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- [00:00]
A
Welcome to the Dr. Gabrielle Lyon show, where cutting edge science meets innovation and practical application for everyone. Today I sit down with a longtime friend and colleague, Dr. Lane Norton. We discuss the real cause of obesity. He covers everything from obesity to the optimal diet to supplementation. I believe that you are going to see a side of Lane that you've never seen before. Now, please sit down with me in conversation with Dr. Lane Norton. Dr. Lane Norton, welcome to the show.
- [00:43]
B
Thanks, Gab. Good to be here.
- [00:45]
A
So you said Gab, which. You are one of the only few people that are allowed to call me Gab. And this is because you made the cut. We have known each other almost 20 years.
- [00:53]
B
Yes, well, I like to have exact numbers, as you know. And you didn't even know when you graduated.
- [00:59]
A
Yeah, well, I mean, you know, details, details.
- [01:01]
B
This is true.
- [01:03]
A
Here's my goal for this podcast. Everybody who listens to this podcast, which is this is a top podcast in the country in medicine, knows who you are. And if you don't, you guys, Lane Norton, you may have seen him shouting on Instagram, talking about randomized control trials. We're gonna talk about all this. But what I love about Lane is, again, I have known him for so long and have believed in this guy since the beginning. He's tried to get rid of me many times. He has not been successful. And here.
- [01:32]
B
Can't seem to shake me.
- [01:33]
A
No, can't seem to shake me. And now you're stuck with me and my husband. It's just like a whole thing. But I want people to get both the other side of you, because you can, let's face it, become and seem to be very aggressive, which you are in many ways, because you are a very well trained scientist. We trained together at the University of Illinois under Dr. Donald Lehman, the goat. The goat. Which has created a certain level of intellectual integrity and scientific rigor and a way of thinking about things that arguably are very creative within the scientific realm, which is unusual.
- [02:10]
B
Yes.
- [02:12]
A
I have many questions for you today. And before I start, did you ever think that you would be in the position that you're in right now?
- [02:23]
B
I didn't. It's so funny when people ask me about, like, my career arc and all that kind of stuff, and I'm like, I had no idea what I wanted to do. I just knew I wanted to do something in fitness, maybe in the bodybuilding space, because I was into bodybuilding when I was young and I basically went to graduate school for a PhD. I. I really didn't even know what a PhD was. To be honest, and when I interviewed.
- [02:48]
A
You come from a very small town in Indiana, Gary, Indiana or close by.
- [02:54]
B
I come from Evansville, Indiana, Evansville, Indiana, which is the fourth biggest town in Indiana. Which means it's like 90,000 people, right?
- [03:00]
A
Yeah.
- [03:00]
B
I always describe it as it was big enough to not be a quaint small town, but small enough to where there wasn't anything going on, you know. So, yeah, when I, when I was looking at going to grad school was basically because I didn't know what I want to do with my life. I did a four year undergrad degree in biochemistry and at the time, if you wanted to make money in the fitness industry, this is circa 2004 when I was graduating. I mean, basically be a personal trainer, start a supplement line, try to be Mr. Olympia, open a gym.
- [03:34]
A
You did a few of those things pretty successfully, minus the Mr. Olympia stage. I mean, you've done a lot of those things pretty successfully.
- [03:40]
B
Yeah, but at the time I didn't really see any of those being a viable path because like I, I didn't come from money, I didn't have a lot of capital, I didn't like the idea of going into a lot of debt. I didn't really like the idea of being a personal trainer. I felt like that would make the gym a chore for me. And so I just kind of went, well, if I can delay the real world by four to six years, hopefully I won't be in an unemployment line with a master's or PhD. Right. And so when I was, when I went to Illinois, I didn't really have strong feelings about doing a master's or PhD. I just wanted to learn more because I.
- [04:12]
A
So wasn't luck that, that you landed in layman's lab.
- [04:16]
B
I'll tell you exactly what happened. I give the same advice to students. It was a little bit of luck for sure. But you know, when I was looking at grad schools, I had heard from people, okay, well, this is a good grad school. Well, this is a good grad school. Well, for anybody who goes to grad school interested in going to grad school, it is much more important to pick the advisor and the topic than it is to pick the school. How having a great school is great, but if you get in a great school with an advisor who's bad, you're gonna have a really bad experience. And I've got many friends who went to grad school who did not have the experience I had. And so I was just kind of going through these different schools Looking through the nutritional science department, the biochemistry departments, like, just seeing, like, who was studying a topic that I was interested in. And after, like, I'd gone through, I don't know, 10 schools, I'm like, this is gonna take forever. And I can't find anybody who's studying the stuff I want to study. So I remembered that I had, like, started to read scientific research on PubMed. PubMed had just gotten started, and you.
- [05:17]
A
Could see PubMed had just gotten started. Like, are you kidding me?
- [05:22]
B
Yeah, I'm old.
- [05:23]
A
And by the way, you're not that old, buddy, because you and I are, like, the same age. But there was a period of time where you and I had to go to the library and look through medical journals, and the amount of information that was being pumped out was significantly less than the amount of information that is being pumped out now. And I just. Why am I saying that? I'm saying that because the level of scientific rigor that I think was happening then is a little bit different, not for everybody, than is somewhat happening now. And you may or may not agree with that. It's just part of what I've seen. And you know who I was talking to about that? Tracy Anthony. Oh, yeah, our mutual friend Tracy Anthony.
- [06:04]
B
Our layman lab graduate, which I don't know.
- [06:06]
A
I think the people that come out of Lehman's lab are at a certain. For the most part, there may be one or two bad apples, maybe not. But really, no, they have good reputation.
- [06:17]
B
I mean, you got Suzanne devcota.
- [06:19]
A
You got Suzanne.
- [06:20]
B
A lot of Josh Anthony. Yeah.
- [06:23]
A
Very good friends of ours. Yeah.
- [06:25]
B
A lot of really good people came out of that lab. And, you know, on PubMed, I just. The. The first paper I looked at that I was like, oh, this is cool.
- [06:33]
A
Was from Tipton, how to have Better Skin. So this is Kevin Tipton. Yeah. Who is an OG in. He. You know, I think he passed away. Okay.
- [06:46]
B
And I emailed him. He wasn't taking graduate students. And then the second paper I read was from Don Layman. And so I emailed him, asked if he's taking graduate students. And it just so happened that his whole crop. Jamie Baum before also.
- [07:00]
A
She's also coming on the podcast. Very good friend.
- [07:02]
B
Yeah, she's awesome. Um, she was graduating, and he was bringing in a new crop of graduate students. And so I went up, interviewed, and I just remember in, like, 10 minutes of talking to him, I was like, I know nothing. Like, I. I was at the peak of Mount Stupid on the. On the dunning. Kruger.
- [07:19]
A
Yeah, yeah. We love.
- [07:20]
B
I felt like I knew so much and within five minutes of talking like nobody. I've never met somebody who one could make complex topics very simple. And not only that, if you talked about something he could tell you how it affected metabolism on a completely like some other biochemical pathway. And so many times I would have ideas and I would bring them to him and he would say well have you considered, you know, X or have you considered how this affects this over here? And it really got me thinking and I loved his background was similar to me. He did an undergrad in biochemistry as well and then his PhD was in nutrition. And so it really got me thinking in like three dimensions in terms of metabolism and realizing as a biochemist and I see this so much on social media now being focused on mechanisms, it's important to understand how these mechanisms function because if you have an outcome there's always a mechanism that's going to support it or mechanisms. But just because you have a mechanism doesn't mean that's going to produce an outcome because oh by the way there's also dozens, hundreds, maybe even thousands of other mechanisms that also affect the outcome that you're looking at and, and always use. A great example is aspirin. So aspirin we know is an anticoagulant, they give it to patients to thin blood but it also activates some pro coagulant pathways as well. But the overall outcome is it's an anticoagulant. And so what I see a lot on social media these days from science based accounts and by the way, for.
- [08:50]
A
Those of you who are not watching this, he just air quoted.
- [08:54]
B
Is present a mechanism and then jump to an outcome. And so you don't want to do this often. Yeah, you don't. I mean I've seen this like for example caffeine, we don't want to take in caffeine because caffeine stimulates cortisol production that's going to make you lay down belly fat. And okay, so what you're presenting is a mechanism that exists, but what do we have? My always, my first question.
- [09:23]
A
Here we go.
- [09:24]
B
My always, my first question is always, well do we have studies that look at like caffeine and visceral fat and, and, and body fat? Oh yeah, we do. And what do they show either neutral or positive effects on adiposity and visceral fat. So if it does activate that pathway, it's obviously activating other pathways that are more than compensating for whatever the negative pathway is.
- [09:46]
A
So let's let you know. You bring up social media, which, by the way, I was thinking about this before. Two things that you didn't know. I called Don and was like, don Lean's coming on the show. By the way, Don Layman, which you guys know, is my best friend, which is been my best friend for over a decade. We talk every day. So I guess that makes me his favorite. Lane and I can bust each other's shops. This is just how it goes.
- [10:09]
B
Well, you know, I gotta let you.
- [10:10]
A
Be better than me at something at one thing, because obviously I'm struggling with the skin. Inside joke, guys. But not so inside. I said, okay, I want to talk to Lane. And, you know, I would say, Lane, your and mind view. We went different paths, but we both serve people. I became a clinician, did a fellowship in nutritional sciences after Layman's lab at WashU and Sam Klein's lab. I don't know if you know Sam Klein, but, you know, extremely well respected metabolic lab. And, you know, I was thinking, okay, well, what are the things that Lane and I agree on and what are the things that we disagree on? And I really struggle to find certain things that we disagree on. Which brings me to a question. And this is. I know, and I was thinking about this. I also talked to dawn that you. And I was like, don, well, what do you disagree with, Laina? There's not very many things, are there? No, but there may be one. Okay, do you know what this is? There may be two. I feel like this is like the.
- [11:14]
B
Q and A. I have a possible LDL cholesterol.
