- Welcome to the Huberman Lab Podcast, where we discuss science and science-based tools for everyday life. I'm Andrew Huberman, and I'm a professor of neurobiology and ophthalmology at Stanford School of Medicine. My guest today is Dr. Lane Norton. Dr. Lane Norton did his training in biochemistry and nutritional sciences, and is one of the world's foremost experts in exercise and nutrition.

He is also an expert in the topic of supplementation and other tools to augment health. Today, we discuss a large number of very important topics in these categories, and we start the conversation by establishing what Dr. Norton's thresholds are for what he accepts as evidence, in particular, actionable evidence.

So what follows is a description of what Dr. Norton really believes is worth paying attention to versus what he believes is worth ignoring in the realms of nutrition, training, and supplementation. So you can be certain that as we start to go through the topics of sugar, GLP-1 agonists, things like Ozempic, artificial sweeteners, whether you should train to failure or not during your resistance training sessions, how much volume of training you need to do, cardiovascular training and its different forms in terms of how they benefit healthspan and lifespan and body composition, protein and its different sources, and on and on.

Indeed, we cover many topics in this episode. You can be sure that all of the information you hear from Dr. Norton is being filtered through that extremely stringent filter that Dr. Norton is so well-known for. And thus, by the end of today's episode, you will be armed not only with the latest information on nutrition, training, and supplementation, but you'll also be armed with your own filter to determine what sorts of health protocols are actionable for you.

Before we begin, I'd like to emphasize that this podcast is separate from my teaching and research roles at Stanford. It is, however, part of my desire and effort to bring zero cost to consumer information about science and science-related tools to the general public. In keeping with that theme, I'd like to thank the sponsors of today's podcast.

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Because I think a big reason why you are considered one of the, if not the most trusted person in the realm of nutrition and training is that you set a very high bar for what you consider science-based fact that motivates action. So to just kind of break this down based on my read of the landscape online, it seems that there's a group of people, I don't know what to call them, purists or something, who, unless there's a randomized controlled trial, so that means in humans, or several, that points in a particular direction, they are very unlikely to adopt a new practice, say, removing a given food or nutrient, adding a given food or nutrient, training a certain way, not training a certain way.

Okay, that's one group. Then there are the people who, if they are told something could be a value, they hear it's worked very well for somebody, maybe they see some before and afters, and it gets mapped to a mechanism that exists in humans and animals, like, oh, there's this molecule, and if this molecule increases, X, Y, and Z happens, and training in this way or eating this way increases that molecule, for instance.

But no randomized controlled trial, then they're willing to try it or adopt it. And then there's a third, probably a fourth category as well, where people say they don't trust science anyway, science is flawed, or the controls required to design a really good experiment are so constrained that they don't mimic the real world well enough, and so they're really just interested in what works.

So they look to people that seem to have achieved the results they want. Feel free to add another group, but which group would you consider yourself in personally? And then where does your evidence that you put out online and today come from? And I already know the answer to the last question, but I think it was important to kind of spell out the landscape.

- So everything you just mentioned would fall into the category of evidence. Everything that we can observe is evidence. But I think what people really struggle with is the idea of different levels of quality of evidence. And if I had to put myself into a group, I have definitely been on the side of, well, there's a case study in this journal, and we're gonna try that now because it must work.

And, or my friend tried this and they said it worked, so I'm gonna try it. And then I've also gone to the group of, well, there's no human randomized control trial, so I don't believe it. And I think now, I'm 42 now, and I've been doing this for two decades.

I think where I'd fall into is it really depends on how the individual is talking about the evidence. Okay, so as you can probably imagine, I get sent a lot of stuff for people to like, oh, debunk this. And a lot of times people will send me things and I'll go, hey, this person said this is their opinion.

That's fine. Like I may disagree with their opinion, but I'm not gonna like rake them over the coals for them saying this is an opinion, or this is my personal experience. That's evidence. It's low quality evidence, but it is evidence. I think I kind of fall in a line of, I ideally wanna see human randomized control trials, but there's also, as you mentioned, practical limitations with how things are implemented.

And I think one of the things that gave me a very unique perspective was the fact that I was doing my PhD in nutrition after I did a bachelor's in biochemistry. So I had that mechanistic understanding. And then I had an absolutely wonderful PhD advisor, Don Lehman, who just, shout out to him, got a Lifetime Achievement Award by the American Society of Nutrition, 20 years too late.

But he was just incredible at being able to understand the small things, but how they impacted the big things and what it looked like overall. It's like a conductor looking at a symphony, right? And understanding how the trumpet sounds affects everything else, but then not getting so tied up in that that he can't hear all the music, right?

And he was so good at that and was so good at getting me to think that way. And so I think where people out in the landscape trying to dissimilate this really struggle is they don't really know, well, this person decided to study, and they equate that as evidence that's equal with any other evidence, right?

And as a researcher, you know, not all evidence is created equal. Not all journal articles are created equal. And I mean, honestly, people who don't have the research background, it's hard to unpack this stuff. So what I would say is you have to be very careful with people who cite studies.

And one of the things I'll say too is there's nothing more dangerous than somebody who's read a biochemistry book because they're gonna see pathway, biochemical pathway, there must be an outcome. So outcomes are what we really care about, right? At the end of the day, and when I say outcomes, gaining muscle mass, losing fat mass, risk of cardiovascular disease, insulin sensitivity, cancer, right?

These are hard outcomes, right? And those outcomes are the summation of dozens, if not hundreds, if not thousands of biochemical pathways, all summing up to an outcome. And just because something has a biochemical pathway doesn't mean it will create an outcome. But if there's an outcome, there's absolutely a mechanism to explain it.

Now, let me give you an example of why this stuff can be so complicated and why it's so easy for people to, if you wanna create a narrative, you can always find a study to create a narrative. Aspirin, we would agree, is an anticoagulant. There's a reason they give it to patients who are at risk for heart disease or a heart attack.

It's 'cause it reduces blood clots, reduces coagulation. It also activates procoagulant pathways. But the overall outcome is anticoagulation. But if I wanted to create a narrative that aspirin was bad for blood clots, I could say, well, look at these biochemical pathways it activates. And you see this, like, for example, I could create a narrative that smoking is not bad for you.

I remember reading a meta-analysis of the effect of smoking on the risk of adenocarcinoma. And there's a forest plot with probably about 50 studies. And most of those studies are to the very far right of the line, which is increases risk. And I think the overall effect was like three or 400% increased risk of adenocarcinoma.

But there were two studies that were to the left of the line, not by much. And it wasn't statistically significant, but I could say, hey, look, I could cite these two studies, PMID, you know, they showed no increased risk of adenocarcinoma and actually might be slightly protective. And by the way, did you know that smoking decreases the risk of Parkinson's by 30 to 40%.

And by the way, that's very consistent in literature. - Yeah, that's true. - So I can start creating this narrative that smoking, but we know smoking's not good for you. It's not good for you. It raises the risk of lung cancer, all different kinds of cancers, cardiovascular disease, massive increase in risk, right?

But I could thread the needle of science using these cherry-picked studies. And so what I'll tell people is if I go into a topic, if I go into something, what I'm looking for highest quality of evidence is first off, do we have some meta-analyses on this topic? - Do you wanna just explain for the general listener what a meta-analysis is?

Just in kind of top contour. - Absolutely. So a meta-analysis is basically where you're trying to compile studies that ask similar questions and look at what is the overall effect? Do we have a consensus in the literature? And usually they're gonna show some kind of forest plot of all these studies.

And however far right or left of the center line is kind of giving you an idea of how powerful the effect was in that study. And then you can see the confidence intervals in terms of how much variability there was. And then you can see the thickness of the dot on there, which shows how much it contributed to the overall analysis by usually how many subjects were in it.

- Right, one study with 10 subjects would have a very small dot compared to a subject with 500 subjects. - Exactly. And so you're trying to, now you can do a bad meta-analysis based on inclusion criteria, and that's where it's important to look at. But let me give you an example of a meta-analysis I cite pretty frequently.

The inclusion criteria is very important to make sure that you answer the question that you wanna answer. And I say this when you're reading scientific studies. I'm like, listen, just because there's a headline in even a paper, just 'cause the conclusion says something, that is the author's opinion, okay?

You need to check to see, did they actually test what they're talking about? And are the tests they use valid, right? So this meta-analysis was looking at lower carb diets versus higher carb diets or low fat diets. And the inclusion criteria, this was done by Kevin Hall of the NIH back in 2017, I wanna say.

And I thought he did a great job at the inclusion criteria, which was we're only gonna include controlled feeding trials where the food is provided to participants, because obviously we know the limitations of free living studies with nutrition. - Right, self-report. People sneak, people forget. - We are going to make sure that these studies equated calories for the reasons we talk about.

You gotta compare apples to apples, right? So a lot of studies will come out saying fasting produced more fat loss, low carb produced, but then they didn't control calories, and it's very likely these people just ate less. So they controlled calories and they controlled protein, which is also important 'cause protein changes the composition of weight loss.

Protein has a thermic effect. Protein increases lean mass retention. So that can change how much fat you lose. And I think that it also had a requirement of like a minimum of four weeks, right? And the outcome was looking at changes in fat mass, not fat oxidation, not energy expenditure.

It actually looked at the outcome that they cared about. And they showed no difference, right? So I thought, well, that's a very well-done meta-analysis because the inclusion criteria make a lot of sense for the question that they wanna answer, which is not, is one diet easier to stick to?

Not, is it more practical? The question was mechanically, do these diets produce differences when we're comparing apples to apples in actual fat loss? And the answer was no, right? So, and then when you look at the other meta-analyses that have been done, they tend to kind of support that, right?

So the first thing I'm gonna look at is all right, these meta-analyses tend to be looked at as kind of the highest form of evidence, right? Because you're compiling a bunch of different studies, which, listen, we know there are bad studies that get done. I think the amount of studies that get like just straight up faked is probably much lower than people think, but- - One hopes, but yeah, I would agree.

I think that people make errors. I do think that a lot of quote unquote bad papers, or let's just say false conclusions, arise from elimination of data that did not fit the person's desired outcome. And the reason I say that is I think it's impossible to control for. So you've got the student or postdoc doing the experiment, the results don't come out the way they would have preferred and then they're, let's just say I've observed before, never in my laboratory, fortunately, but cases where people come up with reasons why that particular experiment wasn't valid because the mice were initially sick or the lot of drug that they used wasn't, it was heading towards expiration, they come up with reasons to exclude rather than outright data fabrication where people literally create results that aren't there.

And there are a number of different examples throughout history where people have done that, but I like to think that those are more rare. - I think that's probably pretty small. My experience is the same as you. I didn't see much of that, or I never saw it observed.

- Usually end up reading about that in the form of retractions in journals that come out. Nowadays, more close to the publications because of AI's ability to scan images and things of that sort. - Yeah, I think, you know, usually if I see a paper and the conclusion, like just straight up, I go, oh, I don't know about that.

When I go in and I read the methods and I read how they analyzed it and I read how they measured things, 99% of the time I walk away and go, okay, I'm not surprised they found what they found, right? Because again, a lot of, and this does happen and it shouldn't, but a lot of studies are set up to kind of find what people want to find.

You can bias things in a certain way. - Well, and what nobody talks about or it's not discussed enough is that a lot of times the way the paper is written poses a question after the results are in. I mean, and this is a really a not correct way to do science.

I mean, in clinical trials, one has to wage a hypothesis, excuse me, wager a hypothesis from the outset and then you go test that hypothesis. You're not asking a question. - And you have to say what you're gonna measure. - Right, exactly. Whereas in more typical laboratory science, people will design an experiment.

They have hypotheses, but then depending on how the experiments work out or don't work out, oftentimes they'll change the question to modify the hypotheses. And one wouldn't, as a reader, as a journal, as a reviewer, one will never know. And so that's a slight of hand that is, I would say, unfortunately is very common in bench science.

- But I will say like, there's very rarely where I say this was a bad study. Often what I'll say is, I don't agree with their conclusion based on their data and their design, but the data is the data, you know? I was just very fortunate, again, to my PhD advisor, I have so much gratitude, 'cause he just right away was like, "Hey, if we're wrong about something, "that's fine," you know?

And I'll give you an example of how results can seem to conflict, but how things are designed. We actually wanted to test, does protein quality make a difference? And we wanted to look at it at like, not low, but like, just kind of like RDA levels of protein. And we saw that protein quality did make a difference at those levels of protein.

But if you look at experiments where people are feeding like high levels of protein, like 1.6 to two grams per kilogram of body weight, you don't really see much difference in, you know, lean mass or protein synthesis with looking at different protein sources. Well, that's because it's much more regulatory on a low end because you're closer to those thresholds that trigger that signaling.

And so, you know, we wanted to show at that level that it made a difference. But then we also acknowledged, okay, at this level, it probably doesn't make as much of a difference. But people can read those things and say, "Well, I don't believe studies 'cause they're conflicting." But no, when you read how it was designed, I can easily say, like I remember there was a, somebody sent me a study and said, "Well, how does this fit with your data?" Which they were comparing rice versus whey protein and found that both stimulated protein synthesis to the same degree.

And I said, "Well, they used 40 grams of protein." Like if you get protein high enough, you can max out protein synthesis regardless of the form of protein you're using. And so that's just like one of those examples, right? So when I'm looking through this stuff, I'm looking at, okay, it doesn't seem to be a consensus in the data.

And then is it like in these meta-analyses, does the inclusion criteria make sense? And then if there's no real agreement amongst the meta-analyses, then I'm looking at, okay, what do the most tightly controlled studies show? Like in the randomized control trials. And then I'm kind of like basing opinion off that.

But you know the hierarchy of evidence, the pyramid, you got meta-analysis, systematic reviews, randomized control trials, you have cohort data, epidemiology and then animal studies tend to get kind of lumped in together. And then you got like case studies and so on and so forth, right? And so all that stuff is valid.

It's all valid. I think where I spend a lot of time on social media is for example, I'll give you a great example. Someone saying, well, you don't wanna eat cruciferous vegetables because they have isocyanthanates in them, which can bind to iodine. And that is going to impair your thyroid function, lower your metabolic rate and cause you weight gain.

And so that's a pathway, that's a mechanism. Is it possible? I suppose it is possible, right? That pathway does exist. Iodine is important for thyroid function. Isocyanthanates do bind to iodine. You can take any food, even organic food, and you can find a compound in it that if you fed it in a high dose, it would have weird effects, right?

And so the question is not, if you eat something, are there compounds in it that maybe activate negative biochemical pathways? The question is, what is the overall outcome? And so when these pathways are promoted versus let's see if we actually have randomized control trials in humans that measure what we actually care about.

And so we do have, like in that particular case, we have randomized control trials looking at, okay, cruciferous vegetable intake and thyroid function, and there's no difference in the outcome. And so what that says, and then no difference in BMR, and then actually people who eat more cruciferous vegetables actually tend to be a little bit leaner, but that could be a little bit of healthy user bias, and they'd probably just eat less calories 'cause they're more satiated.

But it's certainly not going the opposite direction, right? And so the point is, again, if an outcome exists, there is absolutely a mechanism to explain it, but just because a mechanism exists does not mean you're gonna produce an outcome. And I got exposed to this very early 'cause I cut my teeth on the bodybuilding message boards back in the day where it was a bunch of nerds arguing with each other, mostly who had no background arguing, but there were some actual sports scientists and professors who would get on those every once in a while.

This was before social media existed. And I remember I was in biochemistry class, this is 2003, and they're talking about how caffeine inhibits glycogen phosphorylase, which is a mechanism, and it exists. Caffeine inhibits glycogen phosphorylase. And so I made this post on the forums, and I said, well, we should be having caffeine after a workout then 'cause it'll help with glycogen resynthesis 'cause it'll keep glycogen phosphorylase from breaking down glycogen.

And somebody came in and said, you're really like zooming in on a blade of grass instead of zooming out and looking at the forest, right? And biochemists, I was guilty of this, and biochemists by trade, we get very focused on pathways. But if you think about what caffeine does overall, activates the sympathetic nervous system, its function is to, like, you're liberating fuel.

Like you, and some people, when they take caffeine, actually have a rise in blood glucose. So that is, the outcome is actually counter to what that biochemical pathway is. And so we've gotta be really careful with how we promote these biochemical pathways. I mean, I did a really funny post on Twitter where myself and Joseph Sundell, I'm not sure if you're familiar with him, but he's a cancer biologist, great guy.

And we were joking back and forth. I said, you know what, I bet I could, like, come up with a pathway to get people to eat poop. Like, I can make a compelling argument for just eating poop. And then he goes, I'll bet, he's like, I'll take that bet.

I'm like, okay, let's give it a shot. So I'm like, what is some of the most common compounds in human fecal matter? And one of them is butyrate, right? Which is a short chain fatty acid produced by fermentation. Butyrate, and so I did this post where I'm like, here's why you should eat poop to lose fat.

Butyrate increases fat oxidation. I think it activates brown fat, increases insulin sensitivity, decreases inflammation. It's been shown to actually ameliorate the development of obesity in studies. And so I had all these PubMed ideas. Now, what I didn't tell people was, those are all mostly in rodents, right? And it's giving an amount of butyrate that you'd need to eat about 50 to 100 pounds of fecal matter a day in order to get, right?

- Sounding like a worse and worse idea by the moment. - But that is very similar to a lot of the content that is out there, which is find isolated compound, scare people or promote it to be the best thing ever, and then link it to an outcome. And then sometimes you can tie in epidemiology with it as well to support whatever you want.

But again, like I'm not saying, I do things in my training and my nutrition that don't have randomized control trials to support, right? They don't really have anything to support. It's just, it's how I've kind of fallen into doing things. So that's okay. But what I wouldn't do is come out and say, what I do is the best thing ever and here's why, especially if there was human randomized control trials to the counter, that is the biggest thing, right?

If we have human randomized control trials and they're going the opposite direction of a case study or an observation, there's a reason human randomized control trials, I scream about them all the time, and why they're considered the gold standard of evidence. When we look at cohort data, you're just observing people.

There's no intervention. - Maybe explain what cohort data are. Is it comparing two groups? - Sure. So cohort data, you're comparing groups, but you're not having an intervention. So you're tracking them over the course of however, what period of time. A lot of cohort studies, like looking at cardiovascular disease, cancer.

- These people decided to be vegan. These people decided to be, let's just say omnivores. - Those are some of the classic experiments, right? - And they weren't assigned to this experiment. They agreed to join the experiment. They'd been eating this way for a while. You ask them a bunch of questions.

And you look at, okay, over 10 years, over 20 years, who gets whatever more often or less often, right? And then we try to figure out and back calculate, okay, what's the effect and is this real? The problem is you have a lot of bias with those sorts of studies.

Meaning people don't do single habits. They don't isolate habits. I actually put up a reel the other day from my appearance on Stephen Bartlett's podcast, where he said, if I wanna fix my diet, I go to the gym. 'Cause a lot of people do that. If they're training in the gym, they don't wanna waste their effort by having a subpar diet.

Now in reality, eating a healthy diet is more important if you're not going to the gym, right? 'Cause at least you're getting something. But people do this habit coupling. And so it's really hard to disentangle those sorts of things. Now, the reason that human randomized control trials are important is if you're designing an experiment and you randomize, what you are doing by randomly assigning people to groups, you're washing out that bias because you can assume that whatever inherent characteristics that might be coupled to whatever you're gonna try are gonna be randomly distributed and evenly distributed across the groups.

Therefore, we say human randomized control trials are kind of what's needed to establish causation because by randomizing, you can assume whatever differences are observed between the groups are due to your treatment and not due to random chance or data artifacts. Now, randomized control trials, especially in nutrition, have very strong limitations, which is you can't do a randomized control trial for 30 years.

You can't, I mean, I think the longest randomized control trial I heard about in nutrition is like two years long, right? And even then, it's not gonna be a very tightly controlled randomized control trial. I mean, and if you're doing, if you're talking about like the tightest level of control, like a metabolic ward study, four, six weeks, maybe, 'cause you're keeping people in food jail.

And I think where some of this confusion comes from is I think people think that there's just like this pool of people waiting around to be selected for experiments. Like, yes, I'm ready, I've been waiting here. No, there are people like you, like me, like just the average person walking down the street who saw a flyer and goes, okay, I'll volunteer for that.

And the more control you try to establish over their lives, the less likely they are to do it. And you probably gotta pay 'em, you know? I don't know anybody who would do a metabolic ward study without getting paid for it. I mean, you're basically giving up four or six weeks of your life to go do that.

And so while I love human randomized control trials, for some things, they're not always appropriate. For example, if you're trying to look at heart disease and you wanna do a one-year human randomized control trial, looking at say, you know, saturated fat, LDL, cholesterol, those sorts of things, well, how many people have heart attacks within one year after age 60?

I mean, you're gonna look for really small differences between really small numbers, right? And the problem with that is you have no idea about their diet 40 years leading up to that. And we know based on now the Mendelian randomization trials that the risk of LDL is more of like a lifetime exposure risk.

It's not just in this narrow sliver of time. And so I love human randomized control trials, but it's also, I try to tell people, never turn your brain off. Just because something gets published in a certain journal, just 'cause a certain researcher said something, just because it was a certain design, it doesn't make it infallible, okay?

Science is perfect. Science is perfect. Science is what is. But it's done by humans and humans are fallible, imperfect people with their own personal beliefs and biases. And that's why I look at consensus of data first, because yeah, you could, maybe some experiments got faked or maybe they had, but when it's done over, let's take something like creatine monohydrate, right?

You have thousands of experiments done over decades of time in hundreds of different labs with many different funding sources in bunch of different countries under a bunch of different conditions, it works, right? Like if you go to consensus and you type in, does creatine build muscle? It's like 92%, yes, which is crazy.

- Right, consuming five to 10 grams of creatine monohydrate per day is going to benefit strength and muscle mass and likely cognition to some extent. - Yeah, yeah. - I'd like to take a quick break and acknowledge our sponsor, AG1. By now, many of you have heard me say that if I could take just one supplement, that supplement would be AG1.

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Again, that's drinkag1.com/huberman to claim that special offer. - I realize I've been on a long diatribe. - No, no, I wouldn't even call it a diatribe. I think for those listening, this is pure gold because never before, certainly on this podcast or other podcasts, has anyone ever really spelled out how to discern differences in quality of evidence?

- Right. - It's mostly a free world, most places, and people can do what they want, but I think they need to decide what their thresholds are for quality. - Yeah, and I think the one other thing I'll tell people is, I saw this the other day. I saw somebody post, I think it was a comment on one of my posts, and I actually commented back.

