Sugar, Protein & Aging: Two Metabolism PhDs on Surprising New Science

What have you heard about the sugar diet? This is the weirdest nutrition trend I've been seeing. Sour Patch Kids, sodas, fruit juice, in order to improve athletic performance and lose body fat, which is very counterintuitive. Based on this diet, you kind of could design like an ice cream diet that would boost your metabolism, which is pretty crazy.

They didn't actually do any sort of proof of any of the mechanisms.

Well, I'm going to get into that because it looks like FGF21 might defend muscle mass.

I think it's exciting in, in regard to what you alluded to earlier.

We both looked into chlorogenic acid, a really polyphenol found in coffee and yerba mate. What do you know about this molecule? Is it something people should try to get in their diet? All right everyone, I'm here with, uh, Nick Verhoeven from the Physionic channel. Hopefully you guys know him. If you don't, go see our prior, uh, interview on seed oils. We're gonna now be hitting another controversial, uh, and hot topic, the sugar diet. So I'm gonna roll right into it. Uh, Nick, what have you heard about the sugar diet?

Actually very little until I saw your video.

Okay, fine. I guess I'll give my overview, which was, this was something that really caught me off guard. I would say this is the weirdest nutrition trend I've been seeing where there are people, including people that are previously in say the low carb space, say no, now I'm going low fat, low protein, and just eating a bunch of sugar. And when I say a bunch of sugar, I mean like Sour Patch Kids, sodas, fruit juice. I had some Sour Patch Kids, Starburst, Jelly beans, 8 ounces of apple juice, sugar on the bottom, sugar on the top. Sugar. In order to improve athletic performance and lose body fat, which is very counterintuitive. Now, when I saw this happening, there was definitely a part within me that was like, this is BS, and you just wanna call BS and move on. But my lovely audience did twist my arm to go down the rabbit hole on it. And coincidentally, there was a really fascinating trial they came out in the Nature Metabolism, which is one of my favorite journals, on a hormone called FGF21. And the story evolved for me. So let me just confirm, I think I shared that paper with you. Did you have a chance to read it?

I did. Yeah.

So why don't you give us a breakdown of what they did? To remind everybody, if they haven't seen it, like Nick said, a video on this, which you can want if you want the breakdown with all the flashy me making Sour Patch Kid balls and stuff. But if you want the, the measured calm summary, Nick's about to give it to you.

I don't know about that, but I get in general. So I guess the, the study was, had an animal arm and a human arm who's mainly focused on the, the human aspect of, of how a very low protein diet could affect metabolism and weight gain and consumption patterns and things of that nature. But they were specifically focused on a particular hormone that we can get into. I'm sure we will get into it. But the idea being that they gave, it was a pretty small sample size of young, healthy men, and they were told to go from a, their normal nutrition to a very low protein, either very high carbohydrate or very, well, I shouldn't say very because it's not like ketogenic or anything like that. Relatively high fat diet.

It was 9%, 41%, 50%. So 9% protein was low protein and then it was a high carb 70% and then high carb, high fat 41% and 50%.

Yeah. And then they, they measured over, they had a few different kind of studies within this study, but for the main one they measured over 5 weeks to try and they maintained weight. But the only way that they could maintain weight, which was very peculiar, was for the low protein condition because they compared this against a higher protein condition, which I think was double the protein. The low protein condition, they had to increase their food consumption simply to maintain their weight, which was extremely peculiar. So then they were wondering what exactly is happening there. And that's what leads into the story of FGF21.

Yeah, so to double-click on what you just said, they had, they had 3 sub-studies. Basically all these sub-studies in humans where they put them on a low protein diet and 9% of kilocalories to see what it would do to their energy output. Again, all young healthy men. We will get into the limitations and also the studies that are upcoming because I actually had a correspondence with the senior author recently. So they have some follow-up trials coming. But bottom line is, yeah, energy expenditure increased by about 20% irrespective of the other macronutrients. So whether it was a mix of fat and carbs or just mostly carbs, energy expenditure went up by about 20%. So in the first study, I think it was like something 573 calories. I'm converting from megajoules. I don't know why they use megajoules. Who uses megajoules? But whatever.

