would start and I'd do great for like a month, and then things would kind of fall off the rails a little bit. It's kind of stuck, because I was trying to get these good patterns going, and it just wouldn't stick. That was the case up until I was probably 35, 38 or so, a good solid 10, 15 years of just doing the best you can within reason, but not really giving your health any particular focus.

10:04 Becoming a father, and the first health research

10:04Mearns:And then that's when we had a little girl, and that was probably the biggest switch in my thinking. It was like, okay, I'm a little bit of an older dad here, and by the time she is graduating, I might be in really rough shape if I don't actually figure out how to take care of myself properly. So maybe I should look into that a little bit, and I started reading a few books, and eventually that curiosity kind of spiraled a bit and turned into this whole like, okay, holistically, how does this all fit together?

10:35Burres:So you start kind of visiting diet a little bit more, paying a little more attention to diet, working out. Did you get past that one-month mark, where you said you start getting muscle tension? Was there any trick that you needed to do there, or was it just pushing through?

10:56Mearns:Actually, there was, and that was probably my first trip into what you might call biohacking a little bit. I stumbled across someone that had developed a heavy variable resistance system, using latex bands, but in ways that wouldn't cause too much disruption on small joints that couldn't handle that kind of tension. The concept was, by using heavy bands, you're following the strength curve of your muscles. So I would work out, and it would be like this is probably the equivalent of like 200, 300 pounds at the top end, but it's only like 50 at the short end, at the extension.

11:54Mearns:And because of that, my tendons didn't hurt the next day. This whole concept of, hey, the burn that I'm supposed to feel is not there, and because of that the muscle tension shifted. I was definitely causing more resistance in my muscles, but the downside was kind of gone. I was like, hey, I can actually work out, this is pretty cool. I think that was probably the first step into something that kind of changed the way I was looking at health.

12:29 Discovering Dr. Richard Johnson and fructose

12:21Burres:And then when does fructose start to come on the radar?

12:29Mearns:I wouldn't say too long away from that. I read a book that set me down that path. It's by a metabolic researcher that has basically become a hero of mine since, named Richard Johnson. His team out of Colorado has been studying fructose for 20 years now, I'd say, and a lot of what we understand is a result of their team's work. Basically, he started off as a urologist, studying uric acid and kidneys and all that kind of dysfunction, and that led him to upstream realizing that fructose plays a large role in the accumulation of uric acid, and then things spiral from there.

13:21Mearns:So when I started getting interested in this, it was basically just reading one of his books and starting to see that there is an overarching picture of how our bodies are using this as a survival system. Because it not only explained experience and mechanism, but also explained why these things should work, and not from a "hey, sugar is toxic" perspective, but like this is actually something that's deeply rooted in our biology. Perhaps it wouldn't be unreasonable to say that most species wouldn't survive without this. That light bulb moment went off, it was like, actually, this is a miracle that we've broken. That really got me down this road, it was like, okay, I need to look deeper into this and figure out if there's more to this, and really what to do about it, because that wasn't really addressed.

14:21Burres:So talk a little bit about you kind of describing it as a miracle, right? Like, what is the benefit? And then when you say it's broken, I'll follow up with that, but what is this kind of miracle?

14:36 The miracle and the broken: an amplified switch

14:36Mearns:Sure. So you probably have seen this a number of times, but within biology, especially, too much of a good thing can become a bad thing. It's just a simple principle, you see it again and again. But in this case, basically, that seems to be what's happening is fructose, not as a simple sugar, but fructose as a signal, is telling ourselves to conserve. It's actually reducing the conversion of fuel into ATP by reducing the function of your mitochondria somewhat, and so it becomes this little bottleneck within each cell. Because of that, this conservation signal allows animals to conserve fat, conserve water, to use more of the food that they eat without burning it immediately. Just like an eco mode button in your car, that's a good thing, because this world is tough, because abundance is not widely available.

15:44Mearns:And what's kind of crazy to me is that humans have, of all animals, actually have a stronger version of the system. I know you are deeply involved with vitamin C research. So we don't have the ability to synthesize vitamin C, which would otherwise help clear out a lot of the antioxidants that build up from this process. That gives us, in a way, a little bit of an extra when it comes to fructose metabolism, which sounds like a bad thing, but it's actually a benefit if you're the dominant species, and just the species that wants to survive.