They said, "I know I can trust you, "and whatever you say, I know I can take it to the bank." And I said, "I appreciate that, "but I am a flawed human like anybody else. "Please don't turn your brain off." And one of the things I've really tried to do now in this stage of my career is I wanna teach people how to think because if I just give you the information and I'm giving you a fish, great, but I'd rather you understand how I came to these conclusions, you can see my logic and how it tracks, and then you can start applying it elsewhere.

One of the things I say to people is I'm like, "If you want a quick and dirty hack "for knowing who to follow, "try not to listen so much "to exactly the information people say, "but listen to how they say it, okay?" I was just telling you, I was on a podcast the other day where I said, "You know, here's this study.

"I might butcher the details, and if I get the math wrong, "if experts out there wanna comment and correct me, "please do that." Like, that is a way of talking about something where you're saying, "Hey, I could get this wrong," or, "Hey, I might be uncertain." That's very different than saying, you know, just hard, pure, you know, real experts don't really talk like best, worst, always, never.

Like, they don't really use words like that. And one of my favorite phrases that I tell people, it's actually from an economist named Thomas Sowell. He said, "There are no solutions. "There are only trade-offs." And for example, you know, there's data out there that if you lower saturated fat, it may lower your testosterone.

But there's also data out there that saturated fat raises LDL, which is an independent risk factor for cardiovascular disease. Okay, well, there's trade-offs there, right? Like, what do you value more? I would argue that probably the decline in testosterone isn't really physiologically meaningful for most people. But again, there's not a good or bad.

There's trade-offs. And I think when people get talking about biochemical pathways, one of the things I really try to hone in on is like, hey, there's not really good or bad biochemical pathways either. Like, all these things exist for a reason. Like, people, like, one of the things popular is like, well, inflammation, inflammation.

I'm like, hey, you know, like, inflammation does some things that we really need, too. Like, you just don't want, like, no inflammation. Like, it's actually an important physiological process, right? Now, you don't want it to run away, for sure. And so, again, I just give my PhD advisor a lot of credit of, he's like, know what you know, but always question everything, even the things we feel most fundamentally are true, 'cause that is the job of a good scientist.

I'll give you one more story, and then we'll move to another thing. When I did my first experiment, well, actually, sorry. No, this has been like my 15th experiment, 'cause my first 14 blew and didn't work. - A typical graduate career. - Yeah, yeah. And again, very patient man, very supportive.

I honestly cannot give him enough credit. And if you look at the people that came out of that lab, a lot of studs. So, I did an experiment looking at whey protein, or sorry, complete meal with whey protein ingestion and how long the duration of muscle protein synthesis was.

Because most people kind of measured at 60 or 90 minutes, like the snapshot post-prandially for protein synthesis, looking for a peak, and we're like, "Is that really where the peak is? "We don't know. "We're basing this off of purified solutions, "so let's do a duration experiment," right? And my hypothesis was, well, however long leucine is elevated in the blood is gonna be how long protein synthesis stays up.

And when we got the data back on protein synthesis, protein synthesis had come up, peaked at 90 minutes, and by three hours, it'd come back down to baseline. And I went to run the plasma amino acids, and I'm like, "Okay, well, this is what we're gonna see." And that's not what we saw.

So, plasma amino acids, not only were still elevated, they were maxed out, or plateaued, at the highest level they would be at, three hours, where protein synthesis was back to baseline. And so, I said, "Okay, well, it's gotta be mTOR signaling. "mTOR signaling's gotta be turning off, "or something's happening." Nope, mTOR signaling was still elevated, right?

And we saw this through phosphorylation of the binding protein 40BP1, which is a proxy for mTOR activation. And then I said, "Okay, well, maybe leucine "isn't getting into the cell. "Maybe that's why." So, we looked at intracellular leucine, followed the exact path of plasma leucine. And so, then I kept rerunning the plasma data, over and over, I probably ran it five times, right?

And Lehman finally calls me into his office one day, and he goes, "So, where do we stand "with this duration experiment?" And I said, "Yeah, it's almost done. "I just, I gotta run the data again, "'cause the plasma data's gotta be wrong." And he, I saw his little eyebrow go up, you know?

And he goes, "Why do you think that? "Let me see your data." He goes, "Your standard air bars are good. "This looks to be relatively tight data. "How's your technique?" And I'm going through how I, you know, all the steps to analyze plasmino acids. It's not like CSI, by the way, everybody.

You don't just take a pipette, put something in a centrifuge, and all of a sudden you get back data. There's many steps in here. And so, I showed him all that, and he goes, "You know, it sounds like you are trying "to get the data to fit your conclusion, "and what you need to do is change your conclusion "to fit the data." And that one line, again, it just opened my whole world up to one, if I'm wrong, okay, cool.

Like, I care more about getting the right answer than being right, and that's why we were talking earlier. I'm like, there's so much stuff that I just don't believe. I want to see 10, 20 studies before I go, "Yeah," you know. And the other thing I'll tell people is, "Hey, I don't plant my flag real strong very often, "so when you see me do it, I'm not saying I'm not fallible, "but if you see me do it, you probably should pay attention, "'cause I don't usually do that." - I love that description, but now my curiosity is piqued, and you got to tell me.

So, if 90 minutes after ingesting protein, protein synthesis peaks, and then it drops to baseline at three hours, but leucine, one of the key amino acids in mTOR, which is in the pathway of cellular growth and protein synthesis, are still elevated at three hours, what is the conclusion that explains the discrepancy?

- Yeah, so, we actually looked for this for years. So, a few things. There was some other studies that supported that. We called it a refractory response. Actually, we didn't name it that. There was another lab that named it that. Basically, that protein synthesis was becoming refractory to the signal for protein synthesis.

So, just for real quick, I'm gonna try and explain this easily. So, protein synthesis, you know, this sounds like probably a very abstract thing, but it's how your body makes more protein, and whether it's in skeletal muscle, whether it's in the liver, whatever, you have your DNA, which is your genetic code, right?

And then, that gets transcribed to an mRNA. By the way, I'm leaving out a lot of steps here, but just bear with me. That mRNA gets translated by a ribosome into a polypeptide chain or a protein. So, a ribosome is basically attaching to the mRNA, and then, based on the mRNA sequence, is bringing in amino acids to match that sequence.

So, all the proteins in your body are coded for in your DNA, right? So, when it comes to this process, there's a complex called EIF4F, which acts as a scaffold for the ribosome to hook on to the mRNA. And EIF4F, the formation of it, is basically rate-limited by the association of two proteins called EIF4E and EIF4G.

And EIF4E is bound by a binding protein, 4ABP1. And when you stimulate, when leucine stimulates mTOR, mTOR stimulates the phosphorylation of 4ABP1, which makes it unavailable for binding with EIF4E. It can bind to EIF4G. That EIF4F complex can be made, brings the ribosome onto the mRNA, and now it can read, it can translate it.

So, there's a little cellular biology lesson for you. - Yeah, and if people didn't follow that, don't worry about it. What Lane's describing is that the presence of a bunch of molecules involved in protein synthesis is necessary but not sufficient for the protein synthesis. - Right. - Other things have to happen.

- Correct. - And apparently, those other things are not happening after 120 minutes. - So, another lab called it the muscle-full effect. Basically, the idea is like once you've initiated that signal, it kind of runs and then it's done, right? And just pounding more amino acids into the system is not going to further stimulate.

In fact, there was a study done back in, I think it was 2001 by, I want to say by Rennie, another very well-known protein lab, and they infused essential amino acids for six hours and looked at skeletal muscle protein synthesis. And they found it went up and then came back down by two hours and then never went back up, right?

- Good experiment. - Yeah, very interesting. So, we looked at a bunch of different things. The only thing we found that perhaps explained it a little bit, and I'm sure there's other labs that would argue with me on this, and again, this is in rat skeletal muscle, which by the way, is a good model for human protein metabolism, but still.

We looked at intracellular ATP levels and actually found that they were declining kind of in concert with the decline in muscle protein synthesis. And muscle protein synthesis is an ATP-dependent process. But the process of protein turnover is energetically expensive. It's one of the reasons that protein has a higher thermic effect of food.

And so our hypothesis was perhaps by the effect of protein stimulating protein synthesis to start this machinery is energetically expensive enough that eventually you kind of run out of steam. And so you have the signal there, but it just kind of ends, right? Now, there have been other experiments, like Joran Trommelin just published a paper a few months ago that got a bunch of feedback.

It was 100 grams of protein after a resistance training exercise, and saw that it was basically, like a lot more of it was used than we thought would be used. - Right, because for many decades, it has been purported, believed, and propagated that the maximum amount of protein that you can utilize after a meal is 30 grams.

It became like the holy number. And this study essentially showed that more than 30 grams can be used, not just as energy, but for the sake of protein synthesis in muscle, correct? - Yeah. - And how did that study land with you, given that it's one study? Without going into all the details, did that inspire you to change anything about your protein intake after training?

- So, what I tell people is I don't make big shifts, in my opinions, based on single studies. - Yeah, why does that not surprise me? - It shimmies me a little bit, right? So, and even before that study came out, what I had said is I think protein distribution matters, but I think it matters much, much less than total protein intake per day.

'Cause all we need to do is look at some of these resistance training studies with intermittent fasting, where people are eating all their protein in an eight-hour window. And theoretically, you would think they would get less muscle growth, especially based on this refractory data, 'cause less time to stimulate.

But at least in the studies out of Grant Tinsley's lab, I think there's two studies that were very well done where we don't see that. Now, important to point out, they trained during their feeding window, and they had three, they made sure they ate three high-quality, high-protein meals during that eight-hour time, right?

So, at least in that context, there was no difference in the amount of lean mass gained between intermittent fasting groups versus continuous feeding groups. - And in the continuous feeding groups, do you recall what duration they were eating their meals over? Was it probably 12 hours or so? - I don't recall specifically, but I don't recall an actual defined time.

I'd have to go back and look at it. - More than eight hours. - For sure. - I'm so glad we're landing here because my first, let's just call it sort of operational or actionable question, which came from, you know, asking on social media for questions for you, was many, many people, if not in the thousands, asked how to make sure that they're getting enough protein if they're doing something like intermittent fasting.

And I myself fall into this category. I don't do it for any specific purpose. This was long before Sachin Panda started doing his work on time-restricted feeding, AKA intermittent fasting, but I don't tend to want to eat any food until about 11 a.m. Occasionally I wake up hungry, like this morning, and I had some eggs, I was particularly hungry, but I think that's representative of a lot of people.

I want hydration and caffeine in the morning. I want to train in the morning, and then I want to eat pretty soon after I train. But what that means is that I'm eating during an eight to nine hour feeding window. And if I only manage two meals in there and a snack, and I can only assimilate, or excuse me, I can only put 30 grams of protein per meal toward protein synthesis.

We have to be careful not about using it for energy, but toward protein synthesis. Does that mean that I'm not going to hit my target of one gram of protein per pound of desired lean body mass? 'Cause I'm 100 kilograms, I weigh about 220 pounds. I can easily eat 220 grams of protein in a nine hour period.

Like, give me three ribeyes, I'll eat all three. I love ribeye steak, right? But the question is, can I use that? - So, and I'm going to bring this background to that particular experiment. So over time, and when I left grad school, my position was that it matters. Protein distribution matters.

So I'll give you the straight down the line scientific answer, and then I'll give you, if you inject me with truth serum, what I really think answer. And so we did an experiment, again, in rats. We fed them completely same diets, same total calories, protein, carbs, fats. But in one group, they got that pretty much evenly across three meals, and the other group, 70% of their protein was coming at their last meal.

And then the other two meals were like 15% protein, 15% of their daily protein. And 11 weeks, again, 11 weeks out of a rat's life, rodents live 18 to 24 months. That's a big chunk of their life, right? And we did see about a five to 10% difference in the weights of the hind limbs in terms of muscle mass.

- In what direction? - Favoring equal distribution, right? Now again, hard to repeat that study in humans, right? And for the duration it's done. So I came out saying, you know what? That's actually less than I thought we were going to, I thought we were going to find bigger differences than that.

You know, because, I mean, if you're thinking about number of times you're stimulating protein synthesis, I mean, one per day versus three per day, I mean, shouldn't there be like a pretty significant difference there? And it was, I mean, it reached the level of significance, but again, I thought the effect size was smaller than I thought.

And so I kind of walked out saying, you know what? Total protein intake is the most important thing per day. And then if you can distribute it relatively evenly, that's maybe the last five to 10%, right? And you've seen some human studies where it seems to matter, most seem to show it doesn't really matter that much.

Here's what I think. If you're measuring an outcome like lean mass, that doesn't change much in eight weeks, unfortunately. It's very small differences. And so I think it's going to be hard to detect that, but what I'll tell people is, if you're asking, can you build muscle in intermittent fasting?

Absolutely. Can you build a lot of muscle? Probably. If you are a bodybuilder, specific population, or if your goal is to be the most muscular, strongest human being you can possibly become, I think you're probably better off not doing intermittent fasting just because those last, that last 5% may make a big difference.

And you're never going to be able to pick that out of a human randomized control trial in eight weeks. At least I don't think you will. And so, again, I don't have any human data to really back that up, but just based on what I know about signaling and the effects we saw on animals, that's kind of my recommendation.

But most people don't fall in that category. Most people are just worried about, hey, I want to look good, build a little bit of muscle. Intermittent fasting is a perfectly fine tool for doing that. I will say, you know, obviously we haven't studied some of the more extreme forms of fasting in terms of building muscle, right?

Like the 16/8 has been studied, but like I'm thinking of a study that was done without resistance training, alternate day fasting versus continuous kind of normal feeding. - One day no eating, next day eat. - Right, so they did- - Brutal. - They did- - Or at least for somebody like me.

I can't think of anything worse. I'd rather fast for three days in a row and then eat for, you know, four days in a row simply because I know that by day two, it's probably going to get easier, not harder, but on-off fasting eating has got to be just torturous.

- So the way they did it was they did, the continuous group was getting 75% of their maintenance calories per day, so in a deficit. And then the alternate day group was doing 150% and then zero, right? So you're getting an average of 75. And they actually saw differences in lean mass at the end of that study.

The continuous feeding group lost less lean mass than the alternate day fasting group. So that's only one study and it didn't have resistance training. It's possible that a resistance training could attenuate some of that stuff. But what I'll say is, you know, the more extreme forms of fasting probably aren't optimal for lean mass, right?

- Also, can you imagine training on a day of complete fasting? After three hours after that, you're going to be dying. And then you can say, well, you could just train on the days when you eat, but then if you ever train legs hard, which I know you do, or if anyone does, and then the next day, you're not going to eat anything.

The day after training legs properly, my appetite's increased. - Yeah, so I think this is where the rubber kind of meets the road in terms of straight down the line, the randomized control trials say this, but I still do something a little bit different, right? Because the randomized control trials say, eh, protein distribution doesn't really seem to matter, right?

But again, you inject me a true serum, I think it probably does matter a little bit, right? Now, does it matter as much as total protein? Absolutely not. That is by far the biggest lever. But again, if my context is I want to become the most muscular, strongest human being I can be, which I do, 'cause that's where I compete, I'm going to distribute my protein probably over four to five meals per day, right?

And so for you, just personally, what time of day do you wake up and when's your first meal? - So, well, it's summer right now, so kids are off of school. So we're usually getting up around like 7.30, eight o'clock in the morning. And my first meal is usually within an hour.

And then I usually eat within an hour of going to bed, and then I'll have two or three meals in between those. So usually I have about four meals a day. Sometimes I'll have five, if it's just a longer day or just how my timing kind of goes or whatever.

- And does each one of your meals include approximately 30 plus grams of quality protein, some starchy carbohydrate, fibrous carbohydrate, and some fat? - I mean, sometimes they end up being like mostly protein or whatnot, but for the most part, there's a mix in each one. And usually around 50 grams of protein at a meal.

About 235 grams of protein a day. Some people would argue that, oh, that's more than you need. The researchers shown that 1.6 grams per kg maxes out the response. Here's the thing. And again, this is where like scientific experiments are big blunt instruments, okay? They will tell you what not to do more often than they will tell you what to do, okay?

When it comes to protein, my personal opinion, and this is just, I guess, a little bit of intuition based off of 20 years of studying this stuff, is that I don't know if there's an actual amount of protein that maxes out the protein synthesis response. I would bet, if I was a betting man, that it's kind of an asymptote.

You're familiar with? Yeah. So, you're-- - Not everyone's watching. I just drew an asymptote, an asymptote plot. But for those not watching, just think about a plot quickly rising very, very high and then essentially stays stable at the high level. - Yeah. - Maybe with a slight bit of taper.

- Yeah, so it's easier to explain if it's going towards zero. So, an asymptote might be, okay, you start out, you have 10, then five, then two and a half. - Okay, so you're running in the opposite direction. - Right. - Still asymptote going from high to low. - Right.

- So, asymptote can go from low to high, it can go from high to low. - Correct. So, I'm trying to explain it 'cause it makes more sense when people kind of go this way. You never reach zero, but it keeps getting incrementally closer. On the other end, I don't think protein synthesis ever maxes out.

I just think the increment of increase becomes so small that practically there's no difference and you wouldn't see a difference in outcome, right? And so, I think that there's debate over, is it 1.6 grams per kg, 2.4 grams per kg? And there's even been a meta regression that showed up to 3.3 grams per kg had benefits.

I think a lot of this is with protein synthesis, you're looking for small differences between small numbers. It's not a very sensitive analysis to be quite honest with you. And again, we would never be able to pick out those differences. And I'm thinking about, there was a study by Stu Phillips, if people don't know who Stu Phillips is, he's the best researcher going in protein metabolism right now.

But one of the best, so I don't wanna take anybody off. And he did a study probably 15 years ago where they gave people different levels of egg protein. And they looked at five, 10, 20 and 40 grams of egg protein. And their conclusion was that 20 grams of egg protein maximize the protein synthesis response.

But that's because straight down the line, if there's a p-value of more than 0.05, you can't say there's a difference, right? But if you looked at the absolute difference between 20 and 40 grams, I think it was like 11%. And if you look at the graph, it almost looks like the start of an asymptote, right?

Now this was one study, wasn't a huge subject number, but that's kind of where my personal thoughts land on it, that there's, that kind of also support this, okay, 100 grams in a meal, you know, could still be utilized, is I'm not sure if there's a max out. I think there's a practical max out where you get to a point where, hey, you're like slamming down 50 grams more protein for 0.0001% more protein synthesis, it doesn't make sense.

But yeah, we'll never be able to, I doubt we'll be able to pick those numbers out in actual scientific experiments. And the other thing to keep in mind with this whole protein metabolism picture is we're really only talking about one side of this equation. So net gain or loss of skeletal muscle mass is the balance between protein synthesis and protein degradation.

And most of us protein researchers just kind of stick our fingers in our ears and go la, la, la, la when it comes to protein degradation because it's so incredibly hard to measure. And so, yeah, like when we start to put all that stuff together, it's like now this picture gets really complicated.

So what I tell people when it comes to that kind of stuff is listen, you could really get into the weeds on this stuff. The big rocks are about a gram per pound of body weight. If you want to really, for all intents and purposes, max out the anabolic response, you're going to be fine.

- One gram per pound of body weight, which is what Dr. Gabrielle Lyon also essentially recommended. - Right, I'm probably like, you know, real sticklers might be like, no, it's actually more like 0.7 or 0.8. And then it's, well, it's actually based on lean mass, which I agree with.

But just for all intents and purposes, you could say, you know, your body weight, ideal body weight, whatever it is, that number is going to be very sufficient for maxing out muscle building for the majority of people. - And we should probably point out not just for muscle building, unless you disagree, and feel free to, of course, not that I need to tell you that.

Dr. Gabrielle Lyon, when she was here, made a really key point, which is that ingesting sufficient quality protein each day isn't just about building muscle, even for folks that don't want to build muscle, and perhaps even particularly for women who assume that, you know, building muscle can be a runaway process that maybe they're going to build too much muscle.

That's a false assumption, of course, that ingesting one gram of protein per pound of body weight or ideal body weight is going to be beneficial because it's going to improve muscle quality, one's own muscle quality, the health of the muscular tissue. And then she did an excellent job of relating the health of muscular tissue, skeletal muscle, that is, to overall health and longevity.

So I just raise that because I know that many people listening to this probably want to add a little bit of muscle here or there. Some perhaps want to keep the muscle they've gotten loose fat. And some, of course, want to add a lot of muscle. But it sounds like the recommendation is always the same.

Since we need to eat sooner or later, one gram of quality protein per pound of lean body mass or current body weight or desired body weight, that's going to be a good starting place. - Yeah, for sure. And I think I would tend to agree with her. You know, the process, because when you eat protein, you're not just going to start laying down slabs of lean tissue just from eating protein.

There has to be a stimulus, which is resistance training. Or some people would argue you could stretch really hard and get the same thing, which there may be some evidence of that. - With weights and lift them in between stretches. No, I'm just kidding, which is basically weight lifting.

- There actually are studies now where they like put people in like really kind of hardcore stretching for several minutes and they actually see hypertrophy with it. Yeah, very interesting. We could talk about those if you wanted. But the point is either way, it's mechanical tension, right? So that's the stimulus, to build muscle, to lay down lean tissue.

But the process of remodeling is probably beneficial for multiple reasons. So when you eat protein, like we said, synthesis goes up, degradation goes up, right? Because you're stimulating that process. You're stimulating protein turnover. One, that's relatively energetically expensive, all things being equal. So that's where the thermic effect of protein comes from.

'Cause people say, well, it's the urea cycle and this and that. Most of those ATPs you get back in different phases of that cycle. Really, in my opinion, the thermic effect of protein is due to like kind of activation of this futile cycle of you're building more protein, but then you're also breaking down more protein.

And so part of that is you are remodeling. You are making sure that that protein is higher quality in that tissue by continuously breaking it down and building it back up. And so I would probably agree with that. And then it's, again, even if you're at a resistance training program where you're not really building much more muscle anymore, the process of remodeling is probably good for you.

And I would just say, try to ally some of these concerns from people who are concerned about getting too much muscle. So I have been lifting really hard consistently for 25 years. I am very comfortable with saying I train harder than almost anybody else you can possibly imagine. And anybody who has trained around me will back that up, back me up in the comments.

I train very hard. And in a shirt, I look like an athletic guy who lifts. I don't look like a monster, you know? Like you might see pictures of me when I was a bodybuilding show and like very, very lean, and that looks, you know, over the top. But for the most part, I just look kind of athletic.

And I've spent my entire adult life trying to get too big, right? So for most people, unless you're on performance enhancing drugs, or you just have incredible genetics, that's not gonna happen. And if it starts to happen, just back off on your lifting, easy fix. So yeah, I think most people's concern with that is a little bit misplaced.

And the other thing I'll tell people is like, hey, some of these like fitness, like especially like for women, a lot of these fitness models you follow, they show you certain workouts they do, they built that physique by lifting weights, right? And you're thinking that's a toned feature. Well, that person is actually pretty muscular, right?