Yeah.

So the energy expenditure went up massively. They needed to increase their intake by about 573 calories and they still over 5 weeks lost a kilogram without any significant change in lean mass. It was a non-significant change, but also again, they lost a little bit of weight, so it's hard to say what's going on there. And their protein balance actually looked pretty similar. So changes in nitrogen levels in the blood and all that. So it was really surprising to me that protein restriction could cause this degree of increased energy expenditure, which this was not, to be clear, a, a sugar diet study per se,, but it does explain what we're seeing on the sugar diet. So people talking, you know, in the space about spiking their FGF-21 levels on the sugar diet, it's just that the story, the underlying physiology has more to do with the protein restriction. That's a consequence of eating a sugar diet rather than the sugar itself per se. Would you agree with that assessment?

Yeah, absolutely. I mean, it's clear as day when you look at the fact that they were able to replicate the results with a high fat or again, higher fat and higher carbohydrate.

Which is super interesting because it means like it, it, it's counter to common knowledge in a few ways. One, that higher protein is generally better for, for weight. And obviously it's multifactorial. There is a thermic effect of food, which I mean, yes, it's a factor, but you're not hitting 600 calories a day with thermic effect of food. And then there's a society aspect, but also people say, oh, combination of fat and carbs is, you know, bad, but Based on this diet, you kind of could design like an ice cream diet that would boost your metabolism, which is pretty crazy. We will talk about the other extreme, which is a, a ketogenic diet, which they did not study because they didn't do just a high fat. Actually, I'll, I'll just reveal, me and some people are trying to replicate this and we're getting similar results. So from a higher protein ketogenic diet to like a 4:1 ketogenic diet, which is 90% fat, 2 of us have done it thus far and we've both seen a big increase in energy requirements. So it does seem consistent across the spectrum of, it doesn't matter what the other macronutrients are. If you restrict your protein, it does appear energy expenditure increases because of this hormone, FGF-21. Now just to complete the story, then I'm gonna ask more questions for you. Basically, as you said, the body's creating this FGF-21 hormone when you restrict protein and that's leading to changes in fat cells. Which it appears to make them uncoupled. So I actually wanted to get your read on this because I don't know if you picked up on it, but like the, the studies they have to do, their mouse studies to get to do like genetic manipulations to show it's actually the FGF21, FGF21 knockout, et cetera. But it wasn't entirely clear to me how uncoupling was occurring. So the idea was the fat cells were burning off more energy and they implied this mostly from— there was an increase in, I think, a few of the complexes in the electron transport chain. So basically the things that are creating a proton gradient across the mitochondrial inner membrane. And then there was a decrease in the outlet, the ATP synthase. So you're like building up a waterfall, but you're not giving it the right outlet. So it needs to be wasted other places. They didn't go into too much detail though about exactly how that was occurring. They said it wasn't via standard like uncoupling protein. So I think they looked at like UCPs and didn't see a change. They mentioned something about like calcium cycling. Did you have any more thoughts on that or what?

Yeah, definitely. I caught the exact same thing that you did because based off the, the experiments that they did, they did proteomics, but they didn't actually do any sort of proof of any of the mechanisms. So yes, we know that it's through FGF21 based off the, the research that they did do with the, I believe, I guess they were FGF21 knockout mice. But, and there are other studies that have done work on FGF21 and on protein and whatnot, and those find similar results. So this is not specific to this one study, although this is the study that was done with actual nutrition manipulation. But in this study, they proposed a mechanism where you see exactly like you said, you see an upregulation of the mitochondrial proteins that, that allow for the cell to generate energy. So cellular adenosine triphosphate, ATP. However, the terminal protein that actually produces the ATP was reduced. So then of course, like you pointed out, it, it leads to, okay, well then how are, how's the mitochondria able to remove the, the protons that build up in that intermembrane space. And the, the answer was not clear to me at all because if you look at the proteomics data, they show that there's an increase in these mitochondrial proteins, but they don't show any evidence related to UCP, which is this uncoupling protein. They do acknowledge that there were no changes in this uncoupling protein, but then if you look at the diagram that they use, they add an uncoupling protein 7, I I believe is the, is the number that they threw in there. And I, I searched high and low and I just, I couldn't find any evidence for that uncoupling protein 7 to, to be, to be there. Like it, it makes sense, but they just didn't provide any evidence for it. So I agree with them for 90% of the paper. I just don't agree with them on, I, I'll say like, I'll agree with them that it's, it's a plausible mechanism, but they don't provide any evidence that that's the actual mechanism that it, works through.