16:35Mearns:Similarly, we don't have the uricase gene, which would flush out uric acid, which is the step before that. Uric acid develops, that causes stress to your cell, then that stress you want to flush out with vitamin C and antioxidants, and the uric acid, you don't want that in there either, because that's going to lead to the next step. By not having that enzyme, the ability to flush out your uric acid as well, that would also ramp up that whole signal. So then suddenly humans seem to have this extra version of the fructose metabolism switch, so that we could theoretically survive harder times better than any other animal.

17:23Mearns:And then you look out the window, and you've got every animal that is just trying to get by. I remember going for hikes in the desert, and thinking, how do these animals live out here? I've got like four water bottles just for this two-hour hike, and they're not even thinking about this stuff. And yet we're the ones that are metabolically struggling constantly. So I don't believe that our biology is designed for excess, because the world isn't, and yet now that's exactly where we live.

17:55Mearns:We live in constant excess. So then this wonderful system that would help us to survive is now being constantly, chronically activated in so many ways, far beyond sugar. And that is really what is causing long term effects. So you think about it this way, if you've got your eco mode button on your car on, and you forget it exists, and all you're doing is driving around with the foot to the floor, and can't figure out why this sports car is not actually going anywhere. It's like something's broken.

18:41Mearns:And that's really, I think, what the stage that we're at now is, that we're finally realizing that we do run at a higher level of performance, but none of us are actually aware of the dial. Like I mentioned, I grew up with this fast metabolism, I was this scrawny little kid, and anyone that's in that position eventually breaks that, because our metabolism eventually slows down. So we have this innate concept that our metabolism is variable, that we can dial it up or down, and yet we don't know what that dial is. I think this is that dial. This is the one where it's saying, I've been programming my body through my environment to conserve my entire life, and now I can figure out how to actually turn my metabolism up again.

20:33 Nature's eco mode: ripening fruit and migrating birds

19:33Burres:So the broken is just too much access, right? Like we broke it because we have so much access.

19:40Mearns:And then I think the way that I think about it, really, I can learn this from Dr. Stephen Gundry in one of his books. He describes it this way, he's very kind of anti-fruit and fructose specifically, probably. The way that he describes it is, when you are about to go into winter, you need to put on fat because there might not be food, and that is when you actually have access to some fruits or berries. And then when you come out of winter, you probably don't have much fat, because you survived, and you need to put on fat because you don't have any left. Again, fruits and berries, seasonal fruits and berries are available.

20:27Burres:That's the kind of benefit mechanism that you're talking about, right?

20:33Mearns:Exactly. And it's so obvious in nature, just in the ripening process. Fruit is always going to be ripest right before that season of scarcity occurs. And it's not just in northern environments like ours, in tropical environments fruit ripens right before the dry season. It's the same thing, there's a season of scarcity coming, and that scarcity is not just in food, it's also in water. And so you kind of want that maximized version of yourself so that you can survive the difficult time ahead.

21:13Mearns:And that's why it's interesting, because this goes far beyond just what you eat, this same signal is activated in the scarcity itself. For example, you might look at migrating birds, there's a bird that flies from Alaska down to New Zealand, and it's not a small thing, that crossing is insane, what they do, because they can't land. They make this roughly 3,500 mile journey that takes ages, and they need to be able to get there without food, without water, without stopping. So what they do is they build up their reserves really strongly before they leave.

21:58Mearns:And that gains weight, and as they gain weight, they're bottlenecking their cells so that those cells start conserving, so that as they then start expending that energy on that huge journey, they're not giving it all away. Then the moment they take off, when they don't have access to water, that also stimulates the same conservation effect. That dehydration is allowing the stored glucose to be converted into fructose, so that they keep that conservation signal going, and then they can actually get there alive. So it's like this same signal happens across nature, in so many different places, and it's really quite fascinating.