And so again, especially for women, there are exceptions. Some people, some women have very great genetics for building muscle. They usually wind up in track and field, that sort of thing. But it's very hard to get too muscular for a woman. And what I'll say is like, you know, typically muscle looks good, and fat is what makes you kind of look bulky, you know?

So again, I don't want to paint with too broad of a brush, but I would say that you don't really have too much to worry about when it comes to getting too muscular. - I'd like to take a brief break to thank one of our sponsors, Element. Element is an electrolyte drink that has everything you need and nothing you don't.

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Again, that's drinkelement.com/huberman to claim a free sample pack. Since we're sort of in this realm of protein, maybe we build out from there, 'cause a lot of questions related to something akin to the following. So, okay, so somebody strives to get one gram of quality protein per pound of body weight per day.

And I realized that whether somebody follows a pseudo-intermittent fasting thing where their first meal does around 11, and they finish up eating around 8 p.m., or a more traditional eating schedule really is just the addition of one more meal, like in the morning. It's like whether or not you eat breakfast.

And of course, some people shift it the other way. They start with breakfast and they don't eat dinner. But I would argue that in order to, if you have kids or a social life of any kind, most people can deal with sitting across the table with someone just having a cup of coffee for breakfast, but it's sort of awkward.

You limit yourself a lot in life if you can't eat dinner with other people. I don't know, at least- - And that's, again, where the rubber meets the road with what is practically doable, 'cause there've been some of these like circadian rhythm studies that suggest, well, maybe early time-restricted feeding is better than late time-restricted feeding.

The more high-quality, more rigorously controlled, randomized controlled trials are coming out now seems to show that it doesn't really make a big difference. And some of the, again, the measurements you use matter, right? So there was actually a very recent study where they looked at 12 weeks. They provided all the food to participants, equal in protein, calories, the whole deal.

The only difference was one group was eating 80% of their calories before 1 p.m. and they had a eight-hour feeding window in total. The other group had a 12-hour feeding window and were eating over 50% of their calories after 5 p.m., I wanna say. And so really, based on some of the chrononutrition stuff we've seen from some of the lesser well-controlled trials, they were expecting to see differences in glucose metabolism and whatnot, and they just didn't really see a difference in anything.

And I think the only thing they saw a little bit of a difference was in fasting blood glucose. And here's what I tell people. When you see a difference in fasting blood glucose but not HbA1c, you're looking at a transient difference. And what I mean by that is HbA1c is such a great measurement because it's an area on hemoglobin that can be glycosylated.

And so that is very dependent on what is your overall concentration of glucose in the blood over a 24-hour period of time? Because it's exposed the entire time it's in your bloodstream. So whether you're getting glucose spikes at meals or you have higher fasting blood glucose, it's gonna be very reflective of the overall 24-hour area under the curve, right?

So why do some of these studies see a little bit better improvement in lowering fasting blood glucose whereas HbA1c doesn't show up? Well, think about it. If somebody is early time-restricted feeding and they finish most of their food intake before 1 p.m., they have an extra six, seven, eight hours that they're not hardly eating anything.

It doesn't surprise me that the next morning, because they've technically fasted for longer, you have a lower blood glucose. Now, I can't really back this up straight up 'cause nobody's ever measured it, but that, I think, is a logical explanation while you see some of this stuff. And that's why I tell people the measurement you take really matters.

I think fasting blood glucose is a useful measurement, but I put much more value on something like HOMA-IR, euglycemic clamp, or HbA1c. So anyways, I think the early versus late time-restricted is, kind of doesn't matter too much. - Great, you answered a future question right there. - See, I've-- - You're telepathic.

- Mm-hmm. - Uh-huh, that's what you didn't know about 'em. So the scenario here is whether or not meals are distributed evenly through the awake day or stacked a little bit more toward the morning or stacked a little bit more toward the evening, if somebody gets that one gram of quality protein per pound of body weight, then they need to make up the rest of their calories with other stuff.

- Mm-hmm. - And we have, broadly speaking, starches, fibrous, you know, fruits and vegetables, starches, and of course, fats. - Right. - And weight gain and weight loss, I think we both would agree is, or weight maintenance, is going to largely be dictated at this point by whether or not you consume more calories than you burn or not.

So assuming somebody's getting that one gram of quality protein per pound of body weight, is there any data that support, or do you believe, just by your own experience, that there's some value in stacking the starchy carbohydrates toward the earlier part of the day versus the later part of the day?

And this has been an ongoing debate. Like I, for instance, like a nearly pure protein and fat meal for the first meal, plus maybe a salad, some fibrous carbohydrates. And then as they get towards evening, I like more starches and I actually taper off the protein. I find, personally, that matches what I need to do with my brain.

I'm more alert when I'm drinking caffeine and hydrating on a backdrop of slightly lowered carbohydrates. But then as I get towards evening, taper off the caffeine, of course, for me, 'cause I want to sleep well, start ingesting some more starches. It's not starch heavy, but I sleep like a baby.

But everyone would tell me, and does tell me, eating starches late in the day is going to make me fat. Eating starches late in the day is going to do all sorts of terrible things. I find the exact opposite for me. So is there any real evidence that where one places their starches throughout the day matters?

And let's just forget resistance training for the moment, because there is this post-training window where if I train first thing in the morning, I will eat starches at that time. But let's just remove resistance training for the moment. - So again, we're about rubber meets the road in practicality versus what hard line research says.

So I am not real convinced at all that it really matters when you eat your carbohydrates. - Thank you, thank you, my goodness. I knew I brought you here today for a reason. No, I brought you here for many reasons, but- - Is that my bias has been validated?

I can leave now. So I really try to get people focused on the stuff that matters the most, right? So this is, if we're worried about carbohydrate timing, even if there are differences, we are zoomed way in on the blade of grass, right? We're not zooming out all the way.

And I think, hey, if somebody likes to eat more carbohydrate in the morning and that fits their lifestyle, and that is easy for them to continue to do, then I would say do that. - And could I add, in terms of not focusing on a blade of grass, but something that I consider a major lever, if eating fewer carbohydrates in the afternoon and evening doesn't impede your sleep, then you're okay.

But I would argue if anything is interfering with your sleep on a consistent basis, you've got a serious problem. - Yeah, so there are no solutions, only trade-offs, right? And when it comes to carbohydrate intake, you'll hear people say, the data's all over the place, okay, in terms of like timing and how people feel.

Some people say, well, I feel sleepy after I have carbs. Some people have, I feel great after I have carbs. Like I'm ready to go lift. I have a big carb meal before I go lift, you know. It seems to be all over the map. Now, here's the thing what I'll tell people, because people ask me how I eat.

People have wanted me to do a full day of eating video, and I've kind of put it off for a while, 'cause I'm like, so much of the stuff I do, I'm not gonna give you guys a citation for, you know, and I know you're gonna want it. And some of the stuff I do, 'cause I just like doing it that way, right?

Like I grew up in the era of bodybuilding magazines where they said you gotta have a big carbohydrate intake and a big meal before you go train and a big meal after you train. So guess what I did? I got in the habit of eating like that, and it still sticks to this day.

I don't try to tell people it's better doing it that way. Plenty of people have told me, hey, I don't feel good with a lot of my stomach when I go train. Or if I have a carb heavy meal in the morning, I feel tired. The data doesn't really support that in terms of like, you know, on an average response.

But if you know that you feel that way, then by all means avoid, right? Like there's plenty, I remember one time I, so I used to go to a massage therapist in Tampa who would do cupping, and there's really no data to back up the efficacy of cupping. - Is that right?

- Yeah, not much, but she did it. I liked the way it felt. And I'm like, okay, whatever. So I posted a picture of me flexing one time, you know, and there's the cup marks all over, and everybody's like going crazy. Like, how could you do this? I'm like, hey, hey, hey, hey, wait a second.

I never said this does this, and I never made any claims about it. She does it, and I like the way it feels. I'm not saying it does anything. Actually, one of the things about being a scientist is like now I'm impossible to placebo, which is really annoying, 'cause I would love to be able to placebo myself a little bit more.

- 'Cause placebo effect is powerful. - It's powerful, and it's one of the, I was telling you earlier before we started filming, I'm like, it's one of the reasons I just don't believe a lot of stuff, because I know how powerful the power of belief is. I mean, you had Sean Mackey on here.

Your beliefs about pain change your pain, like actually change how much pain you get. It changes your pain experience. So, one of the things I've become big on recently is, hey, what happens in the mind affects the body, and what happens in the body affects the mind. So, just because I don't have a randomized control trial to support something, if we know the RCTs don't say it's worse, right, then you do whatever you like, right?

And I think a lot of people get bent out of shape when I say, well, you know, when they control the variables that need to be controlled, there's no difference between intermittent fasting or just regular old calorie restriction, or there's no difference between low-fat diets and high-fat diets. What people hear is, low-carb sucks.

Intermittent fasting sucks. He said they don't work. No, no, no. This is great. This is great news for everybody. It means you have all the tools at your disposal, and you get to pick the one that fits in your lifestyle best, because that is what makes the difference, is what your overall lifestyle looks like, and we have way too many people worrying about the minutiae who just don't even exercise on a consistent basis, or they don't sleep well on a consistent basis, or they don't manage their psychological stress well, or they try to be perfect with their nutrition, then they fall off the deep end, and what I'm saying is, no, be imperfect, but be consistent with what you do, right?

And so, for you, obviously carbs at night have not made you fat. Like, I have eyeballs, so we can just dispel that myth right now. - Yeah, I would say eating the way I eat now, I'm leaner at 49, even than I was 10 years ago, or 10 years before that.

I was pretty lean then, and I don't put a ton of attention to tracking calories, although, and I want to be very, very clear, I was not paid to say this. I've purchased and use Lane's Carbon app. He happens to be wearing a shirt that says Carbon today, but I've talked about this before on other podcasts and social media, and it's absolutely true that there's no endorsement relationship, but I love the app because that was really the first time, probably since college, 'cause I started lifting when I was 16.

Running and lifting has always been my thing since I was 16, but since college that I used a tool, in this case, Carbon, to basically track what I'm eating, like exactly what I'm eating, and what I like about it is that I can just click on different boxes of things like within the app, and really, it makes it very easy.

Say, oh, like I ate this thing, white rice from this package, and it generally knows products, it knows brands, and it did a really good job of letting me check in and just see how many calories I was consuming, how much protein, how much fat, and from what sources, but one of the major takeaways that at least I got from Carbon was that you can arrange your diet any number of different ways.

In fact, it has like a really nice little slider where you can put in, you want to eat more carbohydrates and less protein even, or you want to have a vegetarian diet, which I don't. I'm an omnivore. I'm an omnivore. My dad's Argentine, I like meat. I like meat.

In fact, I don't even really like fish that much, or chicken, I just like eating meat and eggs, those are my preferred sources, and whey protein. Okay, fine. But you can arrange things within the context of different types of diets, and I think there's real value to tracking precisely what one eats for even short periods of time.

And then I confess, I stopped using the app for it, but then I went back to it, and not because things want to drift. I think some people really need that consistent checking. Other people need to perhaps just kind of eyeball it for themselves. But for me, I've found that knowing exactly what I'm doing for some period of time allows me to explore things in a way that's really effective.

And so I just want to give a nod to Carbon, and I don't do product endorsements on this podcast, I do ad reads and that kind of thing for things I love, but I say that because I think it lands squarely in the context of what we're talking about, which is that I know what works for me.

I also know that some people really love like a giant carb meal in the morning. Some people don't like meat. Some people, and I think what's so beautiful about the way that you've been talking about science and nutrition in particular over the last few years and still here now, is that you don't really seem to care whether or not people are vegan, vegetarian, omnivore, or even carnivore, dare I say.

It's just a matter of how people are couching the advice. - For sure. - And the reason I keep coming back to this is that I really think that you, this discussion, but you in particular are best poised in this whole field of public facing health, nutrition advice to really change the way that the messaging occurs and the way that people hear that messaging.

And I say that with the utmost respect. - That means a lot to me, thank you. - Because most people are not going to go read the meta-analyses. And most people don't know how to parse data. But I think that paying attention to the words that are spoken right before the advice should be, we need to think, come up with something like, that's like the Norton method.

Pay attention to the words provided right before the advice. - Yeah, I think how you say it makes all the difference. And even, take somebody I've had conflict on social media with, which is Paul Saldino, which when he would say something like, "Well, I cut vegetables out of my diet "and I felt like my eczema got better." Okay, that's your experience.

You can't go, on average, that's definitely not reflected in the research. But hey, if you know that you did this thing and you felt better, that's fine. But how we're overgeneralizing to the population is the problem, right? And so I think, I mean, again, I'll say, hey, I calorie cycle a little bit, which again, you can do using the app, right?

You can change your days and what not, give you more calories some days, more calories other days. And I was, I showed a screenshot of it one time and somebody goes, "So why do you do it like that? "Like, is that because it's better this way "for like muscle growth and fat loss?" And I go, "No, 'cause I had a get together "with friends on Saturday "and I knew I was gonna have a couple of beers "and I knew that there was gonna be some fatty food.

"So I put 4,000 calories on that day "and lost the rest of the week." And they're like, "That's it, that's your reasoning?" Like, yeah, like compliance is the biggest one. I will tell people, I'm like, the reason that I, and we talked about this earlier, like I have never used performance enhancing drugs.

I've never even, even when pro-hormones were legal, I didn't use them. - And you're not on TRT. - Not on TRT. - We need to distinguish this because people nowadays like gonna put TRT, well, as long as it's keeping someone's testosterone in the normal reference range, which is somewhere between 300 and 1,200 nanograms per deciliter, then they're like, they're not a, you've never injected a synthetic version of a hormone.

- No, and like my testosterone, even from like age 18, when the first time I had it measured up until like even a year ago, the lowest it's been, I think it's been like 750 and the highest it's been was like 1050. And so I obviously don't need it.

- Yeah, you don't need it. You're well, you're on the upper, you're high normal. - Right. So the reason that I've been able to have so much success, and I get the skepticism, I really do. So many people say, I mean, look at how many people are out beating their chest saying they're drug free and then it comes out that they weren't, right?

But I have been brutally consistent for 25 years. In 25 years, the longest I ever took off of resistance training was seven days and it was after I won world championships in 2022 for M1 93 kilo, you know, so I've been able to be really consistent with my training.

And I always give this comparison of, I think it just really highlights how powerful consistency is. And it relates back to my favorite quote I've ever heard. "The magic you're looking for is in the work you keep attempting to avoid." The work is the hack. If people, and I liked what our friend Peter Attia said this when he was talking about biohacks and why I didn't like the term biohacks.

He said, I don't like that it occupies so much mind space, right? You get people really focused on the minutiae, which is fine if they're already doing the big stuff, if they want to kind of level up a little bit, cool. For me, minutiae is where I live because the difference between me winning a powerlifting meet and me losing world championships is 1%, right?

But for most people, we just got to get inconsistent. If I said, Andrew, I want you to become the best three-point shooter you possibly can be, but you can't get any coaching and you can't even watch any tutorials, right? But all you did for 10 years was go out and shoot three-pointers for two hours a day.

You probably won't go to the NBA, but I bet you'd be pretty good at three-pointers, right? And I feel like if people could just get that message and internalize it more. No, it's not that you didn't have your carb to fat ratio perfect. No, it's not that you ate your carbs at the wrong time.

No, it's not that you didn't get exactly this much protein. It's you just stopped being consistent. You stopped doing it. Yeah, you were really consistent Monday through Friday, and then Saturday and Sunday came and you blew out, right? Like if I'm consistent with my budget Monday through Friday, but then I blow it on the weekend, hey, guess what?

That weekend money still counts and calories are the same way. - And you enjoy resistance training. - I love it, I love it. - Do you do cardiovascular training? Defined as, 'cause people get, I'm starting to catch flack these days when I say cardio, believe it or not. Repetitive motion movement designed to elevate your heart rate for 12 minutes or more.

- So I'll usually do like a five minute warmup on the bike before I train. And then I will also make sure I get at least 10,000 steps on average per day. I usually average more closer to like 11,000, but I don't do a lot of purposeful cardio. Now, what I will tell you is my average heart rate in lifting sessions is about 140 to 150.

So if the definition of cardio is that, then I'm getting cardio. And actually when I've had, you know, most of my markers of metabolic health assessed, I'm very metabolically healthy. I've got good, actually it was funny. I just competed at nationals in late May and won. So I won, and actually, again, very cool kind of side story.

We talked about the injuries I've dealt with. And so I'm 42 now, it's been an eight year journey. And I mean, going from, I've had back pain so bad I couldn't even get up the floor. Needed a cortisone injection in my spine at one point, just to be able to stand up.

And multiple hip injuries, a lot of chronic pain I dealt with. And I'm very proud of myself that I never gave up 'cause in my heart of hearts, I felt like I haven't hit my last PR yet. And at nationals this past year, I actually set a national deadlift record for my age and weight.

- Congratulations. - And it was actually an unofficial world record and qualified for world championships. But one of the team USA coaches, his name's Matt Gary, him and his wife Susie are like, in evidence-based powerlifting, they are the goats. And there is no better game day coach to pick attempts than Matt and Susie Gary.

Other than maybe my coach, Ben Escrow, shout out to Ben. But they were at the meet and we've known each other for 15 years. And the next day I came down into the lobby and they're down eating breakfast. And Matt's like, "Your ears must be burning. We were just talking about you." And I'm like, "Oh, what?" He goes, "You know what I'm impressed with?" He goes, "Your cardiovascular fitness." And you know, powerlifting meets nine lifts, right?

You get three attempts on squat, bench press, deadlift. And so I kind of like looked at him weird. He goes, "We were there between warmups and finishing. It was about four hours. You never sat down. You were yelling the entire time. You're talking the entire time." 'Cause I'm a very extroverted, active person.

Then when I'm firing myself up, it comes out very extra. He's like, "You're yelling the entire time and you never were tired." And again, when I look at my heart rate and I was at the meet, I think the average was like 150 or 160. And so some people would not consider that cardio, but I would say my cardiovascular system does all right.

- I would argue it might be related to you're not getting sick very often. It's very clear that activation of the sympathetic nervous system is one main driver of the immune system. This is why often people observe that they go through a very stressful period of life and then they go on vacation and they get sick, or they're taking care of a loved one and that person either gets better or passes away, there's some ending to that caretaking, and then they get sick.

- I have observed that exact thing. When I went through my first divorce, I was also involved in a lawsuit with a company that I used to own a portion of. It's a very long story, ended up having a good ending for me. And all that stuff kind of resolved itself, the divorce, the lawsuit, everything resolved itself in about a six-week time period.

As soon as it resolved, I got sicker than I ever had been in my entire life. I got the actual influenza. I tell people after that experience in 2018, I go, here's words I'll never use again. I think I might have the flu. No, you know, after you've had it for sure, you know.

But it was like my body had just, maybe it's a little bit of woo, but it was like my body, I dragged it across the finish line and then said, okay, we'll see you in a couple of weeks 'cause we're taking a break. - When you think about human evolution, I mean, these are just so stories.

Anytime people talk about human evolution, by the way, like no one really knows, but the idea that, you know, if there was a famine or you need to take care of children in famine, the idea that you would be more vulnerable to disease at those moments, sure. But it's also true that the catecholamines, dopamine, epinephrine, norepinephrine, activate certain components of the immune system that protect you against things.

I mean, it's not gonna protect you against everything, but it's when you relax and rest finally that you are more vulnerable to incoming infections. - And we see this with pain too, right? Like you had Sean Mackey on talking about this stuff where, you know, I forget who was talking about this.

I remember listening to a podcast with, it wasn't him, but it was another pain expert. And they said, you know, because your beliefs about pain, your stress level, your sleep, like your psychological milieu actually matter in terms of your pain experience. In fact, the single biggest lever I've pulled to get me consistently training and pain-free was becoming more relaxed and less stressed out all the time and managing my psychological stress better.

You know, when you're not vibrating and spun up all the time, your body has, again, this is a little woo-woo-y, but I think you have more energy. I mean, if you look at- - It makes sense. It makes sense. I mean, those catecholamines, I mean, there are other molecules involved too, but that, you know, dopamine, epinephrine, norepinephrine, you know, cocktail is driving us forward in motion and thinking, you know, all the time.

And if you're putting thoughts into one set of things, they're not going elsewhere. Like you said, it's all trade-offs. - I read something from a PhD in psychology who said, "Stop thinking about your problems. "The problem is you're thinking "about your problems too much. "Thinking about it doesn't solve them.

"And just ruminating on them makes it worse." And actually, again, if you look at like pain literature, fibromyalgia, chronic fatigue syndrome, very close ties to psychological stress. And we were talking earlier about like, if you look at the data on mortality, cardiovascular disease, cancer with ACEs scores, which is Adverse Childhood Events Scale.

So zero being best, you were loved as a child, that sort of thing, you had no real big worries, 10 being basically abused. There's like a very, I don't wanna say very tight, but there's a dose response of ACEs scores on the risk of mortality. So what happens in the body affects the mind, and what happens in the mind affects the body.

And we were talking about with pain literature, what happens in the mind affects the body in your pain experience. And even just something like sleep. There was a study done where they looked at military members, and they had eight hours of sleep versus four hours of sleep, and they looked at the risk of acute injury.

236% increased risk in the people getting four hours of sleep versus eight hours. And now here's where people get this wrong. Somebody reached out to me and said, "Well, I got four hours of sleep last night, should I?" No, no, no, one bad night of sleep doesn't do that.

Sleep is a cumulative effect. Just like if you have a week's long worth of bad sleep, but then you sleep 12 hours on the weekend, you're not making up that sleep debt. It's more about what you're doing time over time. - Just like nutrition, just like training. - Exactly.

And so this actually brings me to, I know we kind of have gone down the rabbit hole here, but when you look at, Ben Carpenter did a great example of this. He has a good social media account. He had a jar of blue marbles and a jar of green marbles.

He said, "Let's pretend that this is all junk food. "These green marbles are all junk food, ultra processed. "This blue is minimally processed whole foods, right? "If my diet is mostly junk, and I add one good meal," and he puts a blue marble in the green, "did it change things?" No.

And everybody knows that, right? Like if you eat a mostly junk diet, you have one good, one salad or one good meal, it's not gonna change things. So why does everybody think if we take one from here and put it over here, that it drastically changes things? Because it doesn't.

It's about what you do consistently over the course of time. And so speaking of, we're talking about the mind affecting the body, but then the body also affects the mind. And so there was just a study published, I just covered it on my channel, where they took men with general anxiety disorder and major depressive disorder, and they had them resistance train two times a week for 25 minutes a session, 50 minutes total, eight weeks.