Well, maybe I can get some follow-up on that. The senior author has been very generous with their time and answering some questions, so that's awesome via email. But, um, I sent her my prior video, she was very receptive. I'll send her this conversation when it's all done and we'll see if we can get an answer. If we do, I'll drop it in the associated newsletter and, uh, we'll get more information down below. But I would say by and large, like, I thought it was a fascinating study, and it's one of those areas where just like a good study should open up more questions. And so this is one of the areas of the unknown. We know protein restriction spikes FGF21, at least in lean healthy men. We'll get into other populations in a moment. And that, that is at least based on the animal literature. And we do need to use animal models to show causality 'cause you can't genetically manipulate humans. But this is causal, which is super cool. It's just now like dissecting, well, what exactly is happening in the fat cell? And I guess that'll be the next portion of the story. Now I wanna ask you, do you think Nick Norwitz, if they repeated this, uh, trial in women, older adults, or patients with diabetes and obesity, how well do you think the findings would generalize?

Uh, okay, so, so let me attack two populations. One, uh, let's talk about obese individuals, which I know you covered in your video really well, is that they tend to be resistant to FGF-21. And so, they can have heightened levels of FGF-21 and you would expect them, if you didn't know about that literature, you would expect them, "Oh, okay, then they'll be losing body fat and they're able to increase their metabolism and all that good stuff." But, that turns out not to be the case. It's a little bit like leptin resistance. I mean, you can have an increase in leptin, but you just don't have the receptors just don't respond to it or the intracellular signaling doesn't work for whatever.

Or insulin. Yeah, or insulin.

That's another great example.

Hyperinsulinemia. Yeah. It's a very common pattern in the literature. You have a hormone resistance. So in FGF21, there's a positive relationship with BMI.

Yeah.

But you're not getting more signaling per se if you have obesity, you're just resistant to the hormone. So anyway, continue.

Yeah, exactly. So no, I, I would not expect that these results would be the same for an obese population. I will say, I do wonder though, and I'd be curious on your thoughts, if you were to use a different diet to, to cut a person's weight down, to kind of a normal BMI, would they then resensitize to FGF21? What do you think?

I think they would. I don't think it's a feature. So I should say there are two elements to this. There actually is a feature of genetic heterogeneity. It's very common to have polymorphisms in FGF21. In fact, one, I think the minor allele frequency was like 40-something percent. Bottom line, it's like a toin cost, a coin toss if you have like, you know, variations in this which might make you more susceptible to, you know, adverse or beneficial reactions from protein restriction. That said, I do think the, the lion's share of the effect is metabolic state. So it's in the same way you'd become insulin sensitive if you lost excess adiposity, I think you would become FGF21 sensitive if you had obesity and reversed it. I will say so my prior video I made a prediction which is the effects would not be as powerful in somebody with obesity. I mentioned I had a correspondence with the senior author which I've now put on my Substack post about this, and I asked her that question, to which she replied, we have a study on this that will be submitted for publication soon. And then another answer to a question said, based on this study, It seems like the findings can be generalized to people with obesity.

Wow.

So it seems like, I mean, that, that's, again, we had in our prior conversation, we were talking about seed oils, physiology speculation, and the clinical results. So one of the, like, I, I made a prediction. We'll see if this effect size is the same. It's possible, like, it quote generalized, but it was half the effect size. So I don't know. But I had permission to, to disclose our correspondence. I told her I wouldn't. She said based on the trial they have under, uh, submission, so it'll be published soon. It seems like there is a generalizing effect, which is interesting. I, I, I really am looking forward to seeing what the FGF21 levels are or if there may be something else at play in human context. So TB, but that definitely surprised me.