- [11:17]
A
Yes, that is one. And then the other one is the calories in, calories out insulin obesity model. Okay, I would love to hear it seems like there's this ongoing debate which isn't necessarily a debate so much. You know, at this point with Kevin hall and really some great academic researchers that have been putting this out. But could you describe for me this calories in, calories out model and then this carbohydrate insulin model when it talks about obesity? Because everybody listening wants to either lose weight or just be the best version of themselves. And so really, to do that, one would be foolish to argue that body composition has to play a huge role.
- [12:04]
B
Oh, yeah. So I think we're. We probably don't disagree. I think.
- [12:08]
A
I know, but I had to, like, make it kind of probably.
- [12:10]
B
Maybe with LDL cholesterol we do, but I think with the energy balance, we don't. So I think most people have a fundamental misunderstanding of what energy balance Is, which is the amount of calories, the amount of metabolizable energy you consume. Okay. Versus the amount of energy that you expend on a daily basis. And let me just set this up. These are not independent variables, and this is where a lot of people get crossed up. The amount of calories you consume affects the amount of calories you expend and the amount of. There's evidence that the amount of calories you expend may affect the amount of calories you consume as well.
- [12:48]
A
What do you mean by that?
- [12:49]
B
So there's some evidence that if you increase activity, you, you may increase, you may compensate by eating more. It depends on the activity and the actual. The research tends to suggest that overall exercise has an appetite suppressant effect, that it actually sensitizes you to satiety signals, but you do. So people who exercise on average will eat a little bit more to compensate, but it doesn't fully compensate for the amount of calories they expend. Now that's on average. Right. We report averages in studies. There may be some people who I, I've, I've talked to people say, you know, I don't do cardio because I just know I get so hungry that I end up eating too much. Okay, well if that's the case, then, then don't do that. Right. But on average it has an anorectic effect because it sensitizes you to satiety signals. Now here's where when people hear calories out, they think about exercise. Calories out is far more involved than just what you burn during exercise. So you have one, your resting energy expenditure, which is the amount of calories you burn. Like if I just laid down.
- [13:56]
A
And you never do. But he was just laying there. Yeah.
- [13:59]
B
And didn't move throughout the course of the day. That would be my resting energy expenditure. It's also called bmr, Basal metabolic rate rmr. There's subtle differences in those, but they're essentially the same thing. That's your. That's kind of the cost of keeping the lights on. Then you have your physical activity which goes into two main buckets. The first being exercise, which everyone's aware of. The second is non purposeful full activity, which is called neat. Non exercise activity thermogenesis. And it turns out that NEAT is actually very modifiable. And people who, like. If you look at sort of the obese resistant phenotype. The obese resistant phenotype are typically people that when they eat more, they actually spontaneously become more active without even realizing it. There's A. A study, a very classic study in New England Journal of Medicine from Levine, I think, from 1995. Which were they over? I may. I may butcher the details of the study, but the general directionality will be. Will be correct.
- [15:00]
A
Okay.
- [15:01]
B
I believe they overfed people by like a thousand calories a day for six to eight weeks. And this was in a metabolic ward. So this was like very straightforward for.
- [15:11]
A
You guys listening to metabolic ward. These are studies that are extremely difficult to do.
- [15:14]
B
Food jail.
- [15:15]
A
It is food jail. Do you know I worked in metabolic ward?
- [15:18]
B
Oh, really?
- [15:19]
A
I did at Washu. Basically the patients check in. It's like a. I don't want to dissuade anyone from ever doing a study in a metabolic ward. But it's kind of like a hotel, but not really a hotel. It's like checking into a hospital. Ish kind of thing where you're in your room and the sheets suck and. Yeah, but you're not going anywhere. They're measuring and watching everything. You are laying in bed and you are watching, I don't know, whatever, Tommy the car or whatever, just trolls or something.
- [15:50]
B
They're either providing you with a certain amount of food or they're monitoring your food intake. And they're usually monitoring your daily energy.
- [15:56]
A
Expenditure as well and activity. Everything. At least we did. Yeah.
- [15:59]
B
Yep. So what they found was that on average, I think people gained like 5 kg over the course of this study, but the spread was from 0.8 kilograms to like almost, I think, seven and a half kilograms. And they found that the person who basically didn't gain much weight at all, they spontaneously increased their physical activity. And it wasn't from exercise. They were just pacing, fidgeting, they were just burning more. So that's one aspect of the obese resistant phenotype. Also, people who are obese resistant phenotypes seem to.
- [16:38]
A
Obese resistant, yes. Obese resistant phenotype, huh?
- [16:41]
B
Yeah. So they also seem to have better sensitivity to satiety signals. And another aspect of it, because you'll hear this lot like, oh, this person eats so much and they never gain weight. You see them eat a lot. They also probably don't snack. That is another characteristic of obese resistant phenotype is they tend to eat defined meals rather than snacks because snacking itself is not like unmindful eating doesn't affect satiety the same way that like sitting down for a meal does. Seems weird, but it's true. Like, there's so many things that affect satiety. Plate size, even color has been Shown to affect satiety, utensil size. Like there's a lot of stuff that goes into this psychologically. But getting back to our buckets, you have physical activity, you have neat. And neat is very modifiable. Like they've shown that 10 weight loss can reduce NEAT by up to like 4 or 500 calories a day.
- [17:39]
A
So 10 weight loss will decrease non exercise activity by 10%. Is that what you said? By what percent?
- [17:48]
B
Like 4 or 500 calories a day.
- [17:49]
A
4 or 500 calories a day.
- [17:51]
B
10% of weight loss can induce.
- [17:52]
A
Okay, so basically people are lowering their total body weight and then moving less.
- [17:57]
B
And moving less without realizing it. And then you have your, in the next bucket you have your tef, which is the thermic effect of food, which is like 5 to 10% of your daily energy expenditure. And it's basically like kind of like a car. You don't just put gas in your tank and the car spontaneously starts up. You've got to put some energy in. So that's why you have a battery, right. And you have a starter. So your body has to put energy in to get energy out of the food you eat. And not all food is equal when it comes to that. So for example, fats are like have a t F of 0 to 3%. So if you eat 100 calories from fat, you will net 97 to 100 calories. Carbohydrates like 5 to 10%. So you'll net 90 to 95 calories. A lot of that depends on the fiber content of the carbohydrate, how digestible it is. And then you have protein. And protein is 20 to 30% TEF.
- [18:57]
A
Which is, which is high.
- [18:59]
B
Yeah. So you net 70 to 80 calories. So some people have said, you know, well, I don't want to get too far into this rabbit hole, but no, no, we're not.
- [19:10]
A
I'm keeping you on track.
- [19:11]
B
Protein, you know, can't be stored as fat. And while that's true, you know, protein, the carbons from protein, there's a long way to go from them from amino acids to stored fat.
- [19:23]
A
You definitely can over. It's very difficult. And Jose Antonio has done some of this work where, where he's overfed, I think up to 3.3 grams per kilogram, something like that.
- [19:32]
B
Four actually.
- [19:33]
A
Okay.
- [19:34]
B
And what tends to happen is in the free living studies like that people don't gain body fat and it's, it's because of satiety. Now they've, the studies say that there's no difference in food intake. But I, I would be. I, I think that people are underreporting in one group and, and feel like they're eating more in the protein group, because in the, there's a few metabolic ward trials where they've overfed protein, and they do see that you can increase body fat. But the, the groups getting more protein also had more lean mass and.
- [20:09]
A
Well, we'll circle back to lean mass. Lean mass, you guys, is not just skeletal muscle. Lean mass could be a bigger liver, depending on distribution. And I'm sure maybe, maybe not. This podcast, it is a little nuanced. Maybe we'll circle back. You're smiling because, again, we come from the same lab. So do you believe if, if someone were to say, okay, calories in, calories out, we've identified that calories in is. Is pretty streamlined, right? How many calories are you getting and whether metabolizable. Okay, metabolizable.
- [20:37]
B
So if you have more fiber, you know, that sort of thing, that's, that's going to lower your metabolizable energy. So there's, there's. That, that, that kind of theory. I don't like calling it a theory because I think it's.
- [20:52]
A
I want you guys to listen to Lane's word choices. He is very dynamic and very particular about his statements. And you will also see that with many of the scientists we're having. Heather Lydy on Jamie Baum. I just want to point it out because again, you're amped and you're very entertaining, but your word choices are very particular.
- [21:12]
B
Yeah, well, you learn. You just get it beaten out of you. If you have a good PhD advisor, that if you're going to make a strong statement, you better have really strong evidence to back it up. Yeah, right.
- [21:23]
A
But anyway, calories in, calories out. I want to just bring us back into the, to that model.
- [21:27]
B
That is the, that is the, that's kind of the crux of it, right? Your metabolizable energy in and then the summation of the calories you expend on a daily basis. Now we look at the carb insulin model of obesity. This has a lot of variations. I feel like the goalposts have moved on this a lot. But I'm going to give you my closest interpretation of, of what I think has been popularized, which is you calories in, calories out kind of states that you overeat and become obese in response to the overeating because you're consuming more calories than you expend the carb insulin model says it's not so much that when you eat a high, when you eat high refined carbohydrate, you inhibit lipolysis.
- [22:14]
A
Just the breakdown of fat, right?
- [22:16]
B
So you have, you increase insulin, you inhibit lipolysis. That traps fat and adipose. And since fat is now inaccessible or stored energy is inaccessible to the rest of the body, you overeat in response. And so the, the crux is you don't become fat because you overeat. You become fat from eating too much refined carbohydrate and you overeat in response and then become fat. So I think there's a few kind of really basic reasons that that is not viable. So the first, the first thing I will say is for a hypothesis to be robust, it needs to show up across a broad category, various populations. One of the things that I had said to people who were promoting the carb insulin model of obesity, because they seem to keep changing it and keep like, well, this study didn't quite do this. And so it's not. And I said, well, if your hypothesis requires these extremely tight constraints to actually be true, it's not a very robust hypothesis.