22:45Mearns:It's just this constant: is there tough times ahead? Then let's do what we possibly can to prepare for it, and make sure that we don't die. And if we are running that, not just from sugar, but from dehydration, which is also a high salt diet, or from alcohol, which is sending the same signal of dehydration, or from having too much glucose in our body, like high glycemic carbs, all this caloric excess, that is what gets converted into fructose. Then suddenly we're turning on every single switch in this same biological pathway simultaneously.

23:31Burres:So these biological systems will actually make fructose, right? So in a dehydrated state, in preparing for this, we're in a dehydrated state, maybe alcohol is giving the signal, or even providing some of the fructose. How does fructose metabolism differ from other fuel systems in the body, and why do you believe it has a disproportionate impact on metabolic health?

24:29 Fructose reclassified as a signaling molecule

23:54Mearns:Great question. So sucrose, or table sugar, is 50% glucose and 50% fructose, we know that. And we have very much been focused on glucose, of course, glucose is fuel, we know that, it's fuel. For some reason we kind of think that too much fuel is the root of all evils. Logically, that's problematic, that's like saying too much fuel in your car is the reason it won't go when I hit the gas. So just put that aside for a moment.

24:29Mearns:There was research by that same doctor, Dr. Johnson, maybe three weeks ago, where he just released a review that effectively reclassifies fructose as a signaling molecule. It says that it's not just a calorie, but it is a signal that regulates, and I quote, metabolic health and disease, and it does that by influencing energy. So now you've got sucrose, which is fuel, and a fuel regulator, at the same time. That sounds totally contradictory, but it actually makes a lot of sense, because if you've got this fuel arriving, this excess, don't you want to keep more of it?

25:15Mearns:It would make good sense from a survival biology standpoint. We're eating glucose in various forms, and because we're eating sugar, we're trying to shuttle more and more of that into storage rather than immediately burning it. Because of that, too much glucose can become problematic. But let's think about that car for a second, the problem with too much fuel usually arrives when the fuel turns bad, because you just never used it.

25:57Mearns:And I know that's a loose logic thing, but that concept actually holds up with our biology as well. Because the same doctor has been testing this for a while, and they found an interesting case where they would give rodents high amounts of glucose, and according to this system, that high blood glucose would then turn some of that glucose into fructose. So what he did is he gave those same rodents a fructose kinase inhibitor, so that they couldn't actually metabolize any fructose that was converted, and basically the metabolic dysfunction that we would normally associate with high glucose went away.

26:39Mearns:So it's not the fuel itself that's the problem, it's when we're actually causing this bottleneck inside ourselves. That's really a main reason why, when you put this all together, you start to get this concept that all chronic disease shows a preclinical state of impaired cellular energy, even before we diagnose it and say, okay, this is fatty liver, this is cardiovascular disease. It already shows this preclinical state of poor cellular energy, and this is actually what is causing that poor cellular energy. The entire organism goes into this conservation state, just because it's trying to survive, and eventually those systems start crashing, because you can't have fragile, poor-energy cells that cascade into fragile, poor-energy systems without eventually something breaking.

27:45Burres:So this fructose kinase, so you're giving rats glucose, right? Not sucrose, glucose only, because sucrose is both glucose and fructose, you're giving them glucose. Normally these rats would take some of that and convert it into fructose, right, because it becomes a signaler. And in that study, they gave a fructose kinase inhibitor. What is that, and what is that function? How does that work?

28:17 Inside the cell: the funnel, ATP, and fragmented mitochondria

28:17Mearns:Okay, so I didn't mention this before, we talked about how glucose and fructose compare. Glucose is highly regulated, from an enzymatic step, like the door shuts when the cell has enough glucose, it says, okay, I can't use any more. But fructose does not have that, the enzymatic step is completely unregulated, so you can give all the fructose you want to a cell and it will keep taking it.

28:52Mearns:Which is interesting, it's like, why? But it makes sense from this perspective, because it's not actually a poison to the cell, it's just regulating it down and down in its energy usage, dialing this metabolism step. So fructokinase is that first step, and effectively what it does is it burns your ATP. Normally, when ATP drops to ADP, a tri-phosphate into a dual phosphate, it can be recharged again, like a little rechargeable battery, but this pulls a phosphate out of that step. It's almost like you're degrading your ability to recharge the battery.