Yeah, it surprises me too. Absolutely. I think, I, I think the, the another group though that I would, not in relation to FGF21, but older individuals, if you're consuming a low protein diet, I think that you would start to see some negative effects on lean mass over time. So I think that from which, you know, those, those data aren't quite as interesting 'cause we know that from other papers as well. But the FGF21 angle is by far the most interesting aspect of this. Yeah.

Well, I'm gonna get into that because it looks like FGF21 might defend muscle mass. You sent me a paper, which apparently you didn't read, but he sent me this morning. We're gonna talk about it on that. But I have a few more questions before we get to that. And actually, no, let's just, just get into that. I think over the short term in this trial, they showed that there was an adaptation in basically where, where nitrogen balance adapted. So there wasn't a loss in lean mass, but it was a 5-week trial. So you kind of already answered the question, but I do wanna double down on it. Let's just say FGF21 is muscle sparing to some extent. Question 1, again, you kind of already answered it, but I would like you to reiterate. Do you think, have low protein diet defined as 9% of protein calories from protein would risk muscle loss, let's say in the context of resistant training? And then in addition to that, do you think protein needs would at least be attenuated in the context of high FGF21 signaling? Tackle that as you see fit.

Yeah, that's, that's a tough series of questions. I guess off the top of my head, I would think that, I think that older individuals, because their anabolic signaling in general is dampened compared to younger individuals, that it's possible that the threshold at which we get this kind of, uh, FGF boosting effect may increase, as in they may need to consume more protein to spare their musculature. And yet, because they're so insensitive to the anabolic effects of the amino acids, that you could still get this FGF21 benefit even if you're consuming over, let's say, 9% protein. I don't think that I, and this is pure speculation, obviously. I'm just quick putting that out there. This is just a, a hypothesis I'm just throwing out there. Yeah. So I, I think that's one aspect. The resistance training aspect, it really depends on your goals, right? Like if you're, if you're trying to build muscle, then a 9% protein is going to be woefully short on, on that front. It's not to say that maybe you couldn't, but you'd be, be significantly hampered in your ability. But if you're just trying to maintain musculature, I mean, if with this FGF-21 mechanism, you know, is it possible that it's going to have some sort of effect? Again, I'm trying to, to consolidate this with the literature that's already out there on protein consumption and the effect that it has on muscle growth and things of that nature. And that literature tends to be, you know, much, much higher protein consumption compared to what we see in this trial. And keep in mind that this trial is not in resist— as far as I'm aware, correct me if I'm wrong, is in resistance training individuals.

Yeah, that's interesting. It's interesting to hear the, the first part, what you said about older individuals, because I had kind of an opposite speculation. Okay. Which actually was, yes, older individuals probably have higher protein needs, but I, I, I wasn't confident that the, their anabolic needs would translate into how they respond to the amino acids with respect to AKT21. So a lot of, terminology there, but my idea is, well, yes, maybe you can't get away with 9% protein if you're an older individual, you're gonna need more protein, but maybe you need so much protein that it precludes you from getting below the threshold at which you'll spike FGF21. So either your sweet spot for maintaining mass and getting FGF21 is tighter, or potentially it's nonexistent. So I don't know, it's interesting how we came at it from different angles, but it'll just have to be, I guess, an area of future study. Did what I say make sense?

Yeah, it does. One thing I will quick point out that I really liked about this study is that they compared the amino acid profile in that 9% protein and they still showed that it was above the threshold that like the World Health Organization identifies as necessary, right?

Yeah.

Yeah. So, which was awesome. It's so at least, at least I know it's 5 weeks, but if you were to extend this out for months or years, at least by those metrics, it would indicate that a person could survive on that. And you might be able to reap all the benefits as a result too.