- [23:24]
A
Or could it be that it is efficacious for a very particular type of age population? I don't know. Potential phenotype.
- [23:35]
B
So I would say the first thing to look at is there was a meta analysis of studies looking at various levels of carbohydrate intake in the diet, but they controlled protein and calories. So there's about 20 controlled feeding studies. So this is important because the inclusion criteria for this meta analysis was the. It either had to be metabolic ward or the food had to be provided to participants. So adherence was high because when you provide food to participants, you can get adherence above 90%. When you do free living and just tell them to do whatever, that's when you get like 50, 60% adherence.
- [24:14]
A
Oreos are eaten under the counter, right? Yeah.
- [24:17]
B
So the food was provided to participants. Protein and calories were equated, which is important. Obviously we've got to equate calories. There's a lot of studies out there where they're like, well, this showed more fat loss than this. But then you see, well, they didn't control calories. Okay. Might say something for satiety, but you don't really know if it like mechanistically what it's showing. So they equated calories, equated protein. Important for what we talked about because originally some of the lower carb research, like out of Volek and Finney's lab was showing increased fat loss and better muscle retention. But they weren't equating protein in the studies.
- [24:55]
A
I didn't know that. And for you guys listening Volek infinity, those are old. I don't want to say old school. They've been around a while. Yeah.
- [25:02]
B
Published a lot of really impactful research.
- [25:03]
A
Yes. They are really big into the low carbohydrate ketogenic sphere and world and they produce a lot of good stuff.
- [25:10]
B
Yeah. And I'm not saying anything negative about the research.
- [25:12]
A
Oh, you'll know when he's saying something negative about someone.
- [25:14]
B
Yeah. Actually, Jeff Volek was the first person to ever come up to me at a symposium with a poster I had and complimented me on my poster. So I like Jeff Bullock, you know, lean.
- [25:25]
A
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- [30:27]
B
Not equated in these studies. And so again that's important because of the thermic effect of food and the effects on body composition. So when they equated that, there's like I said, 20 controlled feeding studies, the summation of that showed essentially no difference in fat loss. In fact, there was a slight bit of favoritism towards the lower fat diets, but it wasn't really like, it was like 16 grams, no difference in fat.
- [30:51]
A
Loss regardless of the carbohydrate correct dosing. And do we know how high that dosing went? How high, how many grams per day?
- [30:59]
B
I don't know off hand. So but I, I recall like the spread was like, there was some, several ketogenic studies in there. So there was some pretty big extremes. Then we can look at some of the more, you know, nuanced, like individual studies. I'm thinking about a study from 1997 where again, they provided all the food to participants. They equated protein and calories. One group was getting over 100 grams of sugar per day, the other group was getting less than 10. And this is a study by Surwit and it was a. And they looked at fat loss, they looked at a bunch of other health markers and basically showed that fat loss was exactly the same. Now both groups were in a calorie deficit, right? They were both, I think the diets were like 1200 calories a day. So it was a low calorie diet, but one group was getting over 300 grams of carbohydrate or no, it's probably less than that, but over 100 grams of sugar sucrose. And the other group was getting less than 10. And essentially what they showed was almost all like everything improved, all the markers of health improved. But the one difference was actually LDL cholesterol dropped a little bit more in the, the low sugar group. But they also consume more fiber, which makes sense because we know fiber can reduce the LDL cholesterol. So that was a pretty tightly controlled study. And if refined carbohydrate was gonna cause that, I mean, we would think we would see it. There was another study from Kevin hall where they looked at ketogenic diet versus an isochloric non ketogenic high carb diet. This one did have over 300 grams of carbohydrate a day. And they also looked at C peptide, which is a marker for like, overall insulin secretion during the day. The. The more insulin you secrete, the more C peptide will be in circulation. And they found, I think C peptide was like 40% greater on the. The higher carb diet. But there was actually more actual fat loss in the higher carb diet versus the lower carb diet. And there was. I mean, this was a shorter study, but it was very tightly controlled. They also saw increased nitrogen excretion on the lower carb diet compared to the. But again, proteins equated.
- [33:12]
A
Right.
- [33:13]
B
So when I kind of look through all those, I'm like, okay, well, the carb insulin model, this isn't making sense to me. And then if we look at. Okay, let's take some different aspects of this, they'll say things like, well, you know, fat's inaccessible to the rest of the body. Yeah, but obese people don't have low levels of blood lipids. They have high levels of blood lipids. And then if we look at. There was a study actually where they gave a drug that inhibited lipolysis, and they found that it actually didn't affect fat loss, that people lost the same amount of fat as people who weren't inhibiting lipolysis. And then if we think about semiglutide. So semiglutide.
- [33:58]
A
Ozempic, guys. So either ozempic. So this is a GLP one. Yes.
- [34:02]
B
Regardless of people's feelings about.
- [34:03]
A
There's no moral judgment here with.
- [34:06]
B
Same for me. Same for me. But it. In as far as research literature goes, it is the most effective research weight loss. Beside, like, it's more effective than diet. It's more effective than diet. Like, I.
- [34:17]
A
It's more effective than bariatric surgery.
- [34:19]
B
I am, I am all for lifestyle. I'm not saying don't exercise. I'm not saying don't watch your nutrition, do all those things, but head to head, this drug beats it because it's a very, very powerful appetite suppressant. Now, also part of the low carb insulin model is they say, well, insulin drives up hunger. Guess what GLP1 memetics. Do they increase insulin?
- [34:43]
A
Correct.
- [34:44]
B
So they increase insulin, but they're powerful appetite suppresses yes. So this doesn't jive either. And if you were, and I know Gary Taubes, who's a big proponent of the low carb insulin model, he'll say something to the effect of, well, if you look over time, that's only short term insulin. If you look over time, their insulin goes down. Their basal levels of insulin go down. Yeah, because they lose weight, because they have less adipose tissue. If you reduce adiposity, you'll reduce insulin levels, all other things being equal. But again, your, your hypothesis that you've constructed with the carb insulin model doesn't say that. It says meal insulin release traps fat. And that over time is going to lead to problems. And it's just, it's not supported by the research data.
- [35:34]
A
Now and wait a second. And the reason why I'm bringing this up, Lane, is because on social media, people have access to information more than ever before. And there is a deep disconnect with what I think people think they should do and what will potentially actually move the needle. You know, I think about Jocko, and Jocko says discipline equals freedom. Totally agree with that. And then the next thing above that would be discernment equals right action. And if we are able to discern what is true versus what is questionable, then if we can fall back on good science that has a substantial amount of evidence, then we will have discernment into making right action at the right time at the right moment. Would you agree with that?
- [36:25]
B
Yeah, and I think this is. I was actually talking about this last night with a. I was out at dinner and I was sitting next to a guy at the bar who, he was here on business as well. We got talking and I said, you know, it's really, it's, it's not that complicated. It really isn't. Like if I put down two plates in front of you within a certain range, you know which one is better for you. But the problem isn't an information problem. We have an execution problem and a behavior problem. One of my. I'm going to use a financial example.
- [37:01]
A
Oh, okay.
- [37:02]
B
But I really like what Dave Ramsey said about his debt snowball. I don't know if you're familiar with it, but essentially what Dave Ramsey says is if you're trying to get out of debt, if you have multiple debts, take the smallest one, be as aggressive as you possibly can on that, and pay minimum payments on everything else. Once you knock that one out, move all that money you were paying towards that one, towards the next smallest one, and so on and so forth. And people have criticized this. That's stupid. Like, you should pay down the highest interest rate first. And his response is beautiful. He said, yeah, if we were doing math, that would make sense. But if we were doing math, you wouldn't be in this much debt in the first place, would you? So what we're dealing with is not a math problem. We're dealing with a behavior problem. And I think a lot of people, they mask or excuse inaction through paralysis by analysis or even jumping around.
- [37:56]
A
We have patients that jump around all different kinds of things. Diet to diet to provider to provider. Not so much in our clinic.
- [38:04]
B
Because then you never have to take personal responsibility for your own choices.
- [38:08]
A
And I will say, when it comes to calories in, calories out, I definitely agree it's there. The. There are potentially nuances. For example, I know that during menopause, the data doesn't show that menopause just overtly causes weight gain. I really struggle with this because in my mind I see a lot of patients that go through midlife and calories in, calories out, they go through menopause and then they gain weight. But then I worked on some of the early studies out of Lehman's lab, and these were the first studies of their kind. And really looking at postmenopausal women, diet and exercise and they. And it works. And then, you know, when I think about.
- [38:50]
B
I'm happy to address.
- [38:51]
A
Okay, yes. And then one more thing about this carbohydrate insulin model. I am guessing that. And if you guys notice, Lane is very particular about what is his statements are. I think if the average American is eating 300 grams of carbohydrates a day and are they are sedentary individuals, that is probably too much. We have to think about quality weight loss. If we reduce. I mean, I know, you know, some of the other studies when we reduced carbohydrates to 120 grams, we saw multiple percentage decrease in triglycerides.
- [39:21]
B
Yeah, I will say low carb does seem to have an advantage for reducing triglycerides, whereas like low fat seem to have a little bit more advantage for reducing LDL cholesterol. So it's kind of like your trade offs, you know what I mean? Both can reduce each. Unless you're eating a stupid low carb diet where you're just going crazy on saturated fat and putting butter in your coffee like some of these psychos and.
- [39:43]
A
It just tastes disgusting.
- [39:45]
B
So, you know, I think one of the things to keep in mind is that when you're reducing carbohydrate you're reducing calories by default. And a lot of people, what they think of as high carb foods. When I ask people, well, what they say, well, I'm addicted to carbs. Right. I have a hard time not overeating carbs. Okay, well, what carbs talking about cookies, donuts, ice cream, pizza. Those aren't high carb foods. Those are high carb, high fat foods.
- [40:13]
A
High calorically dense foods.