29:36Mearns:And because of that, the cascade continues, and it ends up that ATP, which was a little battery, is actually converted into uric acid, which is a waste product. That waste product then causes stress to the cell, causes reactive oxygen, and effectively it starts, it doesn't kill the mitochondria, but it starts fragmenting it. We always see pictures of mitochondria, they look like little jelly beans, but in reality those jelly beans can be longer, and they can actually become a network where they connect to each other.

30:18Mearns:When that happens, they're super efficient at converting glucose into energy, into ATP. But what this does is it starts fragmenting that network, so it doesn't kill anything, but it reduces its efficiency, and it literally changes the structure. That basically is what is dialing down our energy. So fructokinase is that front door, it's like if that doesn't happen, then it doesn't start this cascade that eventually leads into not just a transient drop of ATP, but it actually changes the structure of the cell to conserve.

31:04Mearns:And that actually explains why you've got contradictory research, where some research will say you can have a whole pile of fructose and you won't get sick, and then of course we've got other research that basically suggests that fructose is causal of all metabolic disease. If you look a little closer, those studies on high fructose flux are often like a month long, and it's not long enough to cause this structural change where the cell starts reducing its energy output and everything starts to cascade after that. Those other studies go much longer, they basically show that this is fundamentally breaking the metabolic rate and it leads to disease.

31:57Burres:And the fructose kinase inhibitor stops that process from happening.

31:59Mearns:Exactly. So effectively it allows the body to not metabolize fructose, it's not a digestive thing, it's actually within the cell. And normally that would sound like a bad thing, but the body has other means of basically just eliminating it. There's actually a natural experiment, a genetic condition called essential fructosuria, where people don't have this enzyme and they just pee it out, that's why it's named that. They found sweet urine, where there was just high levels of fructose in the urine, the body doesn't use it, it just gets rid of it.

32:39Mearns:And what's fascinating about that is it actually backs this up. Those people with that condition are very healthy, they don't generally ever get metabolic illness. Even finding people that have this is really hard, because how often do you ever do a test for something like that? But when the test is done, it's like, whoa, okay, this might explain why you're actually a pretty healthy person.

33:05Burres:Interesting.

34:04 Mitochondrial dysfunction, hunger, and insulin resistance

34:04Burres:So how does mitochondrial dysfunction alter the way the body stores fat, and then also regulates hunger?

34:11Mearns:Okay, so let's imagine, I don't have one, I need to bring a funnel out here, but imagine a funnel. On the top side of the funnel you've got the glucose going in, that's the fuel itself, and at the center of the funnel it would convert that glucose into energy, ATP. So then you imagine ATP coming out of the funnel. If fructose is pinching the funnel, if that's a variable pinch there, then it starts to explain things. Energy only drips out, so the cell is really functioning at a low state.

34:57Mearns:And if that's the case, it makes a lot of sense logically why it would tell the body that I'm starving, not in a gut way, but in a cellular energy way. That is effectively what happens, it influences ghrelin and leptin, so that our satiety doesn't really exist anymore, and we're always craving more. So then what happens is we go back and we eat more, but that doesn't change the pinch point. If anything it will make it worse, because typically it'll mean more exposure to fructose.

35:28Mearns:So what happens is the top side gets more and more overloaded, where you've got this overspilling funnel full of glucose, but still pinching that little conversion mechanism more and more. And so it actually resolves why cravings exist, why we have caloric excess, because that's part of the challenge with the calories-in-calories-out model. It's like, well, I am already overweight, I am already overfueled, so why am I consuming more than I should? It resolves that kind of concept.

36:07Mearns:It also starts to resolve why insulin resistance develops, and saying it's not actually a cause, but it's an effect. Because if you think about it, if you were to insert too much substrate into those cells, too much glucose into that cell, it would actually cause a toxic reaction, too much substrate, and the cell would start to fail itself. So then if insulin resistance is pushing back and saying, I really can't use any more of this glucose, then it makes perfect sense why insulin resistance would become part of this picture. It's trying to hold up this giant amount of glucose because it simply can't process it, the little factory is just too impaired.

37:01Burres:Yeah, the bottleneck is too restricted. So talk about the paper that you have currently that's under peer review right now.