Yeah. I mean, just doing now, hopefully I don't screw up my mental math for a second, but like 9% protein sounds low, but if you're training and your energy needs are high, you could be getting a decent amount of protein. So like, I'm a pretty small guy. If I'm eating 3,600 calories, you know, let's just round up to 10%, that's 360 calories from protein. Right? And if protein, protein's 4 grams, sorry, 4 kilocalories per gram, that means what, 90 grams of protein for me? And I'm like, that, that is well above what, you know, say standard bodies would recommend is necessary.

That's true.

So, you know, it does, this is a hangup of, of mine, like in terms of protein intake out. I, I tend to go more with like grams per mass versus percent energy intake cuz that varies widely. But 9% is low, but it's not nothing. So we'll have to see. I would love to see how this generalizes. It'd be quite a change in the trend of nutrition science if the whole thing now for weight loss is low protein diets.

But I, I think, I think it's exciting in, in regard to what you alluded to earlier that you can have, you can use a high protein diet. No, just to be clear for anybody listening, it's not like we're sitting here saying that now high protein diets have been debunked.

I don't think you should eat low protein, to be clear. Like, I found it very interesting and it might be legitimacy. It doesn't mean like I'm like rationing my steak into like 2-ounce portions. Right?

Yeah. Yeah. Me either. I mean, to be clear, we might use that for the title of the video, but I mean, in general, we're, we're not saying—

Should Nick share a 2-ounce steak? That'd be a good thumbnail.

But I mean, we are saying that at least there's a new avenue by which a person could lose weight. And it's not like we're talking about a 50-calorie bump. I mean, like you mentioned earlier, it's like a 500-calorie— that's huge. That makes a really big difference.

Well, it's— it was in lean, healthy men. It was about 573 calories. If you have someone with elevated BMI, even if the— even if the percent magnitude of the effect is smaller, there's still gonna be a much larger person. You might get 800, 1,000 calorie metabolic benefit in some people. And it, it's gonna be, your mileage may vary, but especially in someone, let's say, let's say you had a metabolically healthy obese population where they just store a lot of sub-q fat, like the effect size could be astronomical. So, you know, just from an academic physiological angle, it is absolutely fascinating. I do wanna touch quickly on the study you sent me this morning. Actually, I think I have it printed out somewhere here, which was FGF21 promotes longevity in diet-induced obesity through metabolic benefits independent of growth suppression. So, 'cause you didn't read the study, I'll give you a, a primer on what I got from it. But, but effectively what they're showing is if you increase FGF21, which as we've found can be done through protein restriction, it increases lifespan under the context of metabolic challenge in mice quite substantially. And what was really interesting to me in this study was two things. One, the lifespan extension was not a function or did not even associate with a decrease in energy expenditure. So often you think, oh, like say caloric restriction, you're like reducing your metabolic rate, slowing down, becoming like a tortoise or a Greenland shark. And that's, you know, mediating the benefits. That wasn't the case here. Metabolic rate was increased or stayed the same. That was one interesting aspect. Another interesting aspect is there was weight loss, but relatively lean mass increased a lot. So there was enough weight loss, there was some lean mass loss, but there was way more fat loss. So basically these animals became shredded, so to speak. And then the third really interesting thing was they used what's called a conditional knockout, which means they didn't just take the hormone and say, we're getting rid of it throughout the body. They just got rid of the signaling in fat cells. So it was a manipulation, particularly in fat cell metabolism, that extended lifespan, which is pretty profound. So I just threw a whole bunch of stuff at you. React as you see fit and then I'll ask particular questions.

I think just in general, it just speaks to yet another hormone or molecule that is— I mean, to me, I had not looked into this much at all except for when you introduced the first FGF21 study that we just went over. And then, after that, I started looking into it There's, there's another one that's another paper that's called Context Matters for Addressing Controversies in FGF21 Biology.

I love that title.