- [40:14]
B
Correct. And so if you do low carb, it's hard to have pizza, it's hard to have cookies. It's. So you're actually just reducing out those, that variety of foods. Now if you do low fat, you'd have, you'd have a hard time keeping the same things in as well. But I think for some people, low carb because they can have more savory things, it just clicks with them and is a little bit easier. But not for everybody. But what I would say is when you look at. Because people will ask me, well, Lane, how do you, how do you explain the mechanism? Like insulin goes up, it blocks lipolysis, like so how does it, how does this work? What you have to realize is again, you're doing trade offs. Carbs and fats are. Think of those as more of just fuel sources. Protein is kind of your building blocks. I am drastically oversimplifying because you can also use amino acids for fuel. They can be oxidized. But let's just take carbohydrates and fats. And it's so funny when people go, well, Lane's obviously never heard of the Randall cycle. No, I've heard of the Randall cycle.
- [41:19]
A
But have you heard of the reverse Randall cycle by Bob Wolf?
- [41:23]
B
So if you eat. So let's take two extremes. Low carb, high fat, high carb, low fat. If you eat a hike fat, low carb diet, you will increase your rate.
- [41:39]
A
Of fat oxidation because you are eating more.
- [41:43]
B
Because you're eating more fat and you're eating low carbs. So insulin's low. If you eat a low fat, high carb diet, you will not burn nearly as much fat because insulin is higher.
- [41:53]
A
But you would burn more carbohydrates, right?
- [41:56]
B
Correct. Because carbohydrate, once you have maxed out what you can store with glycogen, you have to oxidize it. Why is that? Well, that's because carbohydrate really isn't stored as out of adipose tissue. Like if you look at metabolic tracer studies that examine the fats that wind up as triacylglycerides in adipose, where did those carbons originate from? 98% or over 98% originates from dietary fat. Less than 2% came from carbohydrate. So and again, these are metabolic tracer studies where they've, they've looked, they've labeled carbons and seen where they've gone. Carbohydrate has to be oxidized. So downside is if you're oxidizing carbohydrate, you're not oxidizing fat. But also on a low fat or low fat, high carb diet, okay, you're not burning much fat, but you're also not storing much fat. On a high fat, low carb diet, you're burning a lot of fat, but you're also storing a lot of fat. And fat loss is not just fat burning, it's the amount of fat you burn versus the amount of fat you store. Right. Just like net protein balance is the amount of protein synthesis versus the rate of protein degradation. Right. You could have synthesis go up, theoretically, but if degradation exceeds it, you're still in a net negative protein balance. Right. So same thing over here. You're always storing and burning fat simultaneously. It's the relative rates of each that's going to determine how much actually winds up in adipose tissue.
- [43:20]
A
So if you were to design a diet, which you do actually, you don't, carbon does, which we do have an exciting announcement, but carbon is your nutrition app. If you were to design a diet for a metabolically healthy woman, let's say postmenopausal woman, because again, you know, the evidence doesn't support yet that this change in hormones or increase in fsh, you know, causes some metabolic derangement, especially when training is adequate.
- [43:48]
B
You know, you know what's funny is.
- [43:49]
A
I saw and I'm also saying that very cautiously because I have a feeling that it is going to be variable. But I again, I don't understand.
- [43:57]
B
Everything's variable.
- [43:58]
A
This is the clinician in me over time. But you know, then I look at Stacey Sims who is a postmenopausal woman who just trains like just, she's amazing. And then I see other women that obviously estrogen decreases, their non exercise activity seems to decrease. So you know, so I think a.
- [44:17]
B
Lot of this is what we call false attribution error.
- [44:20]
A
What is that?
- [44:21]
B
Which is basically X happens or sorry, X precedes Y, so you assume that.
- [44:29]
A
X caused Y, so X precedes Y. So you go through menopause and then.
- [44:33]
B
You gain weight and you assume that the menopause caused it on a, like a physiological level.
- [44:38]
A
But there's a redistribution of body fat, so there's a central body fat gain, you know, maybe from the androgen changes and the hormone changes.
- [44:45]
B
I haven't seen that literature. But what we do know is for menopause, we don't really see decreases in energy expenditure. This is Herman Poncer's data. We also don't really see changes in bmr. Now, there is some evidence that if somebody is clinically low in estrogen, if you replace that estrogen, you do get like 100 calorie bump per day, which.
- [45:06]
A
Is not super significant. I mean.
- [45:08]
B
Right.
- [45:08]
A
It's not actually super significant.
- [45:10]
B
That's the thing when you. Even when you look at. When people.
- [45:12]
A
But that is 700 calories a week.
- [45:13]
B
Yeah, no, no, it's. It's.
- [45:14]
A
And we know that typically the people try to reduce it by What? Oh, yeah, 700 calories a week.
- [45:20]
B
But you've got people saying, Well, I eat 1200 calories a day and I can't lose weight. And I'm sorry, I don't believe that. Because even in the most extreme cases, like, say, somebody who's hypothyroid, untreated hypothyroidism. The. The most extreme amount of BMR reduction I could find in the literature from hypothyroidism was 25%. So let's say somebody's BMR is 1200 calories a day. Okay, well, that means that it might drop their BMR by 300 calories. So now it's 900. But that's. That's just their BMR. You still got.
- [46:01]
A
Which is. Which is, like Lane was saying, it's laying on the floor of the podcast studio doing nothing.
- [46:06]
B
So if you're. I guess if you're completely inactive, like, you literally just lay on a couch all day, maybe you burn less than a thousand calories.
- [46:13]
A
I do wonder, because of the way hypothyroidism acts with glucose receptor uptake in the muscle. I often wonder if that would be a group, and I haven't seen the literature, if that would be a group potentially, where a lower carbohydrate diet would work well within their hormonal constraints because of hypothyroidism. Just a thought.
- [46:36]
B
What I would say is what would work better is just getting the thyroid fixed.
- [46:38]
A
Yeah, okay, fair.
- [46:39]
B
And I think I have seen this and the messaging. Some of the reasons that some of these diets get popular and the messaging on social gets Popular is because. And I thought about this a lot. Why do people hate the idea of energy balance, calories in, calories out, and the.
- [46:57]
A
Do they.
- [46:57]
B
You feel like a lot of people.
- [46:59]
A
Do or do you. Or do you feel like they find it because they struggle so much?
- [47:02]
B
I. I think there is in, you cannot get around the implied personal responsibility in calories in, calories out. But if I tell you no, no, no, it was because your hormones changed or no, it's because your. The food companies made you addicted to refined sugar and refined sugar is the cause. If I. That is very attractive to a lot of people because it removes the personal responsibility and it allows them to point the finger at like a larger, more nefarious sort of thing.
- [47:41]
A
So you don't believe as evidence in the literature thus far that going through menopause, because we have a lot of.
- [47:47]
B
Women, I think it makes it more difficult to lose weight, but here's why. Okay, so what happens, you know, menopause is typically mid-40s, 50s, average age, I think is 50. Yeah. So as we get older, what happens? We have more responsibilities, we have more stress. We have kids, stressful jobs, we sleep worse. I mean, this data is pretty clear about this. People drink more alcohol, all that. And what else happens? You don't feel as good because of all those things. You don't feel as energetic. And so you. Part of it is probably you may move less without even realizing it. You're just wiped out at the end of the day. I mean, you know, you have two kids.
- [48:32]
A
Like, yeah, I just drink caffeine and I make it happen. I mean, I'm not a good example. Do not do what I do.
- [48:37]
B
What I'm saying is like, I have two kids too, and I know how exhausted I can be by the end of the day sometimes, you know. And so I think it is more difficult, but I don't think it's because the hormones are somehow reducing your energy expenditure and that's making it more difficult. And again, there is.
- [48:56]
A
I also want to add to that.
- [48:58]
B
Go ahead.
- [48:58]
A
Are you ready? In my clinical practice, we use hormone replacement therapy and we don't see a change in weight. It is not a treatment plan. You do not add progesterone, estrogen, testosterone, and see a decrease in body weight. Will you alone. Right. Will you? With proper dietary changes, keeping protein. We should talk about what you believe and how you suggest people do macronutrient counting. And you guys, for those listening, I worked with Lane multiple times. I have worked with Lane in nutrition multiple times years ago. When I was in college and then residency. I don't know. It's. You're okay. Also, by the way, Lane has a photographic memory. It is the bane of my existence, that in his skin. So what you are hearing, it's ridiculous and somewhat irritating. But anyway, back to the practice. Just. We're like brother and sister. When we replace hormones, it doesn't mean their symptoms go away. They symptomatically get better. Maybe they're sleeping better, maybe there's improvement in mood and cognitive function. But in terms of weight loss, there are two things that are required for recomping body. And I'm not talking about additional anabolic agents and I'm not talking about additional GLP1 or GIP medications. It is resistance training. And this is the work that Don did some of the early studies. Again, thinking ahead, resistance training and maintaining and or increasing dietary protein from the RDA of 0.8 grams per kilogram to 1.6 grams per kilogram. So doubling the RDA, that seems to be within the literature. Just the way to make it happen. If I were to ask you, how do you suggest someone think about structuring a diet? Who is a postmenopausal woman? She is, I don't know, 55, hitting the gym. You know, we should, I want to make sure we talk about exercise. You know, what does her exercise plan look like and how is she designing a diet? Again, I do think that you should talk about carbon because there is a way to make it extremely easy. So what are the macronutrients and how would you think about it? And then what are the practical things? Should they use an app? Should they use something like Lumen? Should they use, I just want to throw that in there. Should they use, I don't know, X, Y and Z? How do you think about it?
- [51:25]
B
So first off, there are many paths to Rome. There's obviously people who have. And I always tell people, if you need to debunk any of this stuff, you just look around people's like, for example, well, you can't lose weight if you're eating refined carbohydrates or a high carb diet. Okay, what about Professor Mark haub, who lost 27 pounds doing a Twinkie diet? Like he was eating 1800 calories a day, but he mostly ate stuff from 711 and protein powder. Like that's what he ate. Right. So. So again, we just have so many examples of. And people, you know, on the plant based side, you'll have people say, well, you know, if you're eating A lot of fat. It gets stored as fat. You can't lose fat. Well, how many examples of low carb diets do we have? Like, it works.