37:08 The peer-reviewed paper: hysteresis and the hole in the bucket

37:08Mearns:So I have no interest in competing with Dr. Johnson's work, they're just brilliant people. But what we started to see is that this is showing a higher causal synthesis of everything that's going on. Their research says, yes, this is causal for metabolic dysfunction.

37:32Burres:When you say this, the excessive glucose is called, fructose is causal?

37:40Mearns:Yeah, because we have so much research that basically, their review just said, it is a regulator of metabolic disease. So if you have too much fructose, then it's very causal when it comes to developing metabolic disease. Our research paper is attempting to create a hypothesis that puts all of this together. Really, the reason that it is causal is because of this energy change, it's shifting how the body produces energy.

38:14Mearns:And there is another doctor named Wallace, who wrote in 2013, some papers that effectively suggested an energetic model of metabolic dysfunction. So it fits this perfectly, he's basically saying cellular energy seems to be one of the major roots of what's happening here. Like we mentioned, you look across chronic disease, and the signal is there, not just poor cellular energy, but it also has this separate signature, we see insulin resistance, we see inflammation, we see high uric acid, we see mitochondrial dysfunction, all sorts of different things. It kind of starts to show that maybe this is all connected.

39:05Mearns:So what our paper is trying to do is show that we've had all of these ideas, and they're all correct, let's just put them in order. We've got this cellular energy issue that's right there with all chronic disease, we've got now fructose metabolism that directly drives a state of low cellular energy. It doesn't say that all chronic disease is caused by this, we know cellular energy can be impacted by any number of things. But the fact is that we are activating fructose metabolism insanely, and unlike we used to, this is a totally modern problem.

39:51Mearns:This is all about our access to sugar, our access to food, anything we want to eat, and as much of it as we possibly want. In fact, those foods are cheaper, and so it makes sense why you would see poorer demographics, for example, have perhaps even more exposure to these outcomes. So fructose metabolism activates it. There is another doctor who suggested a cascade called the cell danger response, and the idea there is that basically a cell at a certain point will come into a defensive posture.

40:33Mearns:Normally it'll do self-repair, it'll work very well, but at a certain point some kind of stress will cause it to basically just hang on to life. And I believe that this is basically causing that posture. So we get this big long chain of fructose dropping cellular energy, putting everything into a defensive posture, and then we start to see dysfunction happen because of it.

41:03Mearns:And what our paper adds to it, besides synthesizing it all, is that we're starting to see that there's a hysteresis effect, which basically means that you can drop into that defensive posture far easier than you can climb out. Because the mitochondria have restructured themselves, because everything is literally running at a conservation posture, then getting back up to that homeostasis of just self-repair and feeling great is a climb. And it doesn't necessarily just mean getting rid of the insult, fructose, it means somehow boosting everything back up to the way it was.

41:55Mearns:So all of this health and wellness stuff for decades has been adding energy into the bucket. We've got everything trying to add antioxidants so we can influence better cellular energy, we've got everything from red light therapy to whatever, where we're trying to stimulate more energy. And this is arguing that there's a hole in the bucket. So everything works completely together, we do need those boosts, and this doesn't take away from any of that. But we, more importantly perhaps, need to patch the hole in the bucket, because then all of a sudden all of that extra work that we're trying to do will actually climb us out of that defensive state.

42:46Burres:Your product is a fructose kinase inhibitor, right? And in one of the interviews that I saw you did with Maddie, you talked about a pharmaceutical company that went down this path, but for some reason they stopped. Can you share that story?

43:05 Why this fits a supplement better than a drug

43:05Mearns:So just to be totally transparent, as a supplement I can't say it's a fructose kinase inhibitor, that would be a drug claim, so we can't say that. But the preclinical research on the ingredients definitely says that that's the function, and that's why we're interested in it. What we observe fits this perfectly. So pharma did go back down this route, and they're continuing to explore this, I don't know the business reasons why they would choose to stop certain trials. But I do think it's possible that this hysteresis effect, of not being able to actually restore, might be part of it.