Yeah, it's came out in April of last year. And, and then obviously this, this one that just released today that you just described. So to me, it in the big picture, I think I'm just really fascinated to learn a lot more about FGF21. And piecing that all together, like figuring out like the nutrition, trying to manipulate nutrition in humans to see increases in FGF21, figuring out the mechanisms, which we still need to do, uh, understanding the longevity effect that it might have. Um, especially to me in the, the first point that you made in, in relation to this study that you don't see a decrease in metabolism, which is absolutely true when a lot of the longevity science speaks to trying to suppress the amount of amino acids that you consume because those tend to promote— well, I don't want to say promote a shorter life or anything like that, but there's just a lot of literature speculating about that kind of stuff. So, this is a new avenue of attacking things and I find it absolutely fascinating.

I want to lean into what you just said, which had to do with amino acids, things like activation of mTOR shortening lifespan because I Yeah. What's impressed me is the degree to which FGF21 physiology does tend to translate to humans and being pretty well conserved. And there's also an argument that's been made that lower protein diets may help promote longevity in humans. You can't really do these controlled trials, but you can speculate based on the physiology. So I'm gonna try to thread this question very carefully. Do you think it's reasonable to speculate based on these data that there is aligned to walk whereby you're getting enough amino acids to support muscle protein synthesis and muscle maintenance so you don't develop frailty in older age, but keeping protein restricted to a point that you do get an FGF21 signal to expand, extend longevity. Is that reasonable?

It's, it's incredibly reasonable. Yeah. And I've been, I've been talking about this since about last year on my channel that we need to, we need to think about— we need to think about nutrition in general, but certainly other aspects of science as not just good or bad, like my nutrition is the best at everything, or it's the— another nutrition is the worst in everything. And the reason why I point that out is because when we're talking about longevity science in relation to protein is we kind of have to make a choice. I, As I read more and more into this literature, maybe it's just a self-fulfilling prophecy ever since I've come to this conclusion that we have to choose our outcome. Do we want to live a healthy life that's full of vitality and you're really strong and you live a pretty good long life, but you're not going to live the longest life that you possibly could live because those two are kind of at odds with one another. They're similar up to a point, and then they start to— in the extremes, they start to diverge from one another. And I think what we're talking about here, this lower protein level, is speaking more to this kind of longevity aspect. Now, there is a little bit of pushback now that I'm learning more about FGF-21, that maybe that could, uh, kind of center both of them, both of these paths a little bit more. But my impression of the literature up to now has been that if you consume a lower protein diet, that there's good evidence, pretty good evidence, like you said, we can't, we don't have any human trials that specifically show this, that you can extend lifespan. And the same thing with calories, but more specifically proteins. And on the, on the flip side, you can increase your protein consumption significantly, and then that'll allow you to build a strong physique, be able to be resilient against disease, things of that nature. But you're probably going to be taking a bit of a hit on your overall longevity. So that's, that's where I stand.

Yeah, I would tend to agree. I think one thing you said that I want to emphasize is we're choosing our outcomes. I think people need to def— they try to defend their diet is best for everything, you know? So somebody has like remarkable recovery story on carnivore, they're like, it can't contribute to any ill health outcomes and it needs to be the best for longevity. And I'm like, I can speak from my experience, like being a patient with IBD. I'm like, I will make my decisions in order to keep my IBD FA and have a good quality of life. I am 29. Not every decision I'm making is optimizing for longevity. So, you know, it is, it is what you're optimizing for. I'll also add, I don't think people probably gonna skewer me for this one, but I do not think what you eat tends to have that big an impact on human longevity. I, I just, I think the bigger factors, if we look at like what are the commonalities of centenarians, it's kind of funny. You have people that you ask like, you know, like what is your diet? You're 116. She's like, I eat cake and bacon every day. Or like, I smoke. It's just like the things that define what is longevity in humans I think are generally beyond diet. Probably social connections, huge sense of purpose. And if you do have the benefit of having a few decades in front of you, I just think technology's advancing so rapidly. That my personal perspective is, you know, titrating your protein from 15% to 10% probably isn't gonna have that meaningful an impact on your longevity. So we talk about this cuz it's fascinating physiology, but I just wanna put it in perspective that I don't think you're gonna get 20 years of life from making sure your chicken portions are only 3 ounces. Do you agree?