- [52:07]
A
Are many passed around?
- [52:08]
B
What works is finding something that you can adhere to. Now, when it comes to the actual nuts and bolts of structuring a diet, the number one most important thing is to get your energy intake correct. Meaning if you want to lose fat, you have to consume less energy than you expend. Now, let me just do a couple of quick caveats on that, because I know there are people say, well, I know I was in a. A calorie deficit. I didn't lose weight. No, you. If you. If you ate the. So everything we eat is a carbon backbone structure, right? You ate those carbons. They have to go somewhere. Okay. And if you got. If you gained body fat, your body did not create carbons out of nowhere. They came from somewhere. Okay? So. And we're very well accounting for those. So we have to get the energy intake right now, what is that? Now, there. There are variances and whatnot, but essentially, like, you're trying to find somebody's daily energy expenditure. This is. You brought up carbon. This is kind of what the app does when it's originally, like, asking you questions and whatnot. And it's usually an equation out there to kind of determine your bmr. And then we're using a questionnaire to determine your physical activity, and then it's kind of taking a stab at it, you know, now you may get it wrong. It may be wrong. Right. Like, you might overestimate, underestimate for, I would say 60 to 70% of people, it's going to be pretty accurate. That's how, you know, bell curves work. Right. But then you adjust based on how you respond. Okay, let me back up.
- [53:51]
A
Yeah, we want nuts and bolts. I want to know how many grams. How are we doing?
- [53:55]
B
Yeah.
- [53:55]
A
Are we thinking about protein in a percentage?
- [53:57]
B
And this is exactly how the app works on the back end in the algorithm.
- [54:01]
A
And the reason I'm bringing up carbon is number one, I think it's amazing, and I may or may not have just recently accepted a position as a director of Women's Health. Very excited about that. Shout out to Mike, who's in Hawaii right now. But also, how do we make things easy for people? And also. But before we talk about carbon, I need you to tell me how many grams of. How are we thinking about protein as a percentage? Which, no, we are probably thinking about it in terms of grams. I know where you Come from? I know the school of thought. Are we thinking about a baseline number? So if the current RDA is 130 grams of carbohydrates, does everybody get that off the bat or do they have to earn that increase in carbon? You know, I think about Shane, my husband, who's running Chicago Marathon.
- [54:47]
B
Right.
- [54:48]
A
If we, you know, we have to account for that and then the fat, where do you. How someone listening at home who doesn't have carbon yet, what are they gonna do?
- [54:55]
B
So again, depending on your goal. If your goal's fat loss.
- [55:01]
A
Yeah, we'll just call it fat loss. Fat loss while muscle, muscle maintenance.
- [55:07]
B
So you get your, you get your, let's just say you get your calories right. Okay. So you have to get the right amount of energy to lose fat and energy deficit. The next step when I construct a diet and this is how the app works as well on the back end is okay, we have the amount of calories that we think is going to be reasonable for somebody to lose fat. Then we set.
- [55:27]
A
What is the deficit do you think? Is it a 10% deficit? How do you begin to think about it?
- [55:33]
B
It just depends on like again, it just depends on how quickly somebody wants to try and lose weight or fat.
- [55:39]
A
And this is somewhat of an experiment. It's interesting because you are an evidence based scientist and even in evidence based practices we still have to adjust and, and kind of go with, I mean there is individuality no matter how you look at it. And the randomized control trials are, you know, broadly speaking, hopefully through populations.
- [56:01]
B
Yeah, I think people, again, I think everybody should have to take a basic statistics course because I think people have a, a hard time understanding like the concept of variants and whatnot. So if we have calories set, the next thing we're going to set is protein because it's the most important macronutrient for the reasons we talked about. Thermic effect to food satiety, body composition. And so I said that as a gram per kilo or gram per pound of lean mass.
- [56:32]
A
See, you and I are different here. Yeah, I don't know my lean mass well.
- [56:36]
B
So again, this is Matt Producer.
- [56:39]
A
What's your lean mass? Why are you trying to get your something out of your man bag?
- [56:43]
B
So the reason I, the reason I say lean mass is because if you have somebody who's very obese, it's really going to overestimate protein if you're giving it based on their, their actual body mass. But again, a lot of people don't know their lean mass like you said, which is why in carbon, when they're signing up, there's questions. If you don't have, like, an actual body fat measurement, then there's some questions about waist circumference and whatnot. We. We make a. We make an estimation of what your. Your body fat is, and from your body fat and your total weight, we can determine your approximate lean mass. People get so hung up on this. It's. It's not a big deal if we're slightly off. Right. So we're.
- [57:21]
A
Could they be, like, ideal body weight?
- [57:23]
B
Ideal body weight, somebody could do as well. So we're looking at, like, around 2 grams per kilo of lean mass. Up to 3 grams per kilo of lean mass is what the app will end up recommending, and that's typically what I recommend as well. Now, 3 grams per kilo lean mass might sound like a lot, but when you consider. If you. If you're not doing total body mass, it winds up around probably 2.2 to 2.4 grams per kilogram of total body mass for somebody with an average body fat, you know, on average. So that's on the upper end. But again, I like protein. But again, in the app, you can adjust within a certain range if you want to. So once you've got calories set, once you've got protein set again, I like around 2 grams per kilogram of lean mass.
- [58:12]
A
Of lean mass, which is interesting. I'm trying to think about what that would be. So if someone was. So if someone was 52kg, and that's their total body weight, you think, Is.
- [58:23]
B
This someone's name Gabrielle Lyon?
- [58:24]
A
No, I'm smaller than that. Yeah, kind of. But I'm. I think I'm actually smaller than 52 kilograms, you know, how much if I'm 100? I don't know, maybe buck 10 if I'm lucky. How much. How many grams of protein would that be?
- [58:39]
B
Right. Around 100 to 110, you know.
- [58:41]
A
Okay, so I probably eat that.
- [58:43]
B
If you're 110 and you're pretty darn lean, my guess is your body fat is somewhere around 12, 13. Body fat, probably not that high, but should be 10.
- [58:55]
A
Just kidding.
- [58:55]
B
You know, you're looking at about 100 pounds of lean mass. That's about 45 kilos. You double that 99. About 100 grams of protein, right?
- [59:03]
A
Yep.
- [59:05]
B
So our app would put you anywhere from like 100 to 150 grams of protein, depending on your personal preference. Right. And so once you've got the protein number set we have to deduct those calories out of your total calorie goal and then you have carbs and fat left. And so what I did as a coach and what the app does is kind of say, what do you, what kind of dietary preference do you have? Do you prefer a little more fat? Do you prefer a little more carb? Do you like a balanced diet? Are you plant based, are you ketogenic? And you can pick any of those things and it will put you and will, you know, distribute the carbohydrates and fats appropriately.
- [59:45]
A
Is there a minimum amount of carbohydrates that you seem to like for an athletic person?
- [59:51]
B
I mean, it depends on the athletic event. If we're talking about somebody doing like actual anaerobic stuff for a lifter, let's.
- [59:59]
A
Say for someone who is lifting, doing resistance training for hypertrophy three days a week, but they're just doing it to maintain skeletal muscle mass, what are you thinking? Do you care?
- [60:10]
B
I'll give you the straight down the line scientific answer and then I'll give you the.
- [60:13]
A
I'm trying to pin him here, guys. I like, I guess yes, yes.
- [60:17]
B
So the straight down the line scientific answer is it doesn't seem to matter that much. It doesn't carbohydrate to fat. There are some individual studies that showed less lean mass accrual on a ketogenic diet versus a non ketogenic diet equated in protein. But there was also a recent meta analysis showing that there really wasn't a difference between high carb, low carb with protein equated. I think if you inject me with Truce serum, I think a little bit of carbohydrate is probably better just because even though carbohydrate insulin is not anabolic in the physiological range, it's, it is anti catabolic, it does inhibit protein degradation. And there was actually a study from Tipton showing that post exercise when they gave carbohydrate with protein or it might have been with amino acids that the net protein balance was more positive when they gave it with carbohydrate.
- [61:09]
A
And then I want to add two things here. So basically the way that I think about it is also muscle glycogen repletion. Right. If you are doing something that is costly from a metabolic standpoint, from an exercise standpoint where you're depleting muscle glycogen, carbohydrates seem like that would be the best route forward.
- [61:28]
B
Now I'll say, like it's pretty hard to deplete muscle glycogen. Unless you're going really hard. Like, it's. So I'll chuckle at these bodybuilders who, like, train for an hour and they're like, having 100 grams of cyclic dextrin right after the workout. I'm like, bro, you didn't even get close to depleting your muscle glycogen.
- [61:44]
A
Which is interesting because if we were to even, you know, think about the exercise component here, if someone is wanting to age, well, how would you think about setting up a training plan? Would you think hypertrophy versus strength versus power? And you would say, well, Gabrielle, how are you defining some of these things? But let's say your mom, okay, we want your mom to train for longevity. How are we going to do that?
- [62:14]
B
So I'll set it up. First of all, I probably should have led with this, but everything is based off, like, what can I get somebody to do consistently?
- [62:22]
A
Let's pretend we get to wave a magic wand. They're gonna do exactly what they tell you.
- [62:26]
B
But you can't do that.
- [62:27]
A
Okay, well, I can't better than you at something. Yes, I'm much more convincing.
- [62:32]
B
Okay, if I.
- [62:34]
A
Our friends, let's pick. Okay, fine. Let's not pick your wand.
- [62:37]
B
So what I would say is that I think both hypertrophy and strength are important for longevity. Hypertrophy because more metabolically active muscle tissue acts as a metabolic sink. It's going to protect you against, you know, metabolic syndrome. It's going to, you know, have better health outcomes, better insulin sensitivity, all that kind of stuff. I think strength is important from the perspective of preventing falls, quality of life. But those two things don't have to be mutually exclusive.