- It's not much training. - I think it was like six hours and 40 minutes of total training over the entire two months. Now, in statistics, you're familiar with an effect size, which is basically how meaningful is an effect, because you can have a significant effect that isn't very meaningful if you have enough subject number.

So when we say things like an effect size, 0.2 is considered small, 0.5 is considered moderate, and 0.8 is considered large, anything above 0.8. SSRIs are typically in the 0.3 to 0.5 range. I think in like best case scenarios, they get up around a 0.8, 0.7, 0.8. The effect size for resistance training two times a week, 25 minutes a day for eight weeks was a 1.7 on major depressive disorder.

- Wow. - Anybody who's a scientist out there, if they hear effect size of 1.7, they do exactly what you did. Their eyebrows go up and they go, "Are they sure that's right?" You don't see effect sizes like that very often. And I want to be very clear, I'm not saying do resistance training in place of SSRIs.

That's a very-- - Of course not. But these individuals had not trained previously. - They hadn't trained before, yeah. They were healthy or actually don't know the specific characteristics, but I knew they were coming from like not training, right? Now, hey, like, listen, both these things could be true.

Maybe somebody needs to get an SSRI because like depressed people don't even want to get out of bed a lot of times, right? So getting them to the gym, even if they know it's going to help them is a hard, it's a hard swing. So maybe coupling that. But that's just resistance training and that affects this, right?

So I think one of the biggest revolutions we're going to see in science is the broad application of biopsychosocial across a bunch of different disciplines and stop thinking about, well, your body's a bag of meat and it's attached to your brain. And if you poke the bag, punch the bag, burn the bag, cut the bag, brain goes owie.

And I think we're going to start thinking about things much differently. And I think it's going to open up a lot more in science. And in fact, honestly, if I had to go back and do a PhD again, it would be in some sort of like psychology or whatnot, because I just think there's so much untapped in that realm.

And I was actually talking about this with somebody the other day and it's pure anecdote. I'm completely speculating. I have yet to see an interview with somebody who's in their nineties or hundreds who sounds really stressed out. They're mostly like DGAF, right? And when you ask them what they did like, most of them say, "Oh, I drink wine every night." Or the one I remember, she was like 110.

She's like, "Yeah, I drink a Dr. Pepper every day," or whatever. It strikes me that, and again, genetics matter, their lifestyle matters. I'm not saying any of that stuff doesn't matter. I don't see, at least in my experience, people who make it old age, they're not usually very spun up all the time.

I just, I haven't observed that. I don't know if you've seen similar observations or- - They seem to enjoy life. I have a grandfather on one side that died earlier, but a grandfather on the other side who lived into his nineties and he ate a steak every day. He smoked till pretty late in life before he eventually quit.

He had ice cream dessert after every dinner. He's Argentine, so they stack their meals toward the end of the day, definitely. He liked walking. I guess the point is that he was always interested in what was in the newspapers, but he wouldn't get riled up about it. He liked walking.

He really enjoyed life. If there's one key characteristic to describe him is he really enjoyed life. Now, he didn't take the best care of himself in the sense that had he perhaps never smoked or quit earlier or dropped the excess calories, he might've lived an additional two or three years, but he was really happy until the end.

- And that's the lesson there is we're not saying that that stuff doesn't matter. He would have gotten better results if he hadn't smoked, if he had paid more attention to his nutrition, that sort of thing. But we have to keep in mind, like what is the hierarchy of importance and the power here, right?

And so I'll give you an example. We're going to zoom in on the blade of grass, but I believe it relates back to this conversation we're having. So we know creatine works 'cause we've got thousands of double-blind placebo-controlled trials showing that creatine works, right? But there was a study where they gave people creatine or didn't give them creatine and then randomly told them if they got it or not.

Meaning you had people who didn't get creatine got creatine, who didn't get it, told they didn't get it, people who got it, told they got it, people who got it, told they didn't get it. And what they found was the results, and I forget what they actually specifically measured, but the results basically were like, not what they got, what they told them, okay?

Now, people will misinterpret that as, well, see, creatine doesn't work. No, no, no, it works. It just means your beliefs about what creatine does are more powerful than what it actually does. Just like actually there's a similar trial with caffeine. And I'm thinking about there was a study, Brad, I don't have the specific citation, but they had two groups of men train drug-free.

One group, they told they were getting steroids. That group gained significantly more strength and muscle mass. Now, I would argue that's probably 'cause they're going into training sessions believing that they can train harder, believing that they will recover better. But that goes to show the power of placebo and the power of belief.

When I say placebo, people think what I'm saying is you're lying about your experience. That is not what I'm saying at all. I think your experience is probably quite valid. What I'm saying is it may not be due to the thing you think it's due to, but your beliefs about the thing.

And so where I get really focused is let's do the big stuff right, because so many people are so worried about little stuff. And one of the things I'll tell them is, hey, I have no data to back this up, but my intuition tells me that the amount of stress you're spending on these small variables is probably killing you faster than if you got those variables wrong.

And if we could just focus on the big rocks first, and if we can pick up some pebbles after we get the big rocks, great, but don't drop the big rocks trying to pick up pebbles. - I love it, and I love this example of the creatine experiment, because just to repeat the conclusion, because I want to make sure that people don't take away the wrong conclusion, creatine works.

- Absolutely. - But your belief about creatine works more in this case. So two things can work, one more than the other, and the placebo, aka belief effects, are very, very powerful. - Exactly. - I completely agree with you there. Wonderful way to set the stage for some of the specific questions that were asked when I said on social media, I'm going to sit down with Lane Norton again.

And I'm very curious about some of these as well. So I'll inject some of my own experience and questions. Training to failure and reps in reserve. We should define these a little bit. And before we get into it, it's fun to have these kinds of conversations nowadays about resistance training, knowing that both men and women should resistance train.

People who want bigger muscles and who don't should resistance train. Because in the past, it was always about like bodybuilding and pre-season football and people going to the military. I think thanks to the great work that you've done, but I'll just give a particular shout out to some of the women in the nutrition and fitness space, namely Dr.

Gabrielle Lyon in terms of menopause, perimenopause, Dr. Mary Claire Haver, and women in that sector really emphasizing the key need for resistance training. There are other names as well, but really championing the importance of resistance training. Training to failure in my book means when you can't move the weight by whatever means anymore in good form, in proper form, that's failure.

So we're not talking about four straps. We're not talking about swaying the upper body or using momentum. So training to failure, you can't move the resistance anymore in good form. And reps in reserve, my understanding is one's own subjective understanding about how close they are to that point of failure.

Do I have that right? - Yeah, so you define failure the way I define failure, which is you cannot take the weight through another concentric repetition without breaking form. Reps in reserve would be an RIR of one means you stopped one rep shy of failure. RIR of two, you stopped two reps shy of failure and so on and so forth, right?

And so I would define those that way. - Okay, so with those definitions in mind, is training to failure more effective at generating strength and hypertrophy increases than if one keeps a few reps in reserve? And of course we have to balance this against all the factors related to recovery, et cetera.

But assuming that one follows a program of doing, and I'm really just trying to cut us right through the middle here. Let's say two or three exercises per muscle group and does after a sufficient warmup, let's say two to five sets that we're going to call work sets. You could imagine an extreme scenario where every single work set is taken to failure.

You could imagine taking only the last set of each exercise to failure. You can imagine taking none of them to failure. Assuming adequate volume is achieved across the week. My understanding is this is 10 to 20 sets per muscle group across the week. It could be distributed across different workouts or all done in one workout.

Is training to failure going to generate more strength and hypertrophy than leaving some repetitions in reserve? So let's start with the extreme scenario. I go to failure on every single set and I do what I need to to recover. It doesn't matter if it's only doing that muscle group once per week or spread out multiple times per week.

I'm doing what I need to to recover in between. My genetics, my hormone status, my sleep, my nutrition, on and on. Is going to failure more effective than not going to failure? - This is going to generate a lot of discussion in the comments. I can't wait to see it.

So I'm going to cite quite a bit of work from my powerlifting coach, Zach Robinson, because he is at FAU, just finished his PhD and did a lot of meta-aggressions and meta-analyses on this exact topic. So I'll give you the answers first that are straight down the line scientific answers and then I'll explain things.

For muscular hypertrophy, you need to get close to failure. But you probably don't need to train to failure to maximize hypertrophy, but you got to get pretty close. You can be stronger, but to maximize strength, you're probably better off not touching failure very often. So there are a few studies now looking at this, showing that, I think there was one study recently, and I can't remember the exact details, but I remember it being pretty well designed.

And the takeaway was, hypertrophy was similar between the groups, but the group that went to failure, or stayed a few reps shy of failure, actually got stronger compared to the group that was taking most sets to failure. - And did they control for total volume of work? - Yes, so- - Okay, 'cause I can imagine not going to failure, you can do more sets because you've got- - And that's exactly- - More quote unquote gas in the tank, right?

- And practically that may be a benefit of stopping shy of failure, right? But yeah, they control for those variables. So when we talk about volume, the way we define that is essentially number of hard sets, which a hard set would be a set close to failure. The general consensus is within five reps of failure is considered a hard set.

Now, what I will tell people is, that may not sound like much, most people have never truly pushed themselves to failure. Okay, and I'll give some practical examples of me. So my best set of squats ever, I did 530 for 10. This was a long time ago. - Yikes.

- I, when I finished that set, I actually, somebody had to come save me because I couldn't fully lock out my lumbar and I couldn't get the bar on my right side all the way back up. So they had to run over in the gym and help me. After that set, I laid down and I physically hardly couldn't move for about 15 minutes.

- So this is, you know, gun to the head type failure. - Yes, you do as many as you can. Your family's been kidnapped. If you don't get these 10 reps, you're, you know. - All those mental games. - That sort of thing. And I mean, I was done.

You know what I mean? And so one of the things I'll tell people is, the first five reps of that set were still hard. They still felt hard, right? And so people will say, "Oh, you stop a rep or two shy of failure. "You're trained like a," I'm like, "So you're telling me "if I stopped two reps shy on that one, "that that's an easy set?" 'Cause it's not, I can tell you that.

And the reason I'm giving this background is because in research studies where they have people who are like beginners or intermediates and they ask them to rate their RIR, they tend to underestimate their RIR, right? So they'll say, you know, during a set, say your RIR, and they might say two.

And what they find is when the researchers push them to true failure, yell at them, crank the music, get them really psyched up, they get five more reps than they think they'll get on average, right? So most people, if you've never actually taken things to true failure, you actually probably don't know what it is.

So I do think it's useful to train to failure at times. - I think you make a very important point, which is that occasionally training to failure gives you a sense of what failure really is for you. And no one can really tell you that, only you can tell you that and experience that.

But if I understand correctly earlier, you said, once you know what failure is for you, then if strength gains are your goal, and I think more and more people, by the way, are training for strength who don't want hypertrophy, at least not across every muscle group. I think when I talk to the general public, which I do a lot, I get the sense that men and women are like, yeah, I'll lift weights.

I can see the value of that. Would love a little bit more muscle here, a little bit more muscle there, but they don't wanna be generally larger. And yet they can understand and appreciate the value of getting stronger everywhere. 'Cause being strong across your whole body is one of the core definitions of health.

- Being strong is fun. So again, for hypertrophy, doesn't seem to matter if you take every set to failure or stop a couple reps shy. I would argue that probably you'd want to leave most reps, most sets shy of failure. And if you're gonna take one to failure, take the last set of an exercise to failure.

'Cause then you can get whatever benefits might be there. But if you take the first set to failure, I mean, imagine if I did that set of 10 with 530 on squats as my first set to... What am I gonna get the next set if I try to do 530?

I can tell you based on how I felt, maybe three reps, maybe, you know? And so your performance is just gonna really drop off a cliff if you're going to true failure on like a compound exercise. Isolation is a little bit different. And so I would say, whereas if you probably could have done like sets with six, seven reps for multiple sets and then have gone to failure on your last one, right?

Now, it may seem a little bit counterintuitive. Why would it be the same for hypertrophy but different for strength? Well, with strength, you also have to think about stimulus to fatigue ratio because fatigue will mass strength, right? And I know this because I've... Like when I overreach for powerlifting competitions, which is basically like we're taking me a little bit past my point of what I can recover from.

I mean, I've had literally before nationals in 2017, I was warming up on deadlift in my last heavy deadlift session, like 10 days before the meet. And I went to pull my final warmup, which is 585, and I couldn't budget off the ground. I was so tired, sore, I couldn't get...

It was like, I couldn't get my body to do what I wanted it to do. 10 days later, I pulled 716, right? It's amazing what fatigue will mask. And so if you're always training to failure, you're gonna be training under pretty high fatigue circumstances. Doesn't really matter for muscle growth 'cause it's really just about doing enough hard sets and putting that mechanical tension on the muscle.

With strength, you also have to think about like, what is the most pure form of strength? It's force production, right? And force is mass times acceleration. So you have a mass component, you have a speed component. And so this is actually Zach Robinson and his company, Data-Driven Strength, who I've been coaching with for three years.

I heard them on a podcast, and he was giving his hypothesis of how to optimize strength in a powerlifter. And I remember thinking, I really like the way this guy is thinking. He's thinking outside the box and it makes a lot of sense. So one of his things was, if you're training close to fatigue all the time, and the goal is strength, think about what that means in terms of your force production.

So let's say you do a set of eight reps, right? Your first few are pretty fast. And then by the end, they're pretty slow. The load hasn't changed. So what happens to your force production? Your force production is going pretty far down. He said, I don't really want my athletes grinding reps in training.

I want them to hit some heavy singles and doubles and triples because they need that because that's a skill. You have to have those neurological, everybody's done this where they go, well, I hit this for 10 reps and here's what my one rep max should be. And then they go in and get stapled with it, right?

Because it doesn't necessarily translate because a one rep max or the purest form of strength is a very specific skill. If you've never trained it, it's very difficult to get accustomed to. So we wanna hit some, his idea was in workouts, we're gonna hit a heavy top set, heavy single, double or triple or whatever it is.

And then our back offsets, instead of taking those close to failure, instead of doing say, well, we'll do, 75% of your training max for sets of eight and have you getting pretty close to failure. Instead of doing three sets of eight, why don't we just do like six sets of four with that weight?

Because now you're doing those first four reps, which you can move that weight faster. You're having greater force production and creating the same good stimulus, but with less fatigue. And so again, that was kind of the hypothesis and he did a meta-analysis, meta-regression that supported this. And now some of the randomized control trials have come out and shown something similar.

And in my experience, I was honestly shocked at, because he had all kinds of stuff to deal with when he first started training me. 'Cause I still was dealing with a lot of back pain, a lot of hip pain. I hadn't really gotten that under control yet. And when I got ready for Worlds in 2022, which I think we did our first podcast like the week after I had won Worlds, I worked up to being able to do like two or three hard sets of squats a week and deadlifts.

And that was all I could do. That was all my body could tolerate before I get pain. And so we did a lot of low load, relatively low, low for me, 60 to 70% 1RM for low rep number sets, but trying to move it as fast as possible to keep that pain under control for me, but to get the stimulus.

And I was shocked at how strong I got because before in 2014, 15, when I was winning open national titles, I mean, I was doing 15, 20 hard sets of squats and deadlifts a week and way more for bench press. And so I always thought, well, that's how much I need to get to that level of strength.

And even now, like, so we've been able to keep progressing it. Now I'm doing probably more like six, seven harder sets of those exercises per week. And I'm basically back to the strongest I've ever been. We're doing way less sets. And I think a lot of it is, we have learned to find the sweet spot with managing that stimulus to fatigue ratio.

So all that to say, if your goal is building strength, it's mostly about, you know, doing enough like heavy lifting that you actually do get stronger. And then if you wanna train closer to failure, you can, because again, most of my audience isn't trying to be a power lifter, right?

- No, but I think a lot of the audience would like to be stronger and not necessarily grow their muscles bigger, except in a few specific places on the body. - And so this would be the protocol. There we go, protocols, little plug. This would be a protocol for probably, not necessarily like growing the most muscle mass, but getting stronger because you're not training so close to failure.

But, you know, obviously you're trying to move, as Zach says, whatever that given load is, you wanna move it as quickly as possible. And so, and there's actually also data to show that like if you train slower purposefully, that it's not as good for strength. So they actually, there was a, I think a meta-analysis recently where they looked at either concentric repetition of more than two seconds or less than two seconds and saw strength outcomes were better in people taking less than two seconds to complete a rep.

- Interesting, so that's the concentric phase, the lowering phase, the eccentric phase. - No, we're not sure about that yet. - Interesting. - So, I mean, we do use some tempo training in my training, but it's mostly because like me doing a slower tempo squat, if my back starts acting up, I can do some squatting and not really hit that pain trigger as much.

So, but I'm still trying to move the concentric as quickly as possible. And so I don't know about that. It doesn't matter how slowly you move the concentric versus how fast you move it. But yeah, what I would say is, when it comes to building muscle, really the world is your oyster.

The research really shows machines versus free weights. - Low reps, high reps. - Low reps, high reps, going to failure, stopping a few reps shy. It all builds the same amount of muscle for the most part. - But you have to work hard. - But you gotta work hard.

Yeah, you gotta be consistent with it. Obviously like the theme of this podcast, right? But you can do it anyway. And if we look at the, I mean, obviously anecdotal, but if we look at the history of the Mr. Olympia is they all train very differently. You know, I mean, Ronnie Coleman.

I mean, I'm sure you remember when the "Unbelievable" came out, his DVD back in like 2001, where he's tossing around 200 pound dumbbells and he's doing seven, 800 pound squats, 600 pound front squats. And everybody's just looking at this like, my God. And then you watch somebody like Phil Heath train, who again, one of the greatest Mr.

Olympia's of all time. Phil mostly did machines, but he built obviously a great amount of muscle. Now people will say, well, they're on steroids. All those guys. - Yeah, it's all controlled. - Trust me, it's an equal playing field 'cause they're all doing it, right? - And the research shows anywhere from whatever, you know, five to 30 repetitions can generate hypertrophy as long as the final few repetitions are really hard and volume is adjusted.

I really like- - There is no hypertrophy rep range like people used to think of as, oh, it's like six to 15 reps is hypertrophy. Now I think practically it makes sense to do a lot of your sets in that range because if you're trying to do 30 reps getting close to failure, I mean, gosh, I'm gonna run out of breath if I'm doing any kind of compound.

- Also if you work out in a- - It's a little boring for me. - Yes, and if you work out in a gym where there are other people, like be kind. You know, like other people are gonna need the space and the equipment. So, you know, it could take forever, you know, 10 sets of 30, like that's impolite.

So we're only half kidding there. One of the more common questions is about training for people 50 years old and older. And I love the fact that we're talking so much about strength. This seems to be one of the key evolutions in this field. Again, in my opinion, the people who've come through this podcast as guests, Dr.

Gabrielle Lyon, yourself, Andy Galpin, who now has his own podcast, The Perform Podcast. Like more and more discussions about strength and training for strength for the general public, not just people who want to be power lifters. So I think there's a lot of carry over there. And I think the more that people hear us say that resistance training can be really powerful for health and longevity and getting strong is one of the best things you can do for your health and longevity, injury protection, et cetera.

Peter Ortega has talked about this and it's not just about building muscle. Want to know how they should adjust their training, if at all, if they are 50 and older. So obviously one of the key things to getting and staying in great shape over time, I always say is avoid getting hurt.

Could we say, okay, don't try anything too novel and crazy without easing into it. Could we also perhaps- - But I would say that goes for anybody, quite frankly. - Okay, could we also say perhaps find the movements that you can do without injury and just keep doing those over and over?

Is there any evidence that mixing up the exercises is important, meaning doing new movements? Or if you find two or three movements that work well for you, can you just stick with those and just work on progressive overload? - I think you can stick with those. I think, you know, muscle, the whole concept of muscle confusion, muscle knows tension and how long it's under that tension and for how many sets it's under that tension.

It doesn't, it's not like, well, this is a, I can tell that this is an incline bench press versus an incline dumbbell. I mean, you know, you might move through different ranges of motion and whatnot, but the tension on the muscle is the tension on the muscle. So what I'd say to people is, I think most people probably change up things too much because there is like a neurological adaptation to doing a specific exercise where you get stronger at it.

And so now you're using more load, you can create more mechanical tension. But if you're always changing things up, you might not take advantage of that full, you know, kind of neurological adaptation. But if you're always doing the same exercises, it's too easy to get comfortable and fall into, well, did I do three sets of 10 and I always do three sets of 10 and I use this weight?

And that's what I do. And now you're no longer progressively overloading. So I think there has to be a balance between enough changing of exercises to kind of promote some novelty, because as you know, novelty, there's a reward center in the brain for that, just changing something. And think about anytime you're gonna try a new workout, you get a little excited about it, you know?

When I was gonna try Zach's way of training, you know, three years ago, I was like, oh, I was very, very excited about it, you know? So I think there is a place for that, but I think people tend to fall into a little bit too much of doing the same thing over and over or constantly changing things 'cause they're always chasing that novelty.

And I think that the reality is probably somewhere in the middle, but specifically for over 50, I think whatever you can do with low pain level and be consistent with that you enjoy, that's what's best for you. I mean, I always tell the story, I had a client who, they loved CrossFit, they loved doing CrossFit.

And they said, you know, I wanna build muscle and I know it's not the best workout for building muscle. I said, it might be for you because if you hate bodybuilding training and you're not motivated to go do it and you don't enjoy it, you're probably not gonna work hard at it.

And so maybe for you a CrossFit workout is the best muscle building workout because if I try to get you to do something else, you'd hate it and would lose motivation. - Right, and it feeds back to that consistency principle that you talked about before. - Exactly, so when we look at like, I think this might be interesting for some of your listeners.

So when we look at how much muscle you can build after a certain age, you can build the same amount of muscle as a percentage of your starting skeletal muscle mass, okay? So what I mean by that is once you're 50, 60, you've usually lost some muscle, okay? And if you've never lifted before, if you go into lift, as a percentage basis, it appears that you will still gain the same amount of lean mass.

But for example, if somebody has 80 kilos of starting lean, most of your podcast listeners are USA, I assume. So let's say somebody has 150 pounds of lean mass when they start, just throwing a random number, and they gain 10% over a couple of years. Now they have 165 pounds of lean mass, they've gained 15 pounds, but the percentage is 10.

If somebody starts and they have 100 and say, 20 pounds of lean mass, 10% of that is 12 pounds, they gained an absolute less amount, but as a percentage, it was similar or same. And we actually see that with women too. Women actually develop as a percentage of their starting lean mass, the same percentage increase in lean mass as men when they do the same level of hard training.

So what I tell people who are, I'll have people say, well, you know, I'm too old to start resistance. No, no, now is the perfect time to start, right now. And honestly, it doesn't take a huge dose. I mean, if you wanna be like, you know, get into powerlifting and like compete at competition, yeah, now it takes a bigger dose, right?