43:55Mearns:I think that fundamentally this is a big deal, that we need to defend our cellular energy. I also think that little climb back out of it is going to be a big part of it, so they're looking for the best way possible of causing a disease state change. And so in a way, this fits a supplement perhaps much better than it fits a drug, if that makes sense.

44:17Burres:Are we trying to block fructose so that it doesn't get into the cell? Or are we trying to break down fructose? In an ideal world, would we make fructose go away entirely, or make fructose sit at the right percentage? What would we ideally want, in your opinion?

44:47Mearns:That's a good question. So if fructose has a biological purpose of conservation, it depends on your goals. If your goal is to conserve energy, then you want exposure to it. If your goal is not to conserve energy, which I would say is like 99% of humans, unfortunately, then it makes sense that we would want to dial that down to the extent possible.

45:17Mearns:Maybe in certain disease states, it's a survival mechanism, right? During COVID, I think I knew someone who was just a machine of a man, working out all the time, owned a gym, and he got COVID and he wasted away because he had no body fat. So we appreciate that fat actually serves a beneficial purpose, it's kind of like a little bit of an insurance policy on our biology, we do need it. You drop down to super low numbers of body fat and it's weird how you actually have the same symptoms of having too much body fat, there's this perfect little spot in the middle where hormone regulation works well and all these other things.

46:17Mearns:So in the same way, if our body is in a really fragile state, then maybe a survival mechanism does make sense. But for most of us, we're finding ourselves where we probably need to drop body weight and open up our cellular energy, because that's really what is the biggest burden. So it depends on what the goal is.

46:43Burres:So do we want to take fructose to zero? Do we never want to take fructose to zero? Where are we operating? Let's say I want 15% body fat, and fructose has a big impact on whether you're storing it or potentially burning it. What do we want to accomplish? Do we chop it off, like a bodybuilder bulking up and then cutting, do we stop it and see where we land? Is that a less elegant but viable solution?

47:19Mearns:As I said, everyone's goals are going to be different, but fructose kinase is a disposable enzyme, and fructose itself is not necessary for biology at all, we don't need that signal. So I would suggest that most people would probably be happier to get rid of it entirely. That said, it's not possible, because if our body is converting glucose into fructose, then you can cut out all the sugar you want, you can never eat fruit again, which I do not recommend, you can never drink alcohol, you can never have high glycemic carbs, keep your glucose levels perfectly level, you can never find yourself in a hypoxic state, that's another activator, you can never have high stress, stress is another activator of converting glucose to fructose.

48:23Mearns:So there's so many inputs here that it's baffling, and they all map back to everything we've talked about for health and wellness for decades. Lower your salt, don't drink so much alcohol, drop your sugar, all of these things, it's all the same thing, because it's all basically mapping to fructose. So you can't eliminate it entirely, but we can turn down all of those signals with diet and lifestyle. And if we could also turn down the enzymatic reaction, where the problem is really happening, that wouldn't be a bad thing, because it almost, I love this concept, it kind of allows us to stop this obsession about health a little bit.

49:12Mearns:The reason that we have these conversations, and health and wellness is a major part of our entertainment industry at this point, is because all of us are struggling. We've got squirrels running around outside that have absolutely no issue with tracking macros and having all these different obsessions about health, but we go and hang out with friends and immediately our conversation turns to a family member that has a major chronic disease and we're worried about them. This is rightly so part of our daily conversation, but if it's all kind of hanging on this one enzyme, then if we turned it down, it could make a big difference to our culture in general, where we can just enjoy food a little bit more liberally without the obsession of whether or not it is a healthy food.

51:09 What a fructokinase inhibitor does, and unboxing SugarShield

50:11Burres:So I think you might have explained this and I missed it, but fructose kinase inhibitor, is that stopping our process of making fructose? Is that interrupting fructose as a signal? Just like the genetic mutation where they just pee out the fructose, if we found this ideal fructose kinase inhibitor, what's happening to the fructose?

50:39Mearns:Yeah, so it effectively mirrors what's happening with that genetic condition, where your body digests it, but any place that it is metabolized, that signal is blunted. So then the ATP drop and the uric acid buildup and all those changes that happen downstream, that's the part that doesn't happen. And yeah, just like that genetic condition, our body just kind of finds a way to eliminate it.