- [63:12]
A
So you could train for hypertrophy and strength at the same time. I mean, there's a great Schoenfeld paper, talks about the strength training continuum.
- [63:19]
B
Yeah, yeah. Like, if you're like, extreme, like with what I do, competing in powerlifting. Yeah, I'm focusing.
- [63:25]
A
It was quite a show, friends. Quite a show.
- [63:27]
B
I'm focusing obviously, more on the strength side, but obviously I've created some significant hypertrophy from that training as well. If you train just for hypertrophy, you have big muscles, but you're probably. You're still going to get stronger.
- [63:40]
A
You're going to get stronger. It would be impossible to not to do progressive overload and get stronger.
- [63:45]
B
Correct. So what I tell most people is, again, find something with resistance training that you enjoy and will push yourself on, because regardless of if it's low Reps, high reps. You have to push yourself to really get the benefits of it.
- [64:01]
A
Is the metabolic adaptation the same in high volume? And I've seen some things out of Stu Phillips lab that does the volume matter? So we're just talking about hypertrophy, which. Actually I called you because I was asking about a statement from, I don't know, I read somewhere something about as we decline, we decrease power, force. And you say, remember I called you about this?
- [64:25]
B
Yeah. Power goes first.
- [64:27]
A
Okay.
- [64:27]
B
Yeah. Because the speed component, I am curious.
- [64:30]
A
As to when we are thinking about what we are required to do. We know that anabolic resistance happens. Skeletal muscle just seems that that breakdown, that degradation, that turnover seems to be higher. You know, I was talking about Don about this. He's like, I'm in my 70s and I just can't put the muscle mass on that I did when I was in my 20s. Hypertrophy becomes more of a challenge, strength becomes more of a challenge. But then power. How do we define power? And power, like you said, has a speed component and is this part of an important component to training?
- [65:05]
B
So power I am not as familiar with. I didn't really do much research on it.
- [65:11]
A
Definitely going to push that needle because I know something here.
- [65:15]
B
So. No, I mean, I think power is, it's kind of like how quickly can you develop force?
- [65:24]
A
Yes.
- [65:24]
B
You know, and so absolute force, like the absolute like force you can apply to a load. That's actually what one of the last things to leave. So if you look at like different athletic events, right, we see like tennis players, sprinters, even like running backs. Like you're, you're pretty much like once you start to get to your mid-20s, you know, like, and obviously like, you know, baseball players last a little bit longer, but again they get to their mid-30s and usually there's a, you know, it starts to tail off.
- [66:06]
A
Depressing. Yeah.
- [66:07]
B
But if you look at like very high level power lifters where it doesn't matter how quickly you develop the force, as long as you develop it, you see that there really isn't a big drop off until people get kind of like as long as the training has been consistent. Do people get in their 50s? I mean, actually, so I set a world squat record back when I was in my. I was 34 years old.
- [66:33]
A
I want to say, let's get that number right.
- [66:35]
B
I was squatted. I squatted £668 at, in the 205 pound body club body weight class. And the guy who broke my record is a guy named David Ricks and he broke my record. He squatted £683 at 57 years old.
- [66:52]
A
That's amazing.
- [66:53]
B
And, and if you watch David squat when he, he, his opener was probably like around just over 600 pounds. So there's. You get three attempts in powerlifting. So openers are usually like your lightest.
- [67:03]
A
And you have a, A meet, not a show. A meet coming up.
- [67:07]
B
Worlds in.
- [67:08]
A
That's in three weeks in af. South Africa.
- [67:11]
B
South Africa. Yeah. So, but like, David's opener looks slow and every attempt looks slow. But, but he very strong.
- [67:20]
A
Okay. So. And also Jeremy, our friend, our mutual friend, Jeremy Lennon, he was on the podcast and, you know, he was talking about how also producing strength that you can get stronger without getting bigger.
- [67:30]
B
Yeah, you can. Yeah. Now what? I will. So I'll tell people this, this is. You won't find this in the literature. So this is if you inject me with true serum, which by the way.
- [67:39]
A
Is probably just a couple bourbons dancing on the table.
- [67:43]
B
So I'll dance on the table without bourbon.
- [67:46]
A
Oh, wow.
- [67:48]
B
So if you want to maximize strength, you probably need to think about trying. So your top end strength is actually probably going to be dictated by how much contractile tissue you have, like your strength potential. And.
- [68:05]
A
Wait, stop, stop. Very important. When do you think you lay that down?
- [68:10]
B
What age you can lay it down. So. So one thing we may, I may disagree with something else with Dr. Lehman. So there was actually a recent study that just got published showing that even people in their 80s who had never resistance trained put on muscle at the same rate as people in their 40s, 50s, and 60s.
- [68:28]
A
I need to see that. I do not. Now here's the rub.
- [68:32]
B
When I say the rate, we're talking about as a percentage of their starting lean mass. Okay? So when you're 20, you have a greater amount of lean mass. And we see this with women, too.
- [68:45]
A
And that was actually on my list here, the rates of muscle growth, men versus women. And how much muscle mass could a woman put on, say in a month versus a woman?
- [68:55]
B
The research shows that it's the same rate as a percentage of your starting lean mass. So. So let's take somebody with who's 50, a woman who's 50 kilos starting lean mass. If they add 10, they add five kilos. If we take a man who's say 75 kilos of starting lean mass, he adds 10%, seven and a half kilos. So the man has added more absolute lean mass.
- [69:17]
A
Because he's bigger.
- [69:18]
B
Because he's bigger overall.
- [69:19]
A
Do you Believe that. I want to ask you a non.
- [69:21]
B
Yes, I do.
- [69:22]
A
And do you believe pound per pound for pound, for example. Let's take out training practices. Could I be as strong as you? Pound for pound?
- [69:33]
B
Well, pound for pound is. So here we're going to.
- [69:35]
A
I don't talk and kill. We like.
- [69:37]
B
Yeah. So pound for pound is not. If you just. Okay, how much can weight weight can somebody lift divided by their body weight? Lighter people will always have an advantage because as your, as your mass, as a body increases in mass, your surface area increases as a function of a square, but your volume increases as a cubed function. And so basically long story short, what that means is people who are heavier so like super heavyweight power lifters are never as strong pound for, as a, on a per pound basis as people who are lighter. So there's some allometric scaling measure like so they have some certain alumetric scaling that will basically equate like that we use to determine who's the best lifter overall. Right?
- [70:25]
A
Definitely me. Yeah.
- [70:27]
B
And joking right now if I go on open powerlifting which, which takes all, every like every meet goes into open powerlifting and they, they crunch all the numbers. It's crazy. The top few are actually women based on body weight. So yeah. In terms of now. Okay, so on an absolute no, a woman will not be as strong as a man. But so let's take a 74 kilo male lifter and then let's take a 72 kilo female lifter. What they're like at elite levels, drug tested, what their lifts look like. Austin Perkins just won worlds and I think he squatted high sixes as a 74 kilo lifter, benched like 450 and deadlifted well over 700 pounds. The top female at that weight class probably squatted just under £500 benched in the. Oh no. Agate would have benched over £300 and deadlifted close to 600 or mid fives. So no, they don't get as strong but also they don't have as much lean mass because they have more body fat at the same level. But even if we go up where a woman would have the same lean mass. No, she doesn't get as strong. Absolutely. As a man and not sure exactly why that is.
- [71:56]
A
We don't know, we don't know why that is. And it's in there. There has to be some differences right. Beyond just the amount of contractile tissue. Is that fair to say?
- [72:03]
B
Yeah, well the other thing to keep in mind is like Lean mass isn't necessarily contractile tissue either, right? Totally. We would really have to get like some detailed studies in terms of skeletal muscle mass. But there is like, if you look at.
- [72:15]
A
But the rates of growth would be the same.
- [72:17]
B
So for rates of growth are similar. Now the. A man has more overall muscular potential because. And I don't want this to get political, but when you are exposed to higher levels of testosterone throughout puberty, one of the effects of testosterone is you get more satellite cell fusion. So muscle cells, I believe, are the only multinucleated cell in the body. So when you took, when all of you took high school biology, you learned that the new. The. The nucleus is the brain of the cell, right?
- [72:52]
A
Yeah, it's different now in urology, something else.
- [72:55]
B
So the muscle, muscle tissue, muscle cells. So a muscle fiber is a single. Is a single cell. It is the only cell that is multinucleated. Right. So you have these satellite cells that sit kind of on the surface of the muscle that can be donated through various different. And testosterone is something that does that to form more myonuclei. And there's some debate whether my nuclear domain theory is legitimate or not.
- [73:24]
A
But I, I don't even know what that. I don't even know what that is. So I might, I might not.
- [73:29]
B
You'll probably know it once I. Yeah.
- [73:31]
A
I might not know it by that name, but we.
- [73:32]
B
So the theory is each nuclei can only control protein synthesis for a certain surface area of the muscle. And so the more myonuclei you can donate, the more overall you can increase muscle protein synthesis. Because if you have, let's say you have one myonuclei that can, that can increase protein synthesis in this defined area, but then you have two now you've doubled the surface area that you can increase muscle protein synthesis over. You can control muscle protein synthesis over. So one of the things that steroids do is they increase drastically the satellite cell fusion and number of myonuclei you.
- [74:10]
A
Have at any age. And it's interesting, you say steroids and I think that they really have a poor connotation. But just from a medical perspective, we have been using people, physicians have been using anabolic agents in the face of hiv, anchexia. So when you hear the word steroid, don't think about.
- [74:32]
B
Barry Bonds.
- [74:32]
A
Yeah, don't think about. That's not what we're talking about. I mean, it is, but who knows? You know, we see it have some advantage.
- [74:43]
B
Yeah, I think I just want to.