But what it takes to get, and I'm just gonna throw a number out, 80%, the majority of the benefits for health, strength, resistance training, you could probably get in three, four sessions of 30 to 40 minutes. You know, you don't have to have a huge input of time. And just look at the depression study we talked about.

Obviously that's not like muscle and strength, but two sessions of 25 minutes, I mean, it is a absurdly low dose that you require. And I think a lot of people, I try to be careful about this too, we'll see how I train, which is two, three hours a day for five days a week, and think that's what's needed.

No, no, that's what, I wanna go win a world championship. That's what's needed for that. It's not needed for you to build muscle and get stronger. And even when I was at grad school across the street, they did a study in frail elderly where they had them, basically they had trouble like standing up from a seated position.

And by the end of a 12 week study of them, like progressively overloading them, which was basically like them just lowering the seat at first, right? And then maybe adding like a little bit of weight. They saw these people built muscle, built bone, got healthier, better quality of life.

And these are people in their seventies. And there was a study in Australia that actually got on the news. Peter Atiyah talked about it with elderly women who I think they were above age 70. And there's some of them in there deadlifting like 150, like upper hundreds in deadlift, you know?

It's incredible how, I took a class called Skeletal Muscle Structure, Function, and Plasticity. Your skeletal muscle is so adaptable. It is such an adaptable tissue. It's amazing. The same thing that can allow somebody to squat, Jesus Oliveira, shout out. Squat over a thousand pounds is the same tissue that can allow somebody to run a hundred miles like David Goggins.

Think about that. That's really incredibly adaptive. And so what I'll tell the people, regardless of your age, your sex, whatever demographic you are in, resistance training for just a couple of times a week for a short period of time will drastically improve the prospects of your quality of life, your longevity.

I mean, if we look at hand grip strength, we look at lean mass, they're all inversely associated with mortality, especially the older you get becomes a stronger association. And I always tell people, I'm like, it's not about the hand grip strength. This is a proxy for just strength overall, right?

There was a study where they looked at pushups and found pushups were inversely associated with mortality. It's not that doing pushups is magic. It's that that is a proxy for that person being strong. And we focus so much of our attention, especially like on falls in the elderly, right?

Well, if they had more bone mass, they wouldn't break their bones. What if they didn't fall in the first place 'cause they were strong enough and had good enough gait and balance to catch themselves? And oh, by the way, nothing better for increasing bone mass than resistance training. So I am a huge fan.

And then we already talked about like the metabolic, like skeletal muscle. Gabrielle touched on it. It was one of the first things Don Lehman said when I came in his lab. He goes, "Skeletal muscle fits every definition of an organ. "And we don't talk about it like an organ.

"We talk about it like it's this inner tissue "that just sits there, and it is not. "It sends out signals to other tissues. "It integrates signals from other tissues. "It is an endocrine organ." And so many people have unhealthy skeletal muscle. And if we treat, and what happens when you resistance train?

What happens when you build muscle? Muscle is a metabolic sink. It is greedy, right? It's sucking up. It's incredible. You can take people who are type two diabetic, and if you get them on a slight calorie deficit, you get them to start exercising. It is incredible how fast their blood markers will start to resolve.

Like they can still be obese, and you'll see their blood markers start to resolve within, like you'll see improvements in weeks. Lehman did a, I wanna say a 16-week study in either diabetic or pre-diabetic women back in like 2003, I wanna say. And he said within four weeks, he said we already saw these blood markers start to resolve.

Like your HbA1c hasn't resolved, but a lot of these other markers started to resolve because at a fundamental level, at least in my opinion, and other metabolism people may disagree, I'm a big fan of Occam's razor, which is plainly stated, all things being equal, the simplest explanation is typically true.

The actual hardcore scientific definition is the hypothesis that requires the least amount of assumptions is usually true. You're putting in so much energy into a system, and you're running out of places to put it. So you have skeletal muscle mass, you have liver, these other tissues in the periphery, and then you have adipose tissue.

And did you know they actually show people who have more adipocytes are actually more resistant to type two diabetes. So they have more smaller fat cells that can soak up more of this stuff. And since type two diabetes is basically too much glucose in the blood, right? And a lack of insulin sensitivity, small adipocytes are more insulin sensitive.

And so what happens is we, at least in adipocyte physiology, we used to think of adipose as also an inert tissue. And now we know that's not true either. - And lots of different cell types. We used to just think that there was brown, beige, and white fat cells, and subcutaneous, and intravisceral.

Now they've done sequencing of different white fat cells, and like 25, probably now 50 different, I mean, different genetics among those cells that respond differently to insulin. I mean, fat is a very interesting and heterogeneous tissue. - It's really interesting. But most fat cells, at least based on the literature I've read, and again, I'm happy to have somebody correct me who's an expert in this, but they can expand to a certain point where it really becomes difficult for them to get bigger.

The integrity of the cell, 'cause you still got a cell wall, you have a plasma membrane and everything, and you have an extracellular matrix that is scaffolding this fat tissue onto your body. And so at a certain size of adipocyte, it basically becomes, you just can't pack any more in there, okay?

And so if you can't put any more in muscle, because muscle isn't, you're not active, and muscle's not moving and churning through substrate, and you can't pack any more into adipose, where does it wind up? It's in your blood. You can't get, and now when your blood levels, it's interesting because there are some people who have all these theories, but like one person, a researcher, was like, well, I think branched-chain amino acids actually cause insulin resistance, 'cause we see them elevated in the blood in type 2 diabetes.

And I was actually in a, it was in a, I was a grad student watching this person present, and I put my hand up, I said, isn't everything elevated in the blood in type 2 diabetes? You know, why are we picking on branched-chain amino acids? So you do have some people who too can become type 2 diabetic who aren't obese.

They tend to have not as many fat cells, which sounds like it'd be an advantage. And if you're lean, or sorry, if you are not overeating, right, and getting enough exercise in, it probably is an advantage because you have less overall fat mass. But you are going to reach that critical mass of an adipocyte of about 100 microns, I think it is, faster because your overall fat cell number.

So at the same fat mass, your fat cells are bigger, and bigger fat cells are less insulin-sensitive. In fact, one of the treatments for type 2 diabetes, sulfonylureas, I think they're called, they're PPAR gamma agonists. They actually increase the production of fat cells. They create new, small fat cells.

Now you have a place to put stuff, and you lower your blood glucose. So very-- - It's a reservoir. - Exactly, and I'm overgeneralizing, to be sure. And again, I hope if I've butchered anything, somebody will come in and correct me. - They will. - But what's amazing is this stuff in the blood, you just gotta get stuff moving.

Like, 'cause you start doing exercise, start controlling your calories a little bit, guess what? You're oxidizing things to the Krebs cycle. You're going through glycolysis. You can now start to pull things in, right? You're using this substrate. You can start to pull things in. And because you're pulling things in, now adipose can start to release some of its free fatty acids into the blood, or some of its triacylglycerides into free fatty acids into the bloodstream, which can also facilitate this.

So using muscle, you are, it is a partitioning effect, and it doesn't take long to start lowering this glucose, blood lipids, these things in the blood. It can actually resolve, you know, at least those markers can start resolving themselves pretty quickly, which is why, you know, when we look at weight loss, what level of weight loss they say is clinically relevant, it's only 5%, right?

Which you'll have obese people, and they'll say, well, 5% weight loss, you see these big benefits in like blood lipids and metabolic health. You wouldn't think with just 5% weight loss you would get that, but you do, because you're just giving a little bit of space to get that stuff in the blood out.

Now, again, this is my, I want to be very clear. This is not a proven thing. I feel pretty strongly that this explains a lot, but again, this is my personal opinion about how these diseases develop and whatnot. But it is, I think it's relatively simple. - Yeah, using, thinking about muscle as an organ, thinking about feeding muscle, we talked about that earlier, thinking about moving muscle, and in particular training for strength, resistance training of different kinds, hypertrophy, yes, but I, you know, I'm kind of given a little bit of a biased vote for more strength training out there across the population for really for the longevity reasons.

I mean, Peter Atiyah has pointed out that the percentage of people who die after a fall, not because of the fall itself, but because of a hip injury or a wrist injury, and then they go immobile, or they're just not exercising as much anymore, then they get an infection, and then it cascades.

In fact, I had a conversation with one of my parents recently on their 79th birthday. I said, you know, in the next five, 10 years, your biggest risk is probably going to be going downstairs or stepping off a curb, not going up, but as Peter's pointed out, going down.

So that eccentric movement, you know, being able to sustain a fall, being able to not fall, to catch yourself, so to speak. - Well, and practically you fall farther going downstairs than you do going upstairs. - Right, than going up. Exactly, and that pattern of falling while going down precedes a lot of infections that end up deadly, right?

So, and, you know, hats off to Peter for really pointing out the relationship between those things, and to you for encouraging people to strength train. Also, I love the idea that I don't have to go to failure if I'm in strength training, 'cause I like training heavy, but the training to the point where the muscles are quaking, even though that's how I initially started training, 'cause I came up in the Mike Mentzer camp, I actually find that it eats into my recovery in a way that maybe is a little more subtle, but meaningful nonetheless, which is that I feel fatigued later in the day.

Whereas if I complete a training session where I can complete every rep, I notice I don't get into that quaking thing. I actually have a lot of mental and physical energy later in the day. - And it's psychologically and emotionally fatiguing as well. - Maybe this one could be out of a brief answer, or maybe not, I don't know.

Are there true age-related changes in metabolism that are independent of decline in muscle mass? I saw a paper, I think it was published in "Science" a few years ago that said that metabolism actually doesn't slow that much as we age. Of course, total muscle mass- - So you mean BMR?

- BMR, basal metabolic rate. In general, well, I should just say, up until that paper came out, I thought, okay, as we get older, our "metabolism slows." Then of course, we have to remember that puberty and childhood is sort of like being on performance-enhancing drugs in the sense that protein synthesis is just massive and ongoing.

But let's just say from age 30 onward, let's say between 30 and 80, assuming that somebody's doing things to maintain muscle mass, is there any reason to believe that their basal metabolic rate actually goes down just as a function of age? - Yeah, you're citing the work from Herman Ponser and really great lab-looking energy expenditure that he does a lot of great stuff.

And so that study was looking at several thousand people, I think, looking at their total daily energy expenditure and really found it's pretty flat from like age 20 to age 70. And then it kind of starts to go down, but you can tie it to the loss of lean mass.

And same thing for basal metabolic rate when they do indirect calimetry. If you look at, and this goes for older people, also women versus men, and then also type two diabetics versus non-type two diabetics, obese versus non-obese, 80, I think the number is like over 80% of the variance in BMR is completely explained by the lean mass, by the amount of lean mass somebody has.

And by the way, the last 20% probably is explained by where that lean mass occurs. Because liver, for example, is a more metabolically active tissue gram per gram than pretty much any other tissue. The skeletal muscle is more metabolically active than fat tissue, but for a lean tissue is actually somewhat like metabolically slow because it's turnover rate is only like 1% to 2% per day.

- You just have a lot of it. - Yeah, right, right. But on an absolute amount of calories you burn, you burn a lot in muscle because you have so much of it. Great point. So things like gut, liver tissues per gram of tissue are very active. So yeah, just doesn't seem to be, for a long time, we spent so much time focused on the metabolism side of things when we're looking at aging, when we're looking at obesity, and we just didn't really find impressive stuff.

So obese people don't have slower metabolisms on average. The research shows that actually on an absolute basis, they're faster than people who are normal weight. When you standardize for lean mass, it ends up being about the same. People who are type two diabetic, same thing. When you standardize for lean mass, if anything, they have a little bit faster BMR.

And so if you think about it, it actually kind of makes a little bit of sense on a biochemical level because if you're insulin resistant, you're also insulin resistant in fat tissue, right? So like, okay, so it makes sense that maybe you waste some more energy because you're not able to put it where you wanna put it, right?

So the people get upset about this because like, oh no, it's gotta be metabolism, metabolism. And then GLP-1 memetics have really kind of shown, no, the answer to this question is very much on the appetite side of things. It's like, we tried to make a bunch of different drugs that would increase metabolism.

We tried to do all these things to increase metabolism and nothing seemed to really make a big difference. And then we came out with the most powerful appetite suppressants in the history of mankind and people are losing large amounts of weight and keeping it off. So I think people got too focused on that metabolism side or what I hear a lot of is from like post-menopausal women, I'll hear somebody say, my metabolism dropped.

What probably happened, you're sleeping less, you're more stressed, you don't feel as good because the hormonal changes, you don't feel as good. And so you spontaneously became less physically active and didn't realize it because our NEAT, like our non-exercise activity thermogenesis, our non-purposeful physical activity that we do, fidgeting, pacing, is actually a large portion of our daily energy expenditure.

And people get this wrong. You can't make yourself do more NEAT because then it's just exercise. If you're purposely doing it, it's exercise. - Bouncing your knee. - It's all subconscious, right? But if you're not sleeping as well and you're feeling worse, spontaneously, you'll just not move as much.

And I know that people, that feels like there's a lot of judgment and shame associated with that, but it is the truth. It is a practical limitation and it may not be metabolism. I guess I'm a little bit pedantic with that, but it still contributes to your overall energy expenditure.

And so again, they've looked at this and I mean, there is some evidence that like if your estrogen drops and you replace that with supplemental estrogen, that that can like help out with like maybe 50 to 100 calorie energy expenditure per day. So if you're replacing something that's like now clinically low.

But my guess is that it would also drive more activity, feeling better, more activity, sleeping better, more activity. - And that's where it's hard to disconnect that, right? So yeah, I think metabolism wise, the results ended up being pretty underwhelming for all this stuff that we just assumed, well, if somebody's overweight, it's 'cause there's low metabolism.

The research didn't pan that out, but I still think it was very interesting. And again, it speaks to like the power of the mind and the connection in the mind of how some of these drugs act. But I do tell people when they say, well, calorie deficit didn't work for me.

And obviously my metabolism was messed up 'cause I had to get on Ozempic to lose weight. I'm like, well, it doesn't really do anything to metabolism like the speed of your metabolism. What happened is you just, you no longer mindlessly snack. You feel, you are now in touch with your satiety signals and that's why you're losing weight.

And that's why these drugs, they work. - All right, so speaking of Ozempic, Munjaro and similar, let's talk about these drugs that are reducing appetite. And in fairness have allowed millions of people to lose substantial amounts of weight and keep it off. This topic tends to get people a little bit riled up on social media, because I think for some reason, people believe that if one gives these drugs the nod, you're essentially saying you don't need to exercise.

But I didn't see anywhere or hear anywhere that the use of any compound, drug or otherwise, is mutually exclusive with taking good care of oneself in other ways too. So what are your thoughts on these compounds and what you're seeing out there? - I think my take is pretty balanced on this, which is I think they appear to be great tools for people reducing their intake and reducing body fat.

And it functions through appetite. I mean, these drugs are GLP-1 mimetics. And so GLP-1 is a hormone secreted by the gut in response to feeding. And it acts on the gut as well as the brain to reduce appetite, slow motility. So it's a satiety hormone essentially. Now it has a very short half-life in the body.

So the reason a lot of people will come out and say, "Well, there's things you can do naturally to increase your GLP-1." This is like talking about, I mean, yes, a BB gun fires a projectile and a tank fires a projectile, but there's a pretty big difference, right? So with GLP-1 mimetics, what's happening is they're taking that protein and changing out some of the amino acids in that protein.

And it basically just gives a much longer half-life. That's why people can take it once a week or whatever it is, 'cause it just stays around much longer. And so if you think about the food environment we live in, which is free access to cheap, hyperpalatable foods, our brains for the most part are probably not equipped to regulate appetite in that environment.

And it really actually is kind of incredible how resilient the human body is, because if you look at when the obesity crisis started, we already had ultra-processed foods available. We had cakes, cookies, all these sorts of things, but the difference was you had to go to the bakery and get it, or there had to be some small barrier, right?

And then, I think kind of the barrier that got flipped was basically now, in the last 30 years, you can go anywhere and get access to cheap, ultra-processed, hyperpalatable, calorically-dense foods. And they just don't have the same effect on satiety that normal food does, where, like I have a Kevin Hall study at NIH where they took people from a minimally-processed diet and switched them to an ultra-processed diet, and they spontaneously increased their caloric intake by 500 calories a day, like overnight.

That may sound like not a big deal to some people listening. That is a very big deal. - It's about a pound per week of increase in body weight. - Yeah, I mean-- - Assuming. - Assuming that there's no increase in energy expenditure, which we know happens over time.

But with these GLP-1 memetics, they're slowing down motility, they're acting on the hypothalamus, they're reducing appetite, and it's a very powerful effect. Now, some of the side effects are nausea. Some people reported kind of like a, not freezing, but like too slow motility, essentially. So there's some GI side effects, which are kind of to be expected with something like this.

And on one side, you've got, it's so funny how everything gets politicized these days, but on one side, you've got people saying, oh, these drugs have no side effects whatsoever, and heck, I think everybody should be on GLP-1s because we're not made to live in this food environment. And then on the other side, you've got people saying, well, this just obliterates the need for hard work, and these people don't take accountability, and I don't really think either of those messages are really useful.

I think there's a lot of nuance here. And I mean, it's a drug, and every drug is gonna have side effects, some worse than others for different people. And so for some people, it's not gonna make sense to take it based on their lifestyle and side effects they get.

But for other people, I did a post on this where I talked about how much weight people lose on average, and so many people in the comments said, I've lost 100 pounds, or I've lost 80 pounds, or whatever it is. - Taking Monjaro or something. - Yeah, one of these GLP-1 memetics.

And again, going back to our conversation of big rocks, people worry about lean mass loss, they worry about, there was a study in, I think, rodents, where they saw an increase in thyroid, I wanna say thyroid cancer or something like that, but it was not really a physiological dose, and again, it's rodents.

People say, well, we don't know what the long-term effects of these drugs are. Well, they've actually been around for diabetes treatment for a couple of decades now. But, I mean, do we know what they do in 50 years? I guess not, but we know what obesity does. So I'm gonna take Ron White's line, which is shoot the alligator closest to the boat.

I think if somebody's very overweight or obese, and they've tried a bunch of different methods, and people say, well, they just haven't been consistent. Okay, so we can live in fantasy land, or we can live in the real world, which is maybe some people just need some more training wheels than other people, okay?

If we could stop putting an ethical judgment on how easy or hard it is for certain people to do certain things. I mean, it's easy for me to say just be consistent because nutrition has never been a problem for me. I've never struggled with my weight, but I struggled in other areas of my life that why can't I just be more consistent?

Why can't I just do the things I know I need to do? I'm sure you would feel the same way about certain things in your life where it's like, well, I know logically what to do, but it's hard for me to do it, right? And so if we look at the burden on the healthcare system of obesity and these type two diabetes, and then all the metabolic diseases associated with them, it's hard for me to imagine a scenario where this is not a big net positive, to be quite frank.

Now, I wanna, this is, as my friend John Deloney says, it's both and, okay? Some people, this is really gonna help them, and it should be done in concert with lifestyle changes and lifestyle education, because we don't want people to go from eating a lot of a crappy diet to a little of a crappy diet, right?

We want them to make better choices overall. But sometimes, again, habit coupling, people don't get motivated and then get results. People start getting results and then get motivated, right? And so a lot of times, people will start losing weight, and now they're motivated to go to the gym. They're motivated to eat better.

It's, it is, it doesn't happen in a linear path. These things are kind of like, you know, like the opposite of a vicious cycle, where this is, you're getting into a good cycle, right? And a lot of people tend to fall into these categories where when things go bad, they go really bad, 'cause it's a vicious cycle.

When things go well, they go really well, 'cause it's a good cycle. And so what I would say is with the concerns about GLP-1s, the one I hear most is loss of lean mass. So in studies, people who use GLP-1 medics, they lose like 30 to 40% of the weight from lean mass, which is a concern.

But by the way, that is similar to the amount of weight from lean mass people use who diet without resistance training or exercise. So I don't think that it's a unique problem to GLP-1s. My guess is when we start getting studies that combine exercise with GLP-1s and look at lean mass retention, we'll probably see pretty similar results.

So I'm not super worried about that. On a practical level, I can see some concern with it, because if you don't have much appetite, you're usually not selecting protein as kind of your first line of what you're gonna pick. And additionally, fiber, you're not usually gonna select as your first.

So I think, again, these are great kind of like, if we think about like training wheels, I think these are great training wheels for people. And through natural, just having less appetite, people start controlling their intake better, and then all these other habits start to fall into place for some people.

And I talked to a friend who, she's a nurse practitioner, and she tried a GLP-1 mimetic, just 'cause she's like, "I'm a nurse, I wanna see what this stuff is like for me." And then she talked to a lot of her clients. And the anecdotal feedback that popped up a lot was, it stopped the food noise in my head.

I wasn't thinking about food all the time. I just stopped thinking about it so much. And if you look at obesity, I mean, again, it really is on the appetite side. We know that obese people have lower sensitivity to satiety signals. They get a greater reward from food. Like I just posted about a study the other day where they gave a milkshake to people, and they didn't really see a dopamine response.

And, but in people with binge eating disorder, when they give something like that, they do see a dopamine response. So a lot of it is contextual, right? And so I think a lot of it's contextual around obesity of, okay, these are people who get a greater reward from food on average.

They're thinking about food more often. They've probably also dealt with people telling them in their entire life or however long that they need to lose weight. And so food is always on their mind in one thing or another. It's kind of like in "Ghostbusters" where they say, don't think about anything bad.

What's the first thing you're gonna do? You're gonna think about something bad, right? And so trying to calm down food noise while knowing that you need to eat less food is probably pretty difficult. So on the whole, I think these drugs are positives. I think it's gonna lower the healthcare burden.

And I think it's gonna help a lot of people. And the other thing I'll say is like, there's been a lot of pushback in the fitness industry by fitness influencers. - Why do you think that is? Like, as if it's gonna take their jobs away. It's like the same way that people fear AI.

Like it somehow get like, like this stuff is here to stay. It benefits many, many people. I feel this way about these GLP-1 mimetics and I, mimetics, excuse me. And I feel the same way about AI. It's like these things could be, yes, potentially used for evil, but you know, also for good.

- If I think back about when I might've had that sort of reaction, I was in my early twenties. And that's when I thought obesity was a choice. I still think there is personal responsibility involved in obesity. But I think my feelings about obesity at that time were, if somebody's obese, they're making the choice.

They don't care about the stuff they eat that mindfully they are choosing to eat these foods knowing this is gonna be the outcome. - Like self-inflicted. - Yeah. And I don't think that's the case at all. I think a lot of people's habits and behaviors are on autopilot, you know?