Yeah, for the most part, I, I think that the, the type of person you're talking about is a person who's already pretty dialed in and in those scenarios, scenarios, I, I agree. I think for a person who's like struggling with obesity or diabetes or whatever, that's where nutrition can have such a powerful impact that, that can propel them literally decades, uh, forward if they're able to reverse it, uh, you know, quickly enough. But, you know, again, those are, those are special, uh, circumstances. We're not talking about the average person. For the average person, yeah, I mean, your nutrition I think does matter to, to a degree. It's just, uh, it's not gonna, you know, it's not gonna be the, the main determining factor. I think genetics plays a massive role.

Yeah, I agree. All right, one more question on this topic and I'm gonna hit you with a few rapid-fire questions.

Okay.

Just for kicks and giggles, which is if you have a question for the senior author, and I'm issuing this to you now as we recorded this, but also any audience members listening, 'cause I might pass it on to her, what would you ask her about either this research on FGF21, the field in general, or upcoming studies?

I think my question, it's not very translation-focused, but I'm very interested just for selfish reasons. I'd like to know the mechanism of action. And I don't think that what they supplied was sufficient evidence or really any evidence of their proposed mechanism. So I would like to see, yeah, I think I would ask, what kind of experiments are you doing to prove or disprove your hypothesis. I think that's really the only one that pops into my head. If I had a little bit more time, I'd probably think of some others as well, certainly.

Okay. All right. Well, bringing us home, I'm going to just ask some rapid-fire questions. You get about 30 seconds to answer. If you don't have a good answer, you can just say pass.

Okay.

All right. Something that I haven't looked into, but I think you have, methylene blue. Blue. Ah, what is it? Is it legitimate? Is it overhyped?

If the hype is supposed to be based on science, then yes, it's currently overhyped. If the hype is based on like a cool mechanism that could hold promise, then no, it's not overhyped.

Okay. That's a good teaser. We can link to some of your content if you have some to suggest below. Okay. I think we both looked into chlorogenic acid, a really interesting polyphenol found in coffee. And yerba mate. What do you know about this molecule? Is it something people should try to get in their diet?

Yeah, I don't think I'd jump out of my way specifically to get chlorogenic acid. I think people get too focused on single molecules, but I mean, if a person's a real big fiend for supplements and making sure everything is optimized, then yeah, I think it's a good candidate. It's got antioxidant properties. There's some studies on reducing blood pressure. It improves glucose tolerance, things of that nature. And there's some cool mechanisms related to cardiovascular disease as well. So yeah, if, if you've got the time and space and money for it, then go for it.

Let me reframe that. I wouldn't recommend supplementing it by itself, but would you agree maybe it's a good extra reason to either have coffee or your maté, whatever you prefer?

100%. Awesome.

All right, this one's a little bit spicy, but since we're talking about longevity, any opinions on Bryan Johnston and Blueprints?

Yeah, he's interesting. I appreciate his journey. I think he's gotten a bit commercial, selling a ton of different things. But, on the other hand, he's also a businessman, so I can't really be too mad at him. But otherwise, I like his experiment that he's doing. I might do things slightly differently if I thought about it a bit more, but Aside from that, I, I like his, I like what he's putting forward.

All right. Animal versus plant protein. Is animal protein superior for muscle building?

Per gram? Yes.

Animal versus plant protein, a part 2 question. Is plant protein superior for longevity?

That's definitely a, a more difficult answer to give, but I would say generally yes.

All right. Anything I should have asked you today that I didn't ask you? Anything you wanna highlight for our combined audiences?

I mean, I guess the only thing I'll highlight just because I feel really passionately about it is, and I know you do too, is I know your mantra is stay curious. I think that just remain nuanced, you know, just try to always take a step back and assess the science for what it is and making sure that you're asking the right questions. Not that we should take any single study as gospel and that we should try to always integrate things into to the overall literature.

All right. Well, thank you so much, uh, Dr. Nick, for joining us. Everybody, you can find him, uh, at Physionic on his YouTube channel. Other social media you want to plug where people can follow you?

No, just type in Physionic, you'll find me.