51:09Burres:Okay, talk about SugarShield. I got some SugarShield right here, you graciously sent me some, I was waiting for this interview before I jump into it. It says on the site, FructoseControl. What am I holding here?

51:23Mearns:So that is a liposomal high dose of luteolin, which is included because of the preclinical research that shows that it inhibits fructose kinase. It also includes tart cherry extract, which is studied for its ability to help with uric acid levels. So in both steps there, it's trying to reduce activation of fructose metabolism as much as possible, and then clear out the byproduct that has been generated by it for so long, so that the mitochondria have this opportunity to relax from their stressed-out state and hopefully start to build up that self-repair a bit.

52:15Burres:So it bookends perfectly with everything else that we've been trying to do for decades.

52:21Mearns:Exactly. I take high doses of vitamin C, I take ubiquinol, I take EGCG, I do all of that stuff as well, because I'm trying to get that mitochondria functioning as fast as possible. But what this does is it tries to protect the energy that's already existing, and protect it from what is very likely its biggest stress.

52:49Burres:So get rid of that bottleneck in the funnel, as you kind of described in the beginning.

52:54Mearns:Exactly.

52:58Burres:What are some of the results, and then we'll get into our wrap-up question. What are some of the results, your feedback you're getting?

53:04 Results: food noise, energy, https://liv3health.com/pages/brain-fog, and the luteolin data

53:04Mearns:They're stellar, like insanely good. I'd say about 80% of people that are taking it find that their food noise is gone within the first month. I'd say on average it's three to four weeks to a point where people are saying, okay, I know it's not a placebo anymore.

53:30Mearns:Energy levels climb in a way that is not like a stimulant, it's like your baseline just raises. And there's definitely evidence of a shift in brain fog, which makes sense because fructose doesn't make it to the brain, doesn't cross the blood-brain barrier, but our brain runs on glucose. Hyperglycemia in the brain still does cause fructose synthesis in the brain, and it's super targeted, so certain areas of the brain are dialing down their energy. This, again, gets rid of the bottleneck so that it dials back up, so brain fog is a huge shift in many people.

54:03Mearns:And then basically what happens with that food noise that drops off, energy increases, clarity increases. Because the food noise drops off, it mirrors what we're seeing in a lot of peptides, like weight loss peptides, our caloric restriction starts happening naturally. You actually gain a little bit of agency over your food choices, it's like, yeah, I'm full, I don't need that anymore, or you can just say no.

54:33Mearns:It's like, actually, that's what happened with me when I first started taking it, we didn't know what to expect at the time, we were just totally experimenting. It was maybe a month in that my wife and I just sort of looked at each other and said, we should make some cocktails, and both of us were like, I don't feel like it. It was enough of a very potent shift in desire that it stood out in our minds.

55:06Mearns:And right at the same time, that whole nine-thirty, ten o'clock craving to go and rummage the cupboards for a bowl of cereal or whatever also disappeared. So because of that, I ended up losing, I think, 25 pounds over the next three months or so, it was just easier.

55:31Mearns:But mechanistically, I should mention that there is an interesting set of randomized control trials on the ingredient itself, luteolin, that we are very interested in. This is not SugarShield, and it's also not liposomal, so legitimately probably a far lower dose than what we have here, but it's baffling how closely it parallels the randomized control trial results that we saw in those pharmaceutical inhibitors. I'm talking a 43% reduction in insulin resistance on HOMA-IR, a 22% reduction in liver fat, massive changes to triglycerides and cholesterol and waist circumference.

56:27Mearns:And honestly, all of those things almost mirrored what the pharmaceutical trials were showing. So I think when you've got the mechanism, you've got the biology, you've got the survival motivations, you've got RCTs that show parallel results, it's just everything lines up so neatly. It's incredible, even to the point where I've looked at this from a historical standpoint, looking at the timeline of our exposure to sugar, and it fits so perfectly, I think it's very fascinating that we're actually seeing real results in people too.

57:16Burres:Very cool. All right, before we get to our wrap-up questions, is there anything we didn't touch on, or any summary you would like to provide our audience?