I can remember very clearly, I dropped my kids off at school one day. I stopped at 7-Eleven to fill up with gas and like grab something from the store, a drink. And there was somebody, there was a obese woman in front of me and she was getting two slices of pizza at 8 a.m.

And at first I kind of had that knee-jerk response of, oh, she's so lazy, of course she'll. And then I thought, you know what? This is probably something she's done for a long time. This is probably a very habit where she goes to 7-Eleven, she gets pizza. Or on Tuesday morning at 8 a.m.

she's around this area and she goes to 7-Eleven and gets pizza. And maybe not, but I think a lot of people out there are like that where their habits and behaviors are very much on autopilot. It's not this mindfulness that we think they're doing. And that translates into other areas.

And the other thing I realized is I'm like, it can't be laziness, like all of it, because there's obese people who are very successful in other areas of their life. So they don't want to work hard. And so, at least not for everybody, that can't be the explanation. And I think with fitness influencers or people who have, you know, they've worked hard, they've built a good physique.

It's almost like, how dare you get results without doing it yourself? I did this without any help, you know? And the reality is you might've had help because your upbringing might have not been food focused. You might not have had a mother who was always on you about food, or you might not have had parents who shamed you if you didn't clean your plate.

You might've had genetics that made you more sensitive to satiety signals. You might've had a phenotype where if you overeat, you tend to just become spontaneously more active. That's part of the obese resistant phenotype. And so you might've had an advantage and you just didn't realize it. So I think if we could just get away from the judgment of stuff and look at, take the judgment, all that stuff out of it.

Does this seem to help people? And is it gonna be a net positive on society? Thomas Sowell said, in order to make compassionate policy, you have to have dispassionate analysis of the data. And the data says this is gonna be massive for our society, and it's a huge benefit.

So regardless of my personal feelings of, "Hey, somebody should be able, look at Ethan Suplee, lost 300 pounds doing it through all hard work and exercise." I'm pretty sure I've talked to Ethan about this and he said, "I think this is great." Because it's hard to get people to believe if people believe what they can see.

And so if they start seeing results, then they can buy in. And yeah, I think overall it's a net positive. So, I mean, maybe studies will come out in 10 years and people are falling over dead from this stuff and we'll say, "Oh, whoopsies." But I mean, you have to shoot the alligator closest to the boat and right now the biggest burden on our healthcare system, I think I'm correct in saying this, and the biggest threat in a lot of ways is how metabolically unhealthy our society is getting.

- Yeah, I think also when people hear about these drugs, they think about the person who's slightly overweight or who is already fit, who wants to be even thinner. And that's not what we're talking about here. And I have a good friend who is an air traffic controller. He works very, very hard, very stressful job, obviously, high consequence job, and he's very overweight.

He's gotta be more than 300 pounds by a significant margin. And he's really struggled over the years. And for years he talked about getting his, quote unquote, "stomach stapled." You know, that's sometimes referred to that way. Couldn't afford the surgery, this sort of thing. And I asked him about it.

I was like, "What's that about?" He's like, "I just need something that's gonna allow me "to move without pain or a little bit less pain." Every time he tries exercising, he injures himself. And he's probably going about that incorrectly, but he doesn't have a lot of time. And he literally has lives in his hands.

He's married now, he may have kids soon. So I haven't spoken to him recently about these drugs, but to me, it seems like that's the perfect candidate for these drugs. If he could eat less with more ease and lose some weight, and then also start exercising, I think that'd be a significant win for him.

So scenarios like that are what I think of. And then also, you know, it's a mostly free world in many places, not all. So if people can afford these things and they wanna take them, like who am I to say they shouldn't take them? You know, I feel like the amount of judgment involved to say that somebody should or should not use a drug is that's safe and potentially helpful for them is like kind of, I mean, that's almost offensive in a way.

- Yeah, I mean, if you had something that, like if we came out with a drug and it's like, it looks like for a lot of people, this can fix opioid addiction, right? - Yeah, you'd give them that drug. - We'd be shouting from the rooftops and celebrating, right?

We wouldn't say, well, you just gotta gut it out and work harder. You know, you just gotta want it more. It's like, no, like there's some, yeah, there is some personal responsibility there and there are choices and things that can be made, but why are we trying to make this barrier so high for people?

Like, let's lower this barrier. - I love that. On the other side of the coin, you've been pretty vocal elsewhere about the fact that sugar is not a drug, you know, because sometimes people will say, you know, sugar is a drug. I would sort of put in the soft argument for my side, soft argument that highly processed foods, or let's just call them high density of taste foods, right?

That combine, you know, processed carbohydrates and fats, you know, at high heats that can be consumed in, you know, where you can easily consume several thousand calories, you know, almost unconsciously, right? I mean, unless you're asleep or in a coma, you can just pop these things in your mouth and keep going.

I don't even know if they taste that good, but people just keep going. That there's a bit of kind of lack of awareness and compulsivity to them. Very different than addiction, of course, because people aren't necessarily going out and robbing people. But maybe just touch on your view of sugar as a substance.

We're not talking about the sugar in fruit. We're talking about candy, ice creams, desserts, "hidden sugars." What are the real risks of these things if people are consuming them still within the confines of their daily caloric needs? So they're not eating excess calories. What's the deal with sugar? - Okay, so this is where it's very important to give the appropriate context and nuance.

I'm glad you set it up the way you did. So I always tell people when it comes to almost anything, have guidelines, not hard rules. Because hard rules will get you to do things that are kind of dumb, right? So for example, if you say, "I'm never gonna eat processed foods." Well, whey protein is processed, but if you look at the data on whey protein, it improves metabolic health, it increases lean mass, body composition, even lowers inflammation.

So I mean, if we're just gonna say all processed foods are bad, well, isn't then whey bad? So guidelines in that nature, same thing for sugar, because obviously, okay, well, added sugar, it doesn't have a big satiety benefit. It's calorically dense, makes food very palatable. I'm gonna come back to that 'cause it's contextual.

But fruit has sugar and biochemically, not really that different. I mean, if you're talking about sucrose, okay, it's a molecule of glucose and fructose. Okay, a lot of fruits have glucose and fructose in them. So if sugar has some inherent lipogenic biochemical toxicity, addictive quality, whatever, we should see similar effects across different sources of sugar.

And we don't see that, right? And even when it comes to some of the processed foods, people don't realize what goes into making something hyperpalatable is complex. It's not just sugar, it's not just fat, it's not just sodium, it's texture, mouthfeel, you mentioned temperature, all these things matter. And in fact, there was actually a study a while back that suggested that texture might actually make a bigger impact on the palatability of a food than even the sugar content.

And let's take it more from a mechanistic level, from your example. If you're in the confines of your calories, what happens? I would say a high sugar diet is still not ideal because it's gonna be hard to get enough fiber in a high sugar diet. But I, long time ago, beginning of grad school, I was under the opinion that sugar and high fructose corn syrup were calorie per calorie, more fattening, metabolically unhealthy.

Now I was at a graduate mixer with a professor named Manny Nakamura, who was at Illinois, and he had done some of the feeding studies in rats with fructose and seen these weird metabolic effects, right? And I overheard him having a conversation with another professor, and I was shocked by what he said, 'cause he's the one that did some of this research.

And the other professor said, "So high fructose corn syrup is bad, and fructose is bad." He goes, "No, it's really just the calories that are in it. "It's easy to overconsume. "People consume it through soda, "and they just eat too much." And the guy was like, "Well, you showed all these things in these mice." He goes, "We fed 'em like over 50% of their calories "were from pure fructose.

"That's pretty much impossible to get through the diet, "unless you're literally doing nothing but drinking soda." And he said, "We showed a pathway, "but that's not practical "in terms of the application to humans." And so I got curious, and I really started going down the literature on sugar, trying to say, "Okay, is he right about this?

"Is it really not calorie per calorie more damaging "than non-sugar carbohydrate?" When you look at sugar intake, it is associated with increased levels of inflammation. It's associated with obesity. But there are what we call confounding variables, which is people who eat a lot of sugar tend to eat a lot of calories.

So if we look at, here's my favorite, human randomized control trials, where we control total calorie intake and sugar intake, what do we see? And probably the best example of this was a study from Surwit back in, I want to say, 1997. And the reason I'm gonna pick out this study is 'cause it had the best controls in it.

So they provided all the food to participants. The protein, carbohydrates, and fats were all the same. It was a, I think it was a 1,200 calorie diet. And they provided all these meals for six weeks and looked at fat loss and some blood lipids and those sorts of things.

And they found that, so one group was getting over 100 grams of sugar a day. I think it was around, I mean, it was based on some like body weight and energy expenditure stuff. But I think it was around like 110 grams of sucrose per day. Right? A lot of sugar.

Other group, like around 10. So 10 times different sugar. And at the end of the study, there was no difference in fat loss. There was no difference in lean mass retention. There was no difference in almost any marker they looked at. The only difference they saw, all the blood markers improved.

The only difference they saw was that LDL cholesterol improved a little bit better in the low sugar group. And that is probably a function of the fact that the low sugar group had more fiber. We know fiber can bind to cholesterol and lower LDL cholesterol in the blood. So when I saw that, I was like, oh man.

And then when I looked through all these other studies with similar kind of controls, they pretty much show the same thing across the board on metabolic health, on inflammation. Like inflammation really isn't different if calories are controlled with high sugar versus low sugar, as long as you're getting enough fiber.

- What about feelings of satiety because- - Well, that is the real downside if you're eating a lot. Like if you're eating a 1200 calorie diet and 400 calories are coming from pure sugar, I mean, you're probably gonna be kind of hungry, right? - Yeah, I'd be extremely hungry.

I mean, I consume artificial sweeteners for the record, but there are enough data and I have enough experience with them to know that sometimes they will curb my appetite. Like they'll get me over the bump, but I've come to associate, it's probably just pure paired placebo association, if there is such a thing, where if I drink a Diet Coke, pretty soon after that, I wanna eat something.

Now I've challenged that by not eating something 'cause I have pretty good discipline and it passes. But I think I've come to associate the sweet taste with wanting to eat something. And nothing to me is more delicious, well, there are many things, like a Diet Coke and a slice of pizza from New York, or a Diet Coke and a burger, or there are these food associations, but I don't think for instance, that sweet taste necessarily stimulates appetite.

But I can imagine if I only had, as you said, 1200 calories a day to eat, and I'm getting 400 of those calories from sugar, like you said, there's not gonna be much, I better be eating a lot of broccoli as well, or else I'm gonna be pretty hungry, just based on my learned relationships between sweet taste and food consumption.

- What I tell people is, I would focus less on like sugar intake. I mean, if you wanna focus on added sugars, that's fine. Focus on calories, protein and your fiber content, right? 'Cause if you're getting enough fiber, it's gonna be hard to eat a lot of junk doing that, right?

And when we look at the sugar intake and calorie levels, all that kind of stuff, actually a great example would be the case of Dr. Mark Halb. Are you familiar with him? He's at Kansas State, he's a nutrition professor. In 2011, he got the name, the Twinkie Diet Professor.

I'm not sure if you saw this, but he-- - I know about the Twinkie defense. - Right, so he asked his students what they thought mattered more for fat loss, the calories you eat or the food choices you make. And they said, most of them said food choices. And he said, okay, let's do an experiment.

Do you think if I do an 1800 calorie diet from ultra processed foods exclusively, that I will lose weight and get healthier? And most of the students said no. And so for 12 weeks, he ate 1800 calories. He called it originally the 7-Eleven diet. He basically was like, if I couldn't get the 7-Eleven, I didn't need it.

Now the caveat is he had a multivitamin and he had some whey protein so that he was getting enough protein 'cause it's hard to get protein from some of those ultra processed foods. But he ate 1800 calories and he lost 27 pounds and all of his blood markers improved and his insulin sensitivity improved.

Now, that seems crazy to a lot of people, but for those people who have worked and looked at blood work with weight loss and whatnot, I mean, it's not that surprising. That is one of the biggest levers for metabolic health. And so when they asked him afterwards, like what a great diet.

Like you could eat all this junk food. And he goes, well, not really. Like it's 1800 calories of junk food. It goes really fast. I was pretty hungry. And honestly, like at first week it was like, oh, this is kind of nice. And then after that, I was like, you know, I'd really like just a really big salad, you know, just something satiating.

So again, no solutions, only trade-offs. There is a benefit to being able to go, well, if I can fit it into my calories, it's okay. As long as I get enough fiber and protein. Yeah, the trade-off is it's a high budget cost, right? Same thing with people's, you know, the data on like moderate alcohol consumption shows that it doesn't impede fat loss.

It doesn't, if you account for the calories in it. But I'll tell people like, hey, do you really like, if you have like two craft beers, do you really wanna spend four or 500 calories on like 24 ounces of fluid that's not gonna impact your satiety at all? And so I think a lot of people view this from a very black and white lens, right?

Where it's like, oh, Lane says, or this person says, I can eat sugar and lose fat, so I can eat as much sugar as I want. No, no, no, no, no. 'Cause there are practical limits to this, right? But take somebody like me, right? If my calorie intake is my budget, I train two, three hours a day.

My maintenance calories are anywhere from 33 to 3,400 calories a day, which is a not crazy amount, but a healthy amount for somebody of my size. I have a decent size budget, right? If I can still get my protein in, get my fiber, hit my micronutrient targets, and I have calories left over for energy filler, sure, just like if somebody makes a million dollars a year and they wanna go buy a sports car, it's not a great investment.

It's not a good investment at all. Why wouldn't they just bank every single cent they make? Well, because maybe for them, having that little reward motivates them to keep doing what they're doing and making that level of money, right? But if you're making, let's take loans out of it, right?

If you're making $100,000 a year, does it make sense to spend $90,000 on a sports car if it means you can't pay your mortgage and you can't save money for retirement, you can't meet your obligations? No, it doesn't make sense, right? And so if you're a small woman, small lean mass wise, who is trying to lose some weight, does it make sense if you're eating 1,200 calories a day to lose weight to spend 300 calories of that on some ultra processed junk food?

I don't think it does. But if you're an Olympic athlete who's burning four or 5,000 calories a day, good luck eating that level of calories from good minimally processed foods, you're going to feel full all the time. - There does seem to be a kind of a requirement in books, sometimes even in podcasts, or to take a stance, like to be anti something.

Because saying, you know, what I personally believe based on my read of the data is that most people should strive to get anywhere from 70 to 90% of their food from non-processed, minimally processed quality foods. And then allow some space for the, you know, some processed food, highly processed foods and sweets and things like that.

But mostly to get the macros right, as we've described them earlier. And what the range will depend on age, will depend on activity level, will depend on prior health history. I mean, there's some people who have enough issues that relate to diet and lack of exercise that when I've seen them get it right and undergo such incredible transformations that like, I also know these people's capacity to fall off the train.

- Right. - And you want to say, you know, maybe make that number a hundred percent so you never go back. 'Cause I've seen them slip before and then the guilt and then they come back, excuse me. So there are two ways to look at it. One is you tell people, listen, you don't have to be perfect, right?

'Cause if perfection is the goal, you're going to fall off. But then there are those individuals like severe alcoholics who quit drinking. You don't say like, "Hey, like you can have a beer on Christmas." You don't say that, right? It's all or none. But anyway, here we're getting into the psychology of it.

- But I think that that's what you're saying right there is that's where the individualization comes in, right? Like it's contextually dependent and it's dependent on the individual and what makes sense for them. And I think we, as people, if we find something that works for us, we're a little bit too quick to want to evangelize everyone else around us because we do want to help, we do have good intentions for the most part, and we overgeneralize.

And I've, you know, for me, again, like counting macros, flexible dieting, when I dealt with a little bit of binge eating when I was young, when I first got into bodybuilding, 'cause I was trying to, you know, eat clean, and I was in college, so my buddies would order pizza or whatever, and I ended up eating like an entire pizza by myself, right?

And so once I allowed myself to just have that, the foods I wanted in moderation, I just got brutally consistent, right? So that, for me, that was the switch that flipped, but other people, that may not be the right solution. And I think we make a bunch of, well, that diet worked for me, and we assume physiology, when actually I think it's much more psychology and just trips that compliance algorithm in somebody's head and it makes sense, and if we could just be willing to say more often, hey, this is what I do, but I like this, and you don't have to do it, maybe try it.

- Yeah, oh, and everyone struggles with different things, and everyone finds certain things easier. Like I'm non-alcoholic, I'm an adult, so I can have a drink or two, I just don't like it, so everyone assumes because I did this episode on alcohol that I'm like anti-alcohol. Like I'm like, if you're an adult and you're non-alcoholic, you don't have issues with, you know, alcohol use disorder or something like, you might guess, like just know the data, right?

But there are certain things like steak, I'm never giving up. Like you could tell me it takes 10 years off my life, and I'm not going to give it up. I'll do other things to offset whatever that, you know, decrease in longevity might be. I don't think that that's a real thing, but I'm just not going to give it up.

It's central to my enjoyment of life, period. Speaking of which, when, if one really wants to wade into the waters of strong opinions and conflicting data, we covered this a bit last time you were on the podcast, but the questions were replete with requests to discuss seed oils. - I'm sure.

- Seed oils. And I must say this whole thing about seed oils has really gotten in my head. Even though I'm a scientist, like the other day I went to my sister's for dinner and she made a really nice dinner. It was for our mom's birthday. And then she made a really nice salad and I love fruits and vegetables.

So it was like salad. And then I looked and I was like, she's made this out with like grapeseed oil. And I was like, why do you use grapeseed oil instead of olive oil? And she's like, well, I ran out of olive oil. And I found myself like looking at the salad, like, is this safe to eat?

And I was like, I heard your voice in my ear. I also heard Paul's voice in my ear. Salad, you know, it was all these people. And I thought, well, I ate the salad, by the way. I really enjoyed it. It was good. Grapeseed oil doesn't taste as good to me as olive oil.

I generally like try and use olive oil, butter, things like that when I cook. But what's the deal with seed oils? I understand that they are calorically dense. You told us that last time. I understand people tend to over-consume them and then blame them for a bunch of things that are not related to their seed oil-ness rather than their calorie containing-ness.

These aren't real words, of course, but you get the idea. But are there any data out there that have your, you know, ears kind of pricked up to the possibility that, assuming equal calories, that there might be something bad about seed oils, or is there zero? And there's no pressure here to answer one way or the other.

Not that you would respond to pressure from me anyway. - So I think it's all about making the appropriate apples to apples comparison, right? 'Cause if we're looking at addition studies of, you know, adding something to a diet, adding omega-6s, linoleic acid, linoleic acid, whatever, well, if you're adding those, you're adding calories, which is a confounding variable, right?

So ideally what the real question is, 'cause the debate tends to be, the people who are anti-seed oil tend to be very pro-saturated fat. And so the question really is, okay, if we swap out these things in a one-to-one ratio, what is the outcome, right? So not, like, when outcome I mean metabolic health, inflammation, those sorts of things.

So in the studies, I have yet to find a good human randomized control trial where they give polyunsaturated fat in place of saturated fat, you know, exchanged at a one-to-one ratio, and see negative, like, actual outcomes. - What about swapping with monounsaturated fats? Like, why are we talking about seed oils versus lard and butter?

Why aren't we talking about seed oils versus olive oil? - Yeah, that's, I've looked less into that just 'cause people ask that question yet less, but it seems like both PUFAs and MUFAs are better than saturated fat in terms of metabolic health and risk of cardiovascular disease, those sorts of things.

- Does anyone have a problem with olive oil? - I'm sure you could find somebody with a problem. - Okay, well, I shouldn't be right. - There's water now. - Terrible way for me to pose the question. Is there any reason to think, like, for the person who isn't sure about seed oils 'cause they've just heard enough negative things, even if there's no basis for it, like me, who's like, I like butter, and I also assume that eating too much butter might not be good for me just 'cause I'm a rational human being based on my read of the data anyway.

So I have some butter, yes, but I like olive oil. Olive oil's tasty, I'm told it's good for me. - Is there any knowledge about anything in olive oil that says, listen, even if you consume it in concert with your caloric thresholds, meaning you're not eating too many calories, is there anything bad in olive oil?

- I'm not aware of anything, but I will say, like, if you extend the logic of the seed oils crowd or anti-seed oils crowd, which actually I'm going to make a new logical fallacy, which is just appeal to seed oils. 'Cause so many times that I've laid out this data, I have people go basically like have a freak out and go, but seed oils, how dare you defend seed oils?

And I'm like, I'm not defending them, I'm just talking about data. - People on X, when I put out questions for your coming on this episode, literally there were multiple people that claim that you are paid off by big seed oil. And I was just like, I have to laugh out loud.

I was like, there might be a lot of companies that are large that make seed oils, but I guarantee they're not paying Lane Norton to say what he's saying. - So I find this actually very funny as somebody whose research was funded by the National Dairy Council, the Egg Nutrition Center, and the National Cattlemen's Beef Association, that somehow I would be the person who would be, you know, and all these things act in opposition too.

It's like, well, you think I'm pro seed oil, but then over here I've been defending meat with this thing, right? And then over here I've been defending, sorry, defending is the wrong word, discussing the data on sugar, which by the way, those would be in opposition to each other 'cause you're-- - And you're very pro fiber.

- Right, right. - So, yeah. - So, and even when I talk about saturated fat, I don't like say it's toxic and it's gonna do, I say, hey, it raises LDL cholesterol, which is an independent risk factor for heart disease. I'm just discussing it, right? So, I'll say what I said online, which is I don't defend nutrients.

They don't need defending. There's not ethical considerations here. If you want to eat them, I don't think you're less of a person. And I find it curious that some people get so emotionally and just like ethically entrenched around certain nutrients. So the logic goes something like, well, you have these multiple double bonds, and so they can be oxidized.

And so that oxidation is gonna cause an increase in inflammation, which is gonna cause heart disease and cancer, okay? Well, olive oil is a monounsaturated fat. It still has a double bond. So by that logic, it would still be worse than saturated fat. So when we look at trading out, and MUFAs would fall in this too, I believe.

If you look at the cohort data, polyunsaturated fats substituted for saturated fats have a stronger effect on reducing heart disease than monounsaturated fats. But monounsaturated fats do still tend to have an effect of reducing the risk of heart disease compared to saturated fat. - Okay, so that would be trading out butter and lard and meat fats for more olive oil.

- Right, and just to add some nuance to it, not all saturated fat is created equal. There are like stearic acid, I believe, doesn't raise LDL cholesterol. But in general, saturated fat is gonna be something that raises cholesterol more. It also, again, and I'm thinking of several randomized control trials where they feed the same calories, they feed the same amount of fat, and they just have people either eat, you know, saturated fat or polyunsaturated fats.