- [74:45]
A
Just say that these things have been.
- [74:46]
B
Demonized because of the kind of the war on drugs and sport and whatnot. And listen, I compete in a drug tested federation. I've never used any illegal anabolic agents. I am.
- [74:59]
A
Or legal anabolic agents for that matter.
- [75:01]
B
Well, I mean I use creatine, which some people. Anabolic agent. But no, I never use steroids, pro hormones, that sort of stuff. But you know, I don't think that the great evil that people have made them out to be either, you know.
- [75:14]
A
No. And we may even see an influence that certain anabolic agents may be helpful in sarcopenia. Again, sarcopenia just got a diagnosis, an ICD, which is an international classification of disease in 2016.
- [75:26]
B
Yeah.
- [75:26]
A
So this is a new thing.
- [75:27]
B
And again to go back to Don Layman and give him a shout out. He was talking about muscle as an endocrine organ 30 years before anybody else.
- [75:35]
A
I know. So the idea that this myonucleodomain theory, when an individual uses anabolic agents, it would increase the satellite cell fusion, is that what you're saying? So the satellite cells are the feeder cells.
- [75:50]
B
So what it does is it kind of takes the, the, the governor off the top end of what you can create. Right.
- [75:57]
A
And interesting.
- [75:58]
B
Okay, this is, this is one of the reasons that again, if we look at men versus at least I believe one of the reasons, if we look at men versus women, why men get more muscular. Absolutely. Again, women can get. Because one, a man's baseline is higher once he's gone through puberty. A man's baseline is higher muscular potential. Yes. Because he's been exposed to higher levels of testosterone during puberty versus a female. So his baseline is higher and his overall top end is higher because of more myonuclei. But again, that's, I think that's also why we see like a similar rate like at post puberty you see a similar rate of muscular development, but you're just not going to get to the same top end as a female as you are as a male.
- [76:45]
A
It's almost like they started later in life. And also testosterone levels, you know, don't go as high even post puberty.
- [76:54]
B
Right.
- [76:54]
A
As, as men. So there's something called that fat free mass index, which I'm sure you've seen. Right. So this is this idea of, you know, is someone natural And I don't care about that, but how much muscle someone could put on. Do you. You're smiling. It's so funny. Right.
- [77:09]
B
People have used this to be like, see, Lane's not.
- [77:11]
A
No, Lane is natural. I may or may not Know, his physician, he is definitely natural. He's a very open book, which I admire very much about you, my friend. This fat free mass index, do you think that there is. You know, I think a lot about our kids. Right. We both have younger kids and I always think if they are sedentary now I really become concerned. Regardless, you know, Robert, you know, I. You have Robert and I have Leonidas. Let's say they're sedentary and they still go through these puberty changes. The influence of testosterone will be helpful, but without that stimulation, you know, I worry about obesity, the obesity epidemics and the sedentary behavior within the changes of skeletal muscle tissue as individuals age. You know, I'm sure you've thought about this quite a bit.
- [78:00]
B
You can look, I mean, there's a very popular image of an MRI out there of a seven year old who's sedentary or. No, sorry, it was a 4, like a 30 or 40 year old that's sedentary versus like a 70 year old Ironman runner. And the muscle tissue is so much higher quality when it's used. Muscle is such a. I took a class called Skeletal Muscle Structure Function and Plasticity. Muscle tissue is perhaps the most adaptable like tissue in the body. It's incredibly adaptable, incredibly resilient, and it really doesn't take a lot to get a big benefit. Like you can probably like 90 minutes of resistance training a week. If you're actually pushing yourself, you probably get 80, 90% of the benefits.
- [78:45]
A
Just right there, I have to stop you. Can we define resistance training? Are you including yoga and Pilates?
- [78:52]
B
No.
- [78:52]
A
Okay, what do you mean now?
- [78:54]
B
I would say.
- [78:55]
A
So you're saying yoga and Pilates. Could you replace yoga and Pilates with resistance training with weights or some kind of progressive overload?
- [79:08]
B
I mean, it just depends on what you want to get out of it. I mean, if you're doing yoga for like meditation.
- [79:13]
A
No, we are not talking about meditation. We are purely talking about jacked and tan and having muscle.
- [79:19]
B
So there is some research now that shows, again, Lehman was Talking about this 20 years ago, that if you stretch a muscle aggressively for a long period of time, that you can create similar hypertrophy as you can with resistance training untrained individuals.
- [79:35]
A
I knew you're gonna bring this up, correct?
- [79:36]
B
Yes, correct. So I, I think I would be very hard pressed to believe that you can create the same response in trained individuals, like you said. And also, like, there was a study looking at calf stretching. Okay. And they showed similar results as resistance training. Now here's what the calf stretching protocol was. It was a contraption they strapped them into that they went to a 7 out of 10 pain level on the stretch and held them there, I believe, for 45 minutes, seven days a week. The calf training protocol, I believe, was like three or four sets of calf training three times a week. I'll take the calf training, thank you very much. You know, to produce similar levels of hypertrophy. But it's cool that it showed as a concept that you could stretch a muscle and make it grow.
- [80:27]
A
Yeah.
- [80:28]
B
But I think resistance training is still the, the, the best way to get there.
- [80:31]
A
Yeah. Throw this out here. So do you think walking is, is enough?
- [80:36]
B
Oh, you're really trying to get it.
- [80:37]
A
No, no, no, I'm kidding.
- [80:38]
B
Listen, so always one of my favorite quotes is by an economist named Thomas Sowell. And one of my favorite things he said is there are no solutions. There are only trade offs. And when anybody makes a claim about something, ask, compared to what? So if we're talking about walking, compared to doing absolutely nothing, hell yeah, walking is better than that.
- [81:00]
A
But if you can walk, could you pick up a resistance band and do something?
- [81:05]
B
For sure. So again, so do you believe that.
- [81:08]
A
If someone can walk, that's the only thing that they can do?
- [81:11]
B
No, I don't. But I will say, I think sometimes people have a drastic lack of confidence with things, and it's almost like a confidence that they don't keep their promises to themselves. And so I have had people where I've said, listen, you know, going from, you know, being obese, completely sedentary, to going to the gym five days a week or four days a week. That's, that's a lot. And I have found what tends to happen. And I'm going to give a, I'm actually giving a talk about this in a few days about coaching.
- [81:44]
A
Oh, you mean tomorrow, Saturday, two days.
- [81:47]
B
Yeah.
- [81:48]
A
Shout out to. Where is it? The pt Dom.
- [81:51]
B
Yeah.
- [81:52]
A
Okay. Sounds like something else, but we'll just call it personal training.
- [81:58]
B
So I think sometimes people need to get the confidence that they'll actually show up for themselves. And sometimes. Yeah, sometimes it's good to like, I've had people say, I'm gonna go to the gym four days a week. I said, okay, maybe that's a great target to shoot for. But also come up with a minimum goal of what you know you can do. Right?
- [82:21]
A
Yeah.
- [82:22]
B
Because I want you to be able to hit something and consistently show up for it. Because if the goal is okay, I'm gonna get in Two days a week and you get in four, awesome.
- [82:31]
A
But if the goal is, like, set the standard lower.
- [82:33]
B
If the goal is I get in two days a week and you get in two days a week, then you still feel good about it. Whereas the goal is to get in four and you get in two, you feel like crap about it. Right? And what tends to happen is people like to think that they make decisions based on logic and data. And the reality is that most of us, myself included in a lot of ways, don't make decisions based on data. We make decisions based on emotion and personal beliefs. And so many people have a response where if it's like the whole, they get one flat tire and then they slash all the other three tires, right? Like, they go off their diet a little bit and all of a sudden they're binging their face off or they miss a training session, they go, well, I already screwed up my week. I'm just gonna not do anything.
- [83:14]
A
No, people are not. They're not doing that. The listener is not doing that. Not anymore.
- [83:18]
B
Right. So the point is, don't let the enemy of good be perfection. Right?
- [83:27]
A
I like that.
- [83:28]
B
So do what you can with what you got where you're at. But if we're talking about absolute best practices, hell yeah. Like, go lift some weights, get stronger, put on some muscle, like that is.
- [83:40]
A
And never break rule number one. And DM me, I'll tell you about rule number one. We gotta talk about supplements. Okay, I want to talk about supplements. I want to talk about fruit, I want to talk about sweeteners. And we have about half an hour to do it because you and I have talked about carbon. Okay, we're not. Okay, supplements. Which supplements have the best evidence? Give me your top three. And I also have a few statements that are. I need a yes or no answer, which can be very difficult for you.
- [84:11]
B
Try to box me in.
- [84:12]
A
Yeah, listen.
- [84:13]
B
Okay, so my Mount Rushmore of supplements is not going to, like, thrill anybody because it's going to be stuff that everybody's aware of. Number one is creatine monohydrate. I, I.
- [84:23]
A
Give me the dose, five grams per day. Do you know that 12 for brain health, they're.
- [84:27]
B
Well, so there was. So for muscle, 5 grams per day, we saturate. There was a recent study that showed an acute 30 gram dose actually improved cognitive function.
- [84:35]
A
This guy, I can never pull. Can you imagine? I would say that. Can you imagine arguing with you? You know, like, just, you know, I'm so excited, I can pull up some X's.
- [84:47]
B
They could probably give you some.
- [84:48]
A
I'm very excited to chat with your, your current beautiful lady, but I would just not want to argue with you. It would just be like, well, that time in 2000.
- [84:56]
B
Okay, but my brain doesn't work that.
- [84:58]
A
Way at 5, 17 and 30 seconds p.m. oh, you're right.
- [85:01]
B
Okay, so this is.
- [85:02]
A
I already know this. Wait, I am going to call you out. Nobody knows this about Lane. He is a freak when it comes to scientific literature and numbers and like ridiculous. If I'm like, Lane. So I would love for you to come to Houston on September 22nd. We're planning on having dinner with everybody this day. In one ear and out the other. Hey, what about that event? This guy, you give him a date or something else? Anything with numbers outside of academics, education or money, forget it.