57:24 Closing case: one disease, and the PCOS reclassification

57:24Mearns:I would just love for people to explore the idea that all chronic disease is one disease. I know how crazy that sounds, but I think all of the systems biology is showing that that's where we're going. We've been talking, especially I'd say insulin resistance in the last year or so, where we're realizing that this is central to so much. PCOS was just reclassified as a metabolic disorder, like four days ago.

58:01Mearns:We're seeing that metabolism is at the center of everything, and it holds logical sense, because if you have no cellular energy, you have a fragile cell, and if that fragile cell then cascades into the whole system, of course disease is going to emerge out of it. So I love that what we're doing here is we are in a very real way trying to say that SugarShield supports your healthy metabolism. And I know that, yes, every supplement says that, but really I think that might be the true root of what we're trying to achieve here, having healthy cells so that chronic disease doesn't emerge out of them.

58:52Mearns:And for as much as we have toxins and environmental issues and viruses and everything else, things that do influence cellular energy, fructose is absolutely saturated in us, and it's the lever that probably is the most movable, and probably the one that moved on us as well, because our biology wants sugar. There's a reason why every single animal loves it, and it doesn't make sense unless it's a survival function, like, of course, that's probably why our tastes developed.

59:21Mearns:So as much as we might want to villainize fructose, or villainize major corporations that are trying to make food easily accessible, this is just us, we like this stuff. So trying to tell people to restrict is a really difficult challenge, but it doesn't change the fact that this is pretty central to our biology. So if we have a way to open things up a little bit more, I feel like it's going to have a major impact.

59:56 Wrap-up: longevity targets, protocols, and where to find LIV3

59:56Burres:Excellent. All right, well, let's get into our wrap-up questions. Chris, do you have a target age that you want to live to?

60:04Mearns:I would say old enough that I still feel good.

60:12Burres:And we don't want that to be next year.

60:16Mearns:No, that's right. I think health span is so important, I remember a chart where it's like people's health just drops like this, and what we want is to be healthy and then die.

60:30Burres:So how long do you think humans can live?

60:35Mearns:A lot longer than we currently do. I think we could probably easily cross a hundred, and I think this is probably the major issue holding us back right now.

60:49Burres:So if we jot down a hundred, how long would you like to live? What two to three protocols, habits, mindsets, let's call them shortcuts, because everybody likes shortcuts, to longevity and healthspan would you share?

61:06Mearns:Definitely doing everything you can to control fructose metabolism. And exercise, exercise is really doing a lot to open up your mitochondrial health more than anything else. I am a strong believer in high intensity resistance training, but in short amounts, and in zone two exercise, just getting movement and allowing your body to use the fuel that it has.

61:43Burres:What are one or two things you think people get absolutely wrong regarding longevity and healthspan?

61:49Mearns:I think that we need to focus on sugar. I think we know it, but I think we need to really take a harder look at that. If reducing sugar is recommended for and helps every single chronic disease, we have to ask why, that is a signal, is that just a coincidence? I think that we've got all these different things going, but I think this is the elephant in the room that we really need to pay attention to.

62:18Burres:Excellent. And Chris, how can people contact you?

62:25Mearns:Our website is liv3health.com, and I have a YouTube channel, it's just a little fledgling thing where I talk about a lot of this stuff, because it branches into every single corner of health. It's called The Fructose Model. And you can find us on Instagram at Try Liv3.

62:55Burres:Excellent. And what in the near future are you excited about?

62:58Mearns:I'm excited to see dialogue shift around this. I think that recent study that reclassifies fructose as a signaling molecule needs a lot of attention, because it literally says it's a regulator of health and disease, and I believe that is absolutely true. I think that if we start to appreciate its role, then we can have some insane downstream effects that will probably shift our culture in the next number of years, not to mention all of the effects within our own families of the results of this problem.

63:35Burres:All right, you can find him at liv3health.com, on YouTube it's The Fructose Model, and Try Liv3 on social media. Excellent, Chris, thank you so much for joining us today.

63:48Mearns:Thank you, it was great to meet you.

63:51Burres:I hope you enjoyed this episode of the Live Beyond the Norms podcast. Make sure to subscribe and follow, also make sure not to be that guy, the guy sharing this podcast with people who are not interested in living beyond the norms.