You see either neutral or positive effects on inflammation. You see neutral positive effects on liver fat. You see neutral positive effects on basically overall metabolic health and insulin sensitivity. So again, and Paul actually counted this one time, and he cited a study looking at, I think it was, I don't wanna say it wrong, but it was like giving Omega-6s and they saw an increase in lipid peroxidation.

I don't think they were comparing it to saturated fat. I could be wrong. But again, this is an example of a mechanism, right? So lipid peroxidation mechanism. We can try to project what that might mean down the road, but when we look at actual levels of inflammation, actual risk for cardiovascular disease, actual insulin sensitivity, actual levels of liver fat, these are outcomes.

We can actually, if we're worried about those, we can actually measure them. And again, some studies show no difference. Some studies, some of the studies I've seen on like inflammation between polyunsaturated fats and saturated fats don't really show a difference in inflammation, but I'm not aware of any that show it going in the opposite direction where substituting in polyunsaturated fats actually raises inflammatory markers like CRP and IL-6, those sorts of things.

And actually one of the things I tell people when they're worried about, you know, fructose activates the novel lipogenesis in the liver. And I'm like, well, here's this study where they overfed fructose and saturated fat by the same amount and saturated fat increased liver fat by 70% more than fructose.

So if you're worried about fructose, you better really be worried about saturated fat. Now again, both, that's an overfeeding study. They were eating excess calories, but again, calorie per calorie, saturated fat was worse for liver fat. So that's kind of where I land on it. I just, you know, maybe I'm missing some data, but when you're looking at these studies, again, I'm looking at not one study, not two studies, I'm looking at 50 studies or however many studies there is on the topic.

And I go on this forest plot, where do they land? And when they're almost all on one side or neutral, I feel pretty confident that that's something not to worry about, right? So let's take another discussion to tie this in. I think this will help people understand how I come to a conclusion about this sort of stuff.

So I do not necessarily think red meat is carcinogenic, even though the IRC has classified it as probably carcinogenic, right? Because when you look at the studies, you can find studies that associate red meat with cancer, and you can find studies that show no association of red meat with cancer.

And so it's kind of all over the place. Now, there's probably more that show the association than don't, but when you look at like studies where they control for overall diet quality, so I'm thinking of a study out of Canada back in 2020, I think the author was Maximova, I wanna say.

They looked at different levels of red meat intake and incidence of cancer, but also with different levels of fruit and vegetable intake. And so what they found was at low levels of fruit and vegetable intake, lower red meat consumption reduced the risk of cancer relative to higher red meat consumption.

But at high levels of fruits and vegetable consumption, I don't think there was a significant difference, but actually the high level of red meat consumption was lower risk than low red meat, high fruit and vegetables. I believe I have that correct in terms of the absolute risk. And I don't know if it was statistically significant, but what that says to me is red meat is more of a proxy of poor overall diet quality.

And if you control for that with some diet proxy of fruit and vegetable intake, you know, if you're eating a lot of red meat and a lot of fruit and vegetables, there's not really a whole lot of room in your diet for a bunch of crap. - You just described the way that I eat and that anytime a friend of mine, and this happens a lot, comes to me and has, you know, 20 to 50 pounds to lose.

You know, well, make it as easy on yourself as possible. You can eat meat, eggs, vegetables, and fruit, and that's all you're gonna do for two months. And most of those guys in this case, they were guys, lost a substantial amount of weight and kept it off. They all exercised as well.

And of course, it's caloric restriction related. - Yeah, hard to overeat those foods. - Yeah, but they're not touching pasta. They're not touching bread. They ask me all the things that, can I do this? And I just said, listen, if it wasn't in the list I just gave you, you're not eating it.

Sounds restrictive. The good news about something like that is that fruit generally tastes good and steak is very satiating, it's delicious. If you don't like meat, I suppose this wouldn't work, but I don't think there's anything magic about that diet. It just gets people below their maintenance calories with relative ease.

- Well, it's simple. You could probably still do it at a restaurant, right? 'Cause you just asked for meat and vegetables, right? - Socially compatible. - So there is some beauty in simplicity. There's beauty in what I do, which is I track everything and I can have whatever I want.

You're gonna have to have some form of restriction to lose weight. You pick the kind of restriction that you can stick to, right? So bringing that all back. So you have this data that's all scattered on meat, right? And then let's look at something like dietary fiber, okay? 'Cause people say, well, you can't establish causation.

This is, some people might say, well, the carnivores might say, well, it's all healthy user bias. If it was healthy user bias, there'd be some disagreement in the data and there's no disagreement in the data. I am not aware of any study looking at dietary fiber intake or fruit and vegetable intake that doesn't show reduced risk of cancer, reduced risk of cardiovascular disease, reduced risk of mortality, usually in a dose response.

And it is very consistent. Now, some studies might show more of a risk reduction versus other studies. But if we're doing a line of a forest plot and this is risk reduction, this is increased risk, everything's on this side, right? - Eating more fruits and vegetables can only be good for you.

- Right, so, and there's like kind of a dose response. So that's when I become, even without randomized control trials necessarily, that's when I get pretty confident, okay, this is a very consistent effect and there's a dose response and we're seeing it in a bunch of different populations across a bunch of different countries in a bunch of different labs.

Okay, I feel confident. And so for somebody to make the claim that seed oils are toxic or that they're bad for you independent of the calories, I mean, you're basically relegated to using animal studies in vitro mechanisms and then epidemiology, which trying to like tie those all together, I mean, that's not really high quality evidence.

Really high quality evidence is that you have the mechanisms. Okay, there's a mechanism, right? 'Cause if there's an outcome, there's a mechanism. The animal data agrees with it. There's a dose response. The human randomized controls trial supported and then the epidemiology supports it. Like in order for something to really truly be strong evidence, we need that.

Now let's take our example of fiber again, right? Epidemiology supports it. We have mechanisms in terms of short chain fatty acid production, in terms of like insoluble fiber, moving, like getting food through the gut faster might be actually better because there's some, I don't wanna use this word lightly, but like some semi-toxic end products of like metabolism in the gut that if they stay around too long, it might have negative interactions with some of the colorectal cells.

And that may be one of the reasons that insoluble fiber helps decrease the risk of colorectal cancer. So we have the mechanisms, the animal studies show it. When we do the human randomized control trials, looking at shorter term surrogate markers, they show it move in the right direction and the epidemiology is in the right direction.

That's when I become very confident about something. So I'm not ready to say like, "Hey, seed oils are really, really good for you and you should have a bunch of them." I'm not saying that. Obviously they're calorically dense, right? People add oil to stuff and it adds calories. But anybody trying to claim that there's strong evidence that they're bad for you, we have very different definitions of what strong evidence is.

And you have to apply your logic symmetrically. If you were going to use a certain level of logic for one thing, you have to apply it to another thing, right? And I'll give you an example of this. When they were talking about the cruciferous vegetables and isocyanthanates and it reduces iodine, I said, "Well, this person was advocating for a meat-based diet." And I'm like, "Okay, well, there's NUE5GC in meat, which by the way, they found antibodies for that in human thyroid." Now, I'm not saying that meat's gonna mess up your thyroid, but if you're worried about the stuff in cruciferous vegetables, don't you have to worry about it in meat too?

Because if you're applying that logic symmetrically, I would actually argue that there's stronger evidence that you're worried about the NUE5GC in meat since you actually see those antibodies show up. So with the seed oil stuff, I'm like, "Okay, let's apply this logic to saturated fat for a moment, all right?" So do we have a mechanism?

We do. Saturated fat raises LDL cholesterol. Well, LDL cholesterol can penetrate the endothelium. We know this. So there gets to be this debate about small oxidized versus large fluffy. Both can penetrate the endothelium. Even large LDL can penetrate the endothelium. Now, small oxidized penetrates more easily, but it carries less total cholesterol and deposits less cholesterol in the endothelium.

Large doesn't penetrate as easily, but per unit of LDL cholesterol, it's depositing more cholesterol because it's bigger. The net effect is both are equally atherogenic. In the end. So we have the mechanism, right? Now let's look at the epidemiology. Well, the epidemiology tends to support it as well. And then if we look at the really what, for me, changed my mind, because I used to be somebody who was on the side of, "Ah, LDL doesn't really matter.

It's HDL to LDL ratio." And was when I saw the Mendelian randomization studies, which for those who aren't familiar, you're basically looking at natural polymorphisms on genes that cause differences in secretion of LDL, right? And since LDL is a lifetime exposure risk, meaning if you're doing a two-year randomized control trial, looking at LDL levels, it says nothing about what they ate before.

And in that timeframe, what's the likelihood people are gonna have heart attacks or some sort of myocardial infarction? It's pretty low. Now that we have all these data banks of blood samples and whatnot from people from all these old studies, they go back and do these analyses. And when they look at LDL cholesterol and plot it, so lifetime exposure to LDL cholesterol, and plot it against the risk of heart disease, I mean, you can pretty much draw a straight line through it.

And so to me, that's pretty strong evidence. If you wanna apply the same logic of, well, we have this, and LDL, by the way, can cause inflammation in the endothelium. So you have that damage to it because of the apolipoprotein, that attracts inflammatory markers. So people are getting some of this cart before the horse.

And then the other thing that sealed it for me was again, like HDL. They looked at the same thing at HDL. Turns out HDL is just kind of a marker of metabolic health. It's good to have high HDL, but HDL itself doesn't appear to be protective because if they raise it with drugs or look at people who secrete more or less, it doesn't seem to independently modulate risk of cardiovascular disease.

So all that to say, saturated fat is really only an issue, I would say, for the LDL, the fact that it can raise LDL. And there is some evidence it's not necessarily good for the gut microbiome because the bile salt in products from emulsifying saturated fat, 'cause it requires more bile, that those might be toxic to some beneficial species of bacteria.

But here's what I'm not saying. I'm not saying don't eat any saturated fat. What I'm saying is, again, your overall diet quality is what matters. I think it's fine to have some saturated fat. I think probably try to keep below seven to 10% of your daily calorie intake. What also matters is there's no solutions, only trade-offs.

And so if somebody says to me, I was able to lose 50 pounds on low carb and everything got better, but my LDL went up a little bit. And they felt like that was the only thing they were able to be consistent with, I'd say on balance, they're probably better off with that slightly elevated LDL than they would be if they kept the 50 pounds on.

Now, I would argue if they had lost the 50 pounds and lowered their LDL, their overall risk would be lower than it is now. But again, we have to look at what can somebody consistently execute. So all that to say, I'm not saying you should consume seed oils. I'm not saying that there's no negative downsides, but if we look at comparing it to a comparable molecule of saturated fat, there's a much more compelling argument that saturated fat is bad for you versus seed oils.

- Thank you for that very thorough and very clear answer. And I just will highlight that you ate a steak last night. So you were by no means anti-meat or saturated fat. - I ate a steak right in front of a vegan. - Okay, not to aggravate them, just because they stuck to their principles, you stuck to yours.

- I was originally going to order fish and they said, "It's okay if you want to get a steak." And I said, "Okay, if you say so." Now they did make a couple of comments in jest during the meal. - Fair enough, fair enough. Let's talk about artificial sweeteners.

- Sweet. Those are the other people that pay me. - That's right. He's kidding, folks. Good goodness. - Yeah, I got to be careful about that. You and I got into a, it wasn't a scrap. We got into a little disagreement about this years ago. So long ago that it's probably not even worth mentioning that, you know, I was somewhat enticed by the data from Dana Small's laboratory, then at Yale, I think now she's up at McGill, looking at some kind of Pavlovian conditioning of artificial sweeteners.

So basically children in that case consuming a high amount of, I think it was either sucralose or saccharin in combination with a meal, kind of standard meal, and look at the insulin response. And then removing the food component sometime later. And what they essentially observed was a conditioned insulin response.

So then you then have these kids just have the sweet tasting non-caloric drink minus the food. And they then saw an elevated insulin response. In other words, the same way that Pavlov got dogs to salivate in response to a bell that was paired with food, then you remove the food and then they just simply salivate in response to the bell.

The idea was, well, maybe you can create a conditioned Pavlovian like response to artificial sweeteners. Okay, I thought it was kind of a cool study. Looking back, I probably wouldn't have covered it the way I did because it's not a typical scenario. I think the more important questions are, is there any evidence that artificial and low calorie or zero calorie sweeteners like Stevia, we have to be very careful here.

- No. - Not all artificial. - That they are somehow dangerous in any of the following ways. One, do they alone increase insulin to levels that are problematic? Two, do they stimulate appetite in a way that's problematic, independent of insulin, or maybe as a consequence of insulin? And then three, what's the story with their potential effect on the gut microbiome?

I think those are the three categories that come to mind. There are probably other categories. And I just want to say for the record, then and now, I'll consume some aspartame every once in a while in the form of a Diet Coke. Stevia seems to be in a lot of the things that I consume and I don't have a problem with that.

So I'm not anti artificial or low calorie sweetener. Although for reasons that are entirely personal and have no scientific basis whatsoever, I avoid things with sucralose in them. I don't really like the taste of it and I have kind of an aversion to it for uninteresting reasons. - And that's a great way to couch that of, I don't have data for this.

Personally, I don't do it. - Yeah, if I see something, I'm like, yeah, no. Aspartame, fine. Stevia gets the thumbs up by me. And I will choose low calorie or zero calorie sodas or drinks or energy drinks when I have the option to have something with sugar. It's just kind of, but I'm not anti sugar either.

I just developed this as a habit. Yeah, I prefer to get my calories from food. - Yeah, you'd prefer to have a steak as opposed to having the cola. - Right, steak, strawberries, blueberries, oatmeal, rice, butter, olive oil, and all the other delicious, wonderful things, as opposed to a Coke.

I'd rather just have a diet Coke and eat a bit more steak. - So let's take the insulin thing first. So interesting mechanism that they're showing there. What I would say is there's been a couple of meta-analyses now looking at different non-nutritive sweeteners and their effects on insulin, and they don't show an effect.

So there's no real effect in it. Let's just kind of play it out logically a little bit. If there was a significant effect on insulin, one of two things is gonna happen. You're gonna see a drop in blood sugar 'cause you're not eating anything, right? So most of us, if we drink a diet soda, we don't then go hypoglycemic, right?

Or if there is an increase in insulin, if blood glucose isn't dropping, then there must be a corresponding increase in glucagon, which is basically offsetting all of insulin's issues. I don't think either of those things happen. I think it's inert, and the research, the meta-analyses tend to show this.

There was a, I'm thinking of two meta-analyses where they looked at these, they looked at glycemia, they looked at insulin sensitivity, and they looked at insulin release, and they just didn't see any effect. Now, when it comes to, what was the second point? - So we have insulin, we have does it stimulate appetite in ways that may or may not be related to insulin?

You ruled out insulin increase. So like, could there be a pairing of like, okay, every time I eat, I have a diet soda. Then if I have a diet soda on its own, does it stimulate the desire to eat, a la the Dana Small study? And by the way, that study was halted.

This is the problem with that study is it was being done in kids. The increases in insulin that they saw in a subset of the kids were so dramatic. This is the way she described it in a talk, so I feel comfortable saying this. Maybe she's changed her tune, but in this online talk, an academic talk, the increases in insulin were so dramatic that they were concerned about the kids becoming pre-diabetic, so they halted the study, which means the totality of the data never came in, means that it's hard to draw a conclusion.

- Okay, when we talk about studies, we're always talking about means and averages, right? I leave open the idea that there could be subsets of populations, that there could be individual responses. I leave all that open. So on average, if that's true, and there is a conditioned response, we're worried about, well, one, is there an effect on appetite, where people are gonna eat more, even if those things don't have calories, they're not gonna make you fat, there's no insulin release.

Okay, they're stimulating you to eat more. Well, if we look at the randomized control trials where they tell people, hey, instead of regular cola, drink diet cola. If that was true, an actual outcome, we would see people on diet soda either not lose weight or gain weight, definitely compared to water, and probably similar compared to a regular cola, maybe a little bit less, but we would expect to see weight gain.

We actually see the exact opposite thing. So we have several randomized control trials now where people comparing not just diet soda, I don't wanna just say diet soda, a lot of them are low, no calorie beverages is kind of what they talk about, 'cause not everything's technically diet soda, but I think people know diet drinks in particular.

Where they're comparing them, they tell people either have cola, either have diet soda, or sorry, diet drink, or just use water. Now, they absolutely, every single one of these trials, they lose weight going to diet drinks, usually a pretty significant amount of weight. - Yeah, and usually, as I recall, pretty significant amount of diet drink, like two liters a day even, like the person will carry around a liter or a two liter of diet drink and sip on it whenever they get thirsty or hungry.

- Yep. - Yeah. - So then what's been interesting is they've done direct comparisons to water, and some studies don't really show a difference, but several studies and several meta-analyses now have shown that when people, if they have either them use water in place of regular soda or diet drinks in place of regular soda, the people actually lose a little bit more weight, and it's statistically significant with the diet drinks.

Now, I don't think diet drinks are fat burners, okay? They're not causing you to have increased energy expenditure, but if you are somebody who is used to a sweet taste, if you switch to water, perhaps you're seeking out that sweetness elsewhere, and so maybe those people are consuming a little bit more sweet food or whatnot, whereas in the diet drink group, maybe that's filled that sweet taste for them.

So I don't get into the, again, this gets, like people get very like ethically charged about what's wrong with drinking water. There's nothing wrong with drinking water. If you can drink water, you feel satiated, and you maintain your body. - I'm just chuckling 'cause if drinking water becomes an issue online, then I might quit.

- No, no, it already has, it already has. - All right, well, I'm not quitting, but that's ridiculous. - Yeah, well, so again, perhaps that mechanism exists, but at least on average, it's obviously washed out by the fact that for whatever reason, for most people who do this, they get a little bit more satiety out of consuming a diet beverage as opposed to substituting water for a beverage.

Now, again, if you're somebody who you can drink water and you don't have an inclination for diet drinks, then don't do it. You don't need it. But again, I look at it as we need to lower the barriers for people to start getting healthy. And unfortunately, a lot of people with the message of just drink water, and they'll say, well, diet soda's just bad for you as regular soda, or it's worse for you than regular soda.

Their intention might be, I just want people to drink water. But the outcome is people go, well, I can't imagine getting my soda, so I'm just gonna drink regular soda then, right? And so while your intention was positive, the outcome is actually kind of disastrous, right? And so we have to disconnect what the intentions of the message are from what it actually produces.

And so that's why I say, hey, if we're moving levers, if somebody is obese and they came to me and they're like, well, I drink five colas a day, I'm like, fantastic, because I'm thinking five diet sodas instead, and now we have just saved 750 calories, and you're gonna start losing weight just by doing that, right, which again, people say, well, what about 100 years down the road or whatever?

I'm like, well, most of these sweeteners have been around for decades now. We do have quite a bit of data on them. But let's say that there is something we don't want. Again, I'm shooting the alligator closest to the boat, right, like we know what obesity does. So, and people who do these diet drinks lose weight, they get more metabolically healthy.

So again, if it comes down to soda or diet soda, by all means, let's do the diet soda. And if there's some small negative effects to it, we'll deal with them. So that brings me to the gut microbiome. Most of the research studies in humans where they use reasonable doses don't really show much effect on the gut microbiome.

However, there are a few with particular sweeteners like sucralose that do show an effect. Now, there was one that got a lot of play and you and I actually talked about this. I think we actually talked on the phone about this. And it was an interesting study. I thought it was well done, but I want to be careful about how overgeneralized it was.

So the first part is in this study, they selected for people who basically, they did a very, very like intense selection process where I think there was over 1500 people who were like originally included in the study and they whittled them down to like a hundred something. Because they wanted people who had really hardly ever used artificial sweeteners in their life.

And that's a pretty small percentage of the population. What they found was a lot of people submitted saying, I don't use them, I've never used them. And then when they did dietary recall logs, like, oh, well, actually you're using it here and you're using it here. So they selected all these people out.

And they found that when they gave them sucralose, that the composition of their gut microbiome changed and they called it dysbiosis. I'll come back to that 'cause that's a scary sounding word. First off, what's interesting is, if you're somebody, that population that they're selecting, those are probably people who have been specifically trying to avoid them.

Because if you're not, even if you don't try to consume them, they're everywhere. So if you haven't been consuming them, it's likely that you're specifically trying to avoid them, which probably means that you have negative thoughts and beliefs around artificial sweeteners. And again, we've discussed the power of belief before.

I'm not saying it was a bad study because of that. I'm just saying we have to be careful about how much we over-interpret this research data. - Are you saying that the potential that those subjects had to believe that zero calorie sweeteners or low calorie sweeteners could be bad for their microbiome might've actually made their gut microbiome more dysbiotic?

- Maybe. I mean, again, we've talked about the power of belief is very powerful. Now, I have no way to support that, right? I'm just saying, be careful before we over-generalize. Plus it was a two week study and- - Just two weeks? - Yes, it was two weeks. Now again, two weeks is enough time to show differences in the gut microbiome.

Actually, a few days is typically enough time. - And only for sucralose. So Stevia, no change. - There was another sweetener that I think had a change. It might've been saccharin. - Saccharin and sucralose are the ones that seem to always show the biggest effects, quote unquote. And I don't know how often those are used in diet drinks these days.

I mean, less and less. I mean, it's usually aspartame, Stevia, more in the kind of wellness, health, fitness crowd drinks. - Sucralose is pretty ubiquitous in a lot of diet products and whatnot. But like being frank, my whey protein powder with outward nutrition is sweetened with sucralose. I mean, it's a great sweetener.

And so some people will take that as well. Of course, he's gonna defend sucralose 'cause it's in his protein. But if I thought it was really bad, I would just use a different sweetener. So what I will say as well is gut dysbiosis sounds bad, but it simply means that the gut microbiome changed.

And I have several friends who are gut microbiome experts. And they'll, when we sit down and talk about this stuff, they're like, I mean, their takeaway is, yeah, in like 50 years, we'll probably have a really good idea of this stuff. But right now, we just know that certain things change it.

We don't really know like if it's a good change, bad change. So I'll give an example. There was another study that did show a gut microbiome shift with sucralose. And they showed some of the species of bacteria that were increased or decreased. And one of the species that was increased, I believe, I'm gonna butcher this so badly.

I think it was Blaudia coccoides was the name of it, or at least how I tried to read it, right? 'Cause these are very like strange Latin words. - Yeah, the names of bacteria are really difficult to pronounce. - Now, what's interesting is this species of bacteria was associated with better metabolic health, lower risk of obesity, better insulin sensitivity.

And so I kind of walked away saying, well, couldn't you make the argument that sucralose actually changed the gut microbiome for the better based on some of this data? And so I'm not saying that. What I'm saying is the following. We don't really know if that change to the gut microbiome is a good change, bad change, or neutral.

We just know that it changes. So if you want to avoid, fine. But if you're somebody who really struggles with moderating your intake and a sucralose is, or an aspartame or whatever have you, helps you moderate that intake, then again, you're shooting the alligator closest to the boat. Let's focus on the big stuff, right?

And that's kind of where I land. And again, I hold open that perhaps my mind will change and adjust. But sucralose has been around a long time. The other thing people bring up is cancer. They'll bring up cancer with artificial sweeteners. I'll give you an example why I'm not worried about this.

First off, you have to keep in mind that negativity bias in the news, all right? Things that are negative are much more likely to get play than things that are positive, okay? Think about how much you hear about this causes cancer, this causes heart diseases, versus this protects against this, this protects against this.

- It's also safer to when the media warns people off things as opposed to towards things, because if they push people towards things, there's more liability. - Right. - Away from things, rarely are they responsible for the opportunity cost there or the trade-off as you referred to it. - Right, so you hear a lot, people are like, oh man, all these studies say that these cause cancer.

So again, I'm gonna give a shout out to Consensus, 'cause it's a great AI tool that basically will give you, like if you ask it a question, and there's some filters that help with that, it will give you kind of like, this percentage of studies say yes, this percentage say possibly, and this percentage say no.

- I've used it a little bit. - Yeah. - It's a great tool. - And if you type in, does aspartame cause cancer, for example, 80% say no. And then like, I think the split is like 13% say possibly and 7% say yes, right? But you would never know that from like listening to social media, watching the news.

But I wanna point out one study in particular that did show an association of aspartame intake with cancer. And it was from the Nutrisanti cohort, I think that was out of France, like 100,000 people. And they looked at like people who didn't use it versus people who were like low-moderate users and then people who were like high users, they categorized them to tertiles.

And between the non-users and the low-moderate users, there was like a, I believe it was like a 15-ish percent relative risk increase in cancer incidents. And that's what got reported in the news. And then that dropped to like a 6% increase risk in the high group. So it did this, which I'm not aware of any carcinogens that they actually decrease in terms of the risks, like carcinogenesis as they go up in like the concentration.

And so to me, you know, one of the things you've got to realize, my PhD advisor used to say, "If you torture the data enough, it will confess what you want it to say." And so if you go through a large group of people and you start trying to associate things with other things, you'll find things, but you gotta be very careful with how strongly you interpret it.

And so for me, again, if I'm feeling strongly about, for me to feel strong about something, there has to be some kind of dose response or at least like if there's a bell curve, sometimes you see that. But, you know, very rarely, especially with cancer stuff, usually this is kind of a linear effect.

And so again, that's where I land right now on artificial sweeteners. I land on them as a useful tool for a lot of people. I don't think they're magic. I think they occupy that sweet taste for a lot of people. And if you can completely avoid them and abstain from them and you're perfectly happy, then by all means do that.

But if they help you maintain a healthy body weight, then by all means do that. - Love it. You've dealt with some injuries. You've dealt with pain. You talked a little bit about how reducing your stress and interpretation of the pain could help. I wanna talk about pain and pain management, but before we do that, a more general question that relates is about recovery tools.

Many, many people want to know, okay, if we were to create the pyramid of the hierarchy of tools for recovery after training, and here let's change out or let's use resistance training and cardiovascular training interchangeably. Some people run hard, other people lift hard or do both. From the moment that session ends, what do you have in your kit of things to maximize recovery over the shortest possible amount of time?

And I can immediately think of sleep as critical, but what are the things that you can do starting from that final repetition? - So I think it's not so time-dependent. Like I said, it's more about what you do over the course of 24 hours and on your day-to-day lifestyle.

But sleep, as you said, also your nutrition, so being consistent with your nutrition. And you don't have to get in ultra-fast digesting, carbohydrate, and 50 grams of weight isolate right after you eat. But it's probably a good idea within a couple hours of finishing your workout that you have a meal with high-quality protein and that you're just eating an overall healthy diet throughout the course of a day.

And we've kind of discussed that at length. - You could do it immediately after your workout. - You can, yeah, you can, absolutely. - Quick, I'm going to layer in an additional question. Is there any evidence that fruit is not good at replenishing glycogen as compared to starch? Because the reason I ask this is that, like if I finish a workout and I have some, like a whey protein shake with a bunch of berries in it and a couple of bananas, assuming equal calories, is that going to replenish glycogen the same way as if I have a couple of scoops of whey protein and a bowl of oatmeal or rice?

- This is going to circle back to our mechanism versus outcome. And this is one where I changed my mind because of seeing outcomes. So the reason this comes up is fructose, your muscles and other tissues lack the enzyme to turn fructose into muscle glycogen. Your liver has that enzyme.

So your liver can take fructose and turn it into liver glycogen. So that has led some people in sports science or research to say, well, don't have fructose after a workout. And actually fructose is kind of a dead carbohydrate, right? 'Cause it's not going to replenish muscle glycogen. And then I was reading a study from Tracy and Josh Anthony, which were, they came out of Lehman's lab and they actually are responsible for really flushing out a lot of the mTOR pathway, a lot of that translation initiation pathway.

Very, very brilliant people. And I was glad I got to see them a few weeks ago when my advisor got his award. Tracy personally taught me how to Western blot. So thank you, Tracy. They did a study where they looked at glycogen replenishment after exercise, giving either sucrose, which is 50% glucose, 50% fructose or pure glucose.

And actually, if I recall correctly, they actually got a little bit better muscle glycogen replenishment with sucrose. Now this, how do you explain it? That seems completely counterintuitive. And there, I believe, again, it's been some time since I read this paper, but I believe the explanation was by providing some fructose, what you're doing is you're kind of satiating the liver's need for glucose.

And so that glucose that does come in from sucrose can then kind of just bypass the liver and be available for muscle. Whereas if you're getting pure glucose, the liver is gonna start picking things off. Now it wasn't, if I recall correctly, it wasn't a big difference in the rate of glycogen replenishment.

But the other thing is people don't realize, well, even though fructose can't be used to replenish muscle glycogen directly, you forget about how the body operates in terms of whole body metabolism. And you can store fructose as glucose, glycogen, in the liver, and then the liver can release that glycogen at some point into the bloodstream, and then that can be taken up by the muscle and turned into muscle glycogen.

So again, what it really boils down to is what are you doing on a 24-hour basis? And what I will say too is the rate of glycogen replenishment gets really tossed around a lot as something really important. For the most part, the rate isn't so important if you're eating enough total carbohydrate on a total daily basis and enough calories, you'll replenish your muscle glycogen.

And most of these people, I always say, dude, you're weight training for an hour. You're gonna do it again in 23 hours. You got plenty of time to replenish that glycogen. You don't need cyclic dextrin or dextrose or whatever. And so I'm not really worried about that. I think where the rate of glycogen replenishment really matters is when you're dealing with athletes who have multiple events in a day, right?

Where it is, they're gonna perform and then they need to replenish quickly before they go to the next event. Or people obviously doing endurance exercise where like Ironman's, triathlons and that sort of thing where getting in that replenishment and keeping it going is very important. But I think for the average person who's just exercising once a day, not really a big deal.

Just make sure you're eating enough total carbohydrates. So for you, the berries and the fruits and the whey protein afterwards, excellent. - Okay, and then perhaps, and then typically I'll do a meal that includes some starch a little bit later in the day. - Yeah. - Great. So nutrition post-workout or in the hour or two post-workout making sure you eat enough in the following hours.

Do you include any kind of stress down regulation? Are you, do you do anything else besides nutrition and sleep to accelerate recovery? - So stress management, like you said. So I am blessed enough that I currently live and home on Tampa Bay and I get to watch the sunset over the water every night.

And that might say, that might seem like a weird thing but I really feel like that has helped with my stress level. - Viewing horizons, we know, just puts you into panoramic vision. We know this from stuff my lab has done. - This is right in your wheelhouse right here.

- Oh yeah, panoramic vision is a, will, you know, come off the accelerator of the sympathetic arm of the autonomic nervous system, which is just nerd speak to say, enjoy those sunrises and sunsets. They are very calm. - I was talking to a friend of mine, we're sitting out.

I said, well, you know, Andrew would approve of the sunset viewing. He might not approve of the bourbon I'm having with it, but. - You don't need my approval anyway. - So whatever, could you just slow down a little bit, you know, and just decompress and feel better. And so, I mean, another thing I'll do is I'll, you know, once the, if I had the kids, once I go to bed, I'll go downstairs and I'll lay on the couch with my cat and I'll play a video game, you know, just relax.

- Yeah, decompress. - Just decompress, you know. - Things you enjoy. - Yeah, I think things you enjoy, like, obviously like, you can't drink a 12 pack of beer and have that be conducive to that sort of thing. But the other thing I will say is I think a lot of people focus too much, especially with resistance training, there's some evidence that being just overall active lifestyle, like going out, I remember when I was first getting into lifting, like back in the early 2000s, the guy's like, I go in and I lift and then I lay down the rest of the day.

Right, 'cause I gotta recover, right? I think the research actually suggests that you're better off like having kind of an overall active lifestyle, you know, that, yeah, it's important to rest and recover, but it's probably important to move your body throughout the day. You know, active recovery does have some good data on it.

- Awesome. Earlier, we were talking about protein. Actually, several times we talked about protein and I neglected to ask a question that is very timely because I just did an episode, a solo episode of this podcast recently about skin health and appearance. And I looked at the data on ingesting collagen.

Could be from bone broth or other sources of collagen. Typically it's powdered collagens, anywhere from five to 30 grams of collagen. And I was kind of surprised at the results. I also talked to some dermatologists. Basically the results say in these papers, these meta, the meta analysis I looked at, and in speaking with these dermatologists that the conclusion was that regular consumption of collagen on the order of anywhere from five to 30 grams per day, with a little bit of vitamin C, a couple hundred milligrams of vitamin C for whatever pathway related reason, seemed to improve skin appearance.

Fewer wrinkles, reduction in wrinkles, more skin tautness, appearance of moisture, et cetera. These are subjective measures, right? I don't think they were calibrating the skin and looking at tensile strength and things like that. But people felt they looked younger, et cetera. And I was surprised, really surprised, because without making this too long a question or story, a few years back, there were some claims by not-to-be-named individuals on Instagram saying, "Well, if you want to improve the function of your liver, "eat liver.

"If you want to improve the function of your heart, "eat heart." If you want, and you and I were just like, "No." You're the nutrition biochemistry guy. I'm the neuroscience guy. I have a little bit of a background in cold physiology that I rarely talk about, but in any case.

- But you know physiology. - Yeah, I mean, there is, we both agree, there's like zero evidence that ingesting a protein, which of course is broken down into its amino acid constituents in the gut, would somehow lead to selective shuttling of those amino acids from liver that you ingest to your liver.

That just is like a, there's only one word for that. It's like a crazy unsubstantiated claim. And then some papers were sent my way, which were in a different language. And like, I was trying to, anyway, zero minus one evidence, as I would say. And yet the whole notion that consuming collagen protein, which Dr.

Gabrielle Lyon told me is actually a pretty low quality protein on the kind of protein quality scale. It's like tendon and toenails and all this stuff, gross, but yeah, that's what it is. Somehow leads to improvements in actual collagen, which is of course is a native protein of the body.

So I went digging. I just want to, before I get your answer, I went digging and I found, again, a not to be named individual has this kind of wild story on the internet that, ah, well, this is because it's broken down into the dipeptides and tripeptides in the gut that somehow inform the body that there's an injury in the collagen.

And we have quote unquote, breakdown of collagen, AKA injury, I don't know, breakdown of collagen and elastin in the skin all the time. And then the body recognizes the presence of those dipeptides and tripeptides. So little groups of twos or three peptides, not just one, and sends those selectively to the skin.

And so it's like, once again, it's like, it makes sense as a mechanism if it were true, but I just had to like roll my eyes. I was like, oh no. Okay, I'm going to pitch this over to Lane, as I am right now. So Lane, take it away.

What's the story? Does ingesting collagen improve skin appearance? And does it, do we have any idea what the mechanism might be? - Okay. - So I have a long question folks, but I had to set the stage. Well, first off, I will never make somebody apologize for giving a long winded preamble, right?

Because you know how long I'm about to go. - We're both scientists. - So I will tell you, I actually, like after I commented on that post, I went and looked up some more research and I've actually changed my mind a little bit. Okay, which probably wouldn't surprise you.

I haven't completely changed my mind, but I've shifted a little bit. So first off, my first thought was exactly what your thought was. This is all getting broken down to constitutive amino acids. It's not like you're taking collagen and just like putting it in the place you want it.

Like just, you know, like that sort of thing. So my skepticism was also because one of the highest quality protein metabolism labs out there, where Jordan Tromblin is, is Luke Van Loon. Luke Van Loon's lab is one of the best protein metabolism labs in the world. And they were publishing research back when I was in graduate school.

In fact, I think Jordan and I were actually in graduate school at the same time. So they did a study where they looked at after exercise, giving either whey protein or collagen protein. And they looked at skeletal muscle protein synthesis and they looked at connective tissue protein synthesis. Right?

And they saw no difference between whey protein and collagen protein in connective tissue synthesis after exercise. And so, but by the way, collagen did not stimulate muscle protein synthesis, even at like 25 grams, I think it was. Which most protein sources, even like plant protein sources, will stimulate muscle protein synthesis at like 25 grams.

- So it's very low quality. - So it's low quality in terms of skeletal muscle. Anybody who's telling you like, "Collagen's good for building muscle." I mean, it's better than no amino acids, but it's one of the worst you can get in terms of all protein sources. So that study, again, since I know this lab, I have a lot of trust of the data that comes out of there.

Right? And it was a well-designed studies, well-executed study. But then there's these meta-analysis out there, looking at skin, looking at, you know, even like some we're trying to make associations with connective tissue injuries and whatnot. And again, I'm always a little bit, have the heebie-jeebies when we jump straight to, we have an outcome, but we don't know what the mechanism is.

Right? And then I started reading a review by Luke Van Loon, actually. And it was talking about like the, so the collagen is three alpha helixes. So if you think about DNA, right? It's a double helix, right? So think about three helixes. And an alpha helix just refers to the way a protein is shaped.

And they are, they have a very large amount of glycine. So glycine is an non-essential amino acid. And every third residue in collagen, in the three alpha helixes, every third residue is a glycine molecule. So 33% of collagen is glycine. And then I want to say 10% is proline.

And then another like 10% ish is hydroxyproline. So proline that's had a hydroxyl molecule added to it. And that's done, apparently the hydro, nobody needs to know this, but just for fun stuff, the hydroxyproline helps stabilize the structure because of the hydrogen bonding with hydroxyl molecules, which I found interesting.

So you have these three amino acids and amino acid derivatives that make up over half the amino acids in the collagen protein. And, well, my next thing was, well, a lot of non-essential amino acids, if you give them in the diet, they don't really raise non-essential amino acids in the plasma because the gut, liver, extract a bunch of them.

Glycine is different. If you give, there was a study looking at giving just one gram of pure glycine and looking at the rise in plasma glycine. And I think it went up, like I think the like native level of glycine in the plasma, something like 250 micromolar. And after giving a gram of it, it went up to like 400 micromolar.

I'm giving my best estimate based on the graph I saw. And so then I got thinking, okay, that's, I guess, possible if you have more glycine and proline. I didn't look, I didn't see the proline data, but if you have more glycine and proline that's winding up in the plasma, not that they're being directed to those tissues, but since those tissues use so much of that amino acid, perhaps it does help.

And then if you look at like whey protein versus collagen and the content of glycine and proline, I think collagen has like three to 10 times the amount of glycine and proline in it compared to whey protein. So am I ready to say collagen helps skin and connective tissue and whatnot?

I'm not, 'cause I'm still, you know, this study looking at connective tissue synthesis doesn't show anything. So the mechanism is incomplete, but there is a plausible, at least they've shown that glycine can go up in the plasma from taking it in. And it is a big component of collagen.

- So why aren't we just suggesting that people take glycine instead of collagen? - Well, I think what they would say is like, there's, because you're getting hydroxyproline in the collagen that you're taking, that probably, I don't know how much hydroxyproline is typically in the diet, you know? But I would say, again, I am a little bit nervous about like a lot of these subjective measurements of skin appearance and skin tightness.

I mean, I'm not saying faking data. I'm just saying that data is easy to get wrong because it is subjective, right? It's less, the more subjective things are, the more bias you introduce. So I hold open the idea that supplemental collagen could help with skin, hair, nails. I'm not convinced by the data, and I'm not going to tell people to spend their money on it just yet, but I'm going to stop short of saying that I think it's BS.

And I've actually changed my tune slightly on that from looking in this data a little bit further. - Thank you for that very thorough answer and very clear answer. If nothing else, it tells us that collagen protein is going to be least ideal for post-workout protein because of the fact that it's, you know, it lacks significant amounts of leucine, et cetera.

So it might be good for skin. Definitely not a great protein for dietary protein reasons. - No, it's very, very low in the branch amino acids, like the lowest in leucine of any protein source I'm aware of. I think it's like 2% leucine, which is like most, even like the worst plant-based sources of leucine are like 6.5% leucine.

So like the worst sources of protein in the diet are still like three times more leucine than you get in collagen protein, so. - And a quality whey protein would be the highest leucine available. - Oh, it'd be 11, 12, 13%, yeah. - Eggs, whey protein. - Eggs are going to be around 9% leucine.

You know, beef, chicken, most your animal sources are around 8%, and then most of your plant sources are 8% and under. - Great, well, Dr. Lane Norton, thank you for coming back here for the second time on the podcast. I must say it's a true pleasure to sit down with you and discuss training, nutrition, supplementation, recovery, pain management, stress, life advice, and for so many reasons.

A, you're, you know, a serious scientist, you know, in our business of science, that really means something. You're serious about the science and you're a lighthearted guy in the right context, but you're a serious scientist. You believe in the process and you provide the nuance, even though that might not be convenient to what somebody wants or convenient to the discussion.

- By the way, not convenient for me either. I'd rather this stuff be so simple, you know? - Right, sure, sure, you're like the rest of us. And at the same time, I really appreciate it because we are now also colleagues in the public health, public facing landscape, social media it's sometimes called, but a lot of landscapes, podcasts, YouTube, et cetera.

And it's required, it's needed that people like you exist. And I will go so far to say that, you know, and I'm not alone in this, right? Because I've talked about this with Rogan and with Dr. Gabrielle Lyon, excuse me, and others, you know, in an ocean of noise, some of which has validity, right?

But in an ocean of noise about nutrition and training and all these different things and how to, evidence-based blank and science-based that, you really clearly are pure signal. Like you're going to take as much time and as much effort to communicate the real signal. And you today have really defined for us, for you what is real versus not real versus a maybe.

And I just want people to hear that loud and clear because I think sometimes people pay attention to how spirited you are and they miss the fact that in that spirited nature and in the nuance and in the, look, we're both long-winded at times. Like I know, because I know this for myself, but I certainly know it for you that, that comes from a place of respect for the science and respect for your audience.

That is not being dismissive. That's actually respect for them. It would be disrespectful to just give them the answer they want or give them a quick answer without the explanation. So I just really want to extend like a real voice of gratitude for you, for what you did for us today, just far too much to list off.

It's all so valuable, just so, so valuable. And also what you do on social media and the way you do it. And look, I also really love and respect your fighting spirit because you're fighting, you're fighting for truth, you're fighting for good. And I also love the posts and the pictures of your kids.

They're delightful. And it's great to see that the balance in your life you've created. So I could go on and on, but I'm going to cut this short by just saying a giant thank you for being the signal among all the noise. - Well, speak for yourself of being long-winded 'cause I'm not, but honestly, I appreciate that.

That means a lot to me. You know, I recognize how valuable your platform is and how many people want to be on it. And the fact that I've been asked to come on again, I really appreciate it. And to be able to have the opportunity to disseminate this information and not just talk about the studies, but talk about, hey, here's a method of thinking.

Here's a way to approach this stuff. And I mean, you kind of pointed out like, I would love to be able to say, yeah, seed oils are bad. Like, I'd love to give you that answer, but I can't do it. I can't make myself do it because I look at the evidence.

And I'm glad you said spirited. I do feel like I do have some fighting spirit, but at the end of the day, I tell people, you know, I'm human. I've got my own biases, my own beliefs, and I like making money like anybody. But I, and I like to be right.

But at the end of the day, I want to help. And I believe that if I continue to execute on that mission, that, you know, financial stuff will take care of itself. And at the end of the day, I just want to be a net positive on the world.

So thank you for giving me that chance. - It's been a true pleasure, and you're absolutely more than net positive on the world. And we'll just have to have you come back and talk to us again before long. Thank you so much. - Anytime, thank you. - Thank you for joining me for today's discussion with Dr.

Lane Norton. To learn more about his work, please see the links in our show note captions. If you're learning from and or enjoying this podcast, please subscribe to our YouTube channel. That's a terrific zero cost way to support us. In addition, please be sure to follow the podcast on both Spotify and Apple.

And on both Spotify and Apple, you can leave us up to a five-star review. Please also check out the sponsors mentioned at the beginning and throughout today's episode. That's the best way to support this podcast. If you have questions for me or comments about the podcast, or guests or topics that you'd like me to consider for the Huberman Lab Podcast, please put those in the comment section on YouTube.

I do read all the comments. For those of you that haven't heard, I have a new book coming out. It's my very first book. It's entitled "Protocols, an Operating Manual for the Human Body." This is a book that I've been working on for more than five years, and that's based on more than 30 years of research and experience.

And it covers protocols for everything from sleep, to exercise, to stress control, protocols related to focus and motivation. And of course, I provide the scientific substantiation for the protocols that are included. The book is now available by presale at protocolsbook.com. There you can find links to various vendors. You can pick the one that you like best.

Again, the book is called "Protocols, an Operating Manual for the Human Body." If you're not already following me on social media, I am Huberman Lab on all social media platforms. So that's Instagram, Twitter, now known as X, Threads, Facebook, and LinkedIn. And on all those platforms, I discuss science and science-related tools, some of which overlap with the contents of the Huberman Lab podcast, but much of which is distinct from the contents of the Huberman Lab podcast.

Again, that's Huberman Lab on all social media platforms. If you haven't already subscribed to our Neural Network Newsletter, our Neural Network Newsletter is a zero cost monthly newsletter that includes what we call protocols, which are brief one to three page PDFs that cover things such as neuroplasticity and learning, dopamine optimization, how to get better sleep, things like deliberate cold exposure.

We have a foundational fitness protocol. We have a protocol all about habit forming and much more. To sign up, again, at completely zero cost, you simply go to HubermanLab.com, go to the menu function in the corner, scroll down to newsletter, and you provide your email. I should point out that we do not share your email with anybody.

Thank you for joining me for today's discussion with Dr. Lane Norton. And last, but certainly not least, thank you for your interest in science. (upbeat music) (upbeat music)