- [85:38]
B
Yeah.
- [85:39]
A
Did anyone know that about you?
- [85:40]
B
Probably not. My girl definitely knows.
- [85:44]
A
Yes, of course.
- [85:45]
B
Because I think it actually gave her like a hard time for a while because she was kind of like. Like I would struggle with dates, times, recalling certain things in conversation. Yes, it should be like.
- [85:58]
A
It's called.
- [85:58]
B
How can you like this?
- [86:00]
A
It's called man brain.
- [86:01]
B
Yeah, man brain.
- [86:02]
A
Yes, man. So I don't want to deter you, but yes, we have to close this out because people do not know this about you.
- [86:06]
B
No. So, and, and I, I never actually realized like that. I just thought study wise, that that's how people work. No, and layman, last year we were all at an event and he goes, yeah, I've never met anybody who could just.
- [86:19]
A
I just like the bane of mine. Between that and your skin, it's a. The bane of my existence.
- [86:23]
B
So, yeah, I, I don't know why I got that way. I just had a photographic memory when it came to studies and you know, it just kind of worked out.
- [86:34]
A
Creatine. So 5 grams, 30 grams for muscle.
- [86:38]
B
30 grams acutely for. So I don't, so I don't actually know that. I forget. You got one, you got one. Now the question I would have is, okay, would you get the same benefits if you just like took that 5 gram maintenance dose and over time you would get there? Perhaps the 30 gram dose is just a saturating effect early on it would make sense. Who knows? Hopefully that cognitive research is going to expand more. But I honestly have a really people like, well, do I need creatine? No, you don't need it. But I have a hard time making the argument against taking it, to be honest.
- [87:15]
A
And do you know the, you know how much creatine you would get in A cooked steak?
- [87:21]
B
Yes.
- [87:21]
A
One pound. A pound.
- [87:23]
B
A pound. You get about half a gram of bioavailable creatine.
- [87:26]
A
I mean, so that would be what, two and a half pounds of. Wait, you would have to eat five.
- [87:32]
B
To get a half grams.
- [87:33]
A
Yeah, yeah, no, thanks.
- [87:35]
B
Yeah, it's, it's a little bit more that. I think I worked out the math.
- [87:38]
A
Because everybody wants that.
- [87:40]
B
There was a claim from the carnivore community that all you need to do is eat red meat. And I'm like, oh, well, you need to eat about seven and a half pounds of red meat.
- [87:48]
A
Well, it does make cooking much easier. And menu choices. What is your next. What is your next supplement?
- [87:53]
B
Let me finish with creatine.
- [87:54]
A
All right. I'm just trying to keep you on track.
- [87:56]
B
You don't need a load. If you have gastrointestinal side effects from it, split it into two, two and a half gram doses. That will help with the gastrointestinal discomfort. Also, any form of creatine other than monohydrate in my opinion, is a waste of money. All the studies looking at different forms of creatine, creatine monohydrate performs just as well or better. And it's the cheapest version. So get that. If you want to go a little bit more bougie, get the micronized version. It's more soluble, mixes up better. Next one, caffeine, the original nootropic, the original cognitive enhancer. I'll take it very consistently. Show caffeine will. It actually increases BMR slightly, may improve fat loss just a little bit. Cognitive, like task recall stuff, people are better at performance. People get a little bit better at how much.
- [88:48]
A
What's the kind of dose?
- [88:51]
B
So if you want like strength and power stuff, you got to get like 3 to 6 milligrams per kilogram. So pretty high dose. If you're looking at like anti fatigue cognitive stuff, probably around like 100 to 200 milligrams of caffeine.
- [89:09]
A
So basically it's how crazy do you want to feel?
- [89:13]
B
Yeah, so for me, as a super ADHD person, I'm kind of a caffeine junkie. You know, I, I'll have about 500 milligrams of caffeine before I train. But I'm also like, you know, if you're adhd, stimulants don't affect you the same way. I just, that doesn't make me like, it just makes me very focused. So I like caffeine. Obviously there's the, you know, the, the impact on sleep. Again, no solutions, only trade offs. If you are someone who trains later in the day, the half life of caffeine is six hours. You're probably like, let's say you're going to train like 5pm you're probably better off having your caffeine dose like maybe like three hours earlier. And that way, you know, after six hours, at least half of it's out of your system.
- [90:05]
A
And some people are fast metabolizers and some people are.
- [90:08]
B
Yeah, there is some slow.
- [90:08]
A
There's some genetic variants. I think it's comt. It's just a snp, but again, that's one snp. So some people, you know, caffeine affects them. Other people, they're able to metabolize it very fast.
- [90:19]
B
Yeah. And again, look again, when we do studies, we report averages. If you know that you're somebody gets really jittery with caffeine intake, you know, take in the amount of caffeine that you feel like you can tolerate. Hmm. And then whey protein. So whey protein, just.
- [90:34]
A
Why whey as opposed to something else?
- [90:36]
B
Well, one, it's. It tastes good, even like unflavored whey actually has like a little bit of sweetness to it. It's easy to flavor, it mixes up well, the consistency is good, it's not super expensive, and it's very high in leucine. So, Lucy, what's that? So leucine is the amino acid responsible for triggering muscle protein synthesis. Now I would consider whey protein, of the popular proteins out there, the highest quality protein, very bioavailable. Great. PD cause. PD cause is an amino acid score corrected for digestibility that kind of assesses like, does it supply all the essential amino acids? And whey does, and it's very high in the branch chains, very high in leucine.
- [91:20]
A
What about the alpha lactobumin and lactoferrin? Are those immunoglobulins? I mean, I know that they're highly available and present in the concentrate, the whole whey. What about the whey isolate, does that also have alpha lactalbumin, lactoferrin, which are again, immunoglobulins that are good for gastrointestinal health and immunity. Potentially good for immunity and gastrointestinal.
- [91:49]
B
Yeah, so what I'll tell people is whey concentrate has those, and it's less expensive, usually a little bit higher in carbohydrate, higher in lactose, higher in fat is a weight concentrate. But you're getting some of those other things that we're talking about. That are maybe beneficial for like gut health immunity, those sorts of things. Weight isolate, less of those, but also virtually devoid of lactose, very low in carbohydrate, very low in fat. So it really just depends. A lot of people have difficulty tolerating a straight way concentrate. Oh yeah, a lot of the most. A lot of people can tolerate like a blend. So like kind of an isolate concentrate blend.
- [92:31]
A
And do you like that over a rice pea blend? For exactly those reasons. I mean, I am biased. I do like whey isolate over that because rice p blend. I mean, yeah, there are probably other bioactive compounds that we just don't know. But I think whey we have a pretty good understanding of what's in it.
- [92:50]
B
I like whey isolate and that's what my company Outwork Nutrition sells as a protein because I wanted something that most people could take in. So isolate. It's very low carb, very low fat, it still tastes good.
- [93:02]
A
I wouldn't know because you haven't sent me any. I mean, look, he's looking over his shoulder.
- [93:08]
B
All you gotta do asking you shall receive. I'm asking you shall receive. So I, I like a way isolate just because I know most people are gonna be able to tolerate it. There are some people who do have, are really sensitive to the lactob humans in a whey that still don't tolerate away isolate. Very small percentage of the population for them you can do away hydrolyzed. Now they're increasing in levels of cost. Like concentrate is the cheapest whey isolate. A little more expensive whey hydrolysate is more expensive. Hydrolyzed is enzymatically digested. So those, those polypeptide chains get chopped up with enzymes. So that will almost. I can't imagine somebody not being able to tolerate away hydrolysate. The downside is it's more expensive and it doesn't taste as good. But if you want a good high quality whey and you're somebody who, you know, you get a lot of gastrointestinal discomfort with whey isolate or whey concentrate. Whey hydrolysate would be an option.
- [94:09]
A
What else you got for me? So we have creatine, caffeine, caffeine and whey. Is that it?
- [94:15]
B
That's my Mount Rushmore of supplements.
- [94:18]
A
I'm so excited to share with you guys a scientific breakthrough to support our long term health and wellness. C15 is the first essential fatty acid to be discovered. And get this, 90 years, that was omega 3 fatty acids. You've heard of the freshman 15. But let's talk about something positive. Our primary source of C15 has long been whole fat dairy products. Unfortunately I don't eat those. You might not either. And our C15 levels have gone down because many of us are eating a lot less of them. Additionally, our C15 levels naturally decline as we get older. Now C15 works in a number of ways. It helps repair damaged cells, it may protect us from future breakdown, could potentially boost mitochondrial energy output, activates pathways in the body to help regulate sleep, mood and natural repair mechanisms that of course support our overall health. Now it ends up many of us are deficient in this saturated fat C15, which results in obviously weaker cells, potentially less energy. Fatty 15, when you take it orally, is highly absorbable and it can actually help with cellular repair. It is made from a patented pure oxidative resistant process. It is vegan friendly. No fillers, no allergens, no preservatives. It is 100% pure. Fatty 15 is on a mission to help you replenish your C15 levels and restore your long term health. You can get an Additional get this 15% off their 90 day subscription starter kit by going to fatty15.comdrlion and you can using the code D R L Y O N at checkout. Here's how I've been using AG1 with my unsweet Texas tea and half a shot of ketones. I have to tell you I feel really good about that kind of decision. AG1 covers what I lack in my diet. It comes from whole food sources that are synergistic. It is the difference between eating components of a stew, for example, rather than the entire cooked stew itself. AG1 has vitamins, minerals, adaptogens and bioactive ingredients from whole foods like citrus, bioflavonoids. The synergy of the parts amplifies the effectiveness of AG1. It contains prebiotics, probiotics, gut supporting ingredients. In fact, in a research study, 97% of participants felt digestion improved after 90 days of drinking AG1. In another clinical trial, AG1 was shown to increase healthy bacteria in the gut by 2.9 times. AG1's formula takes a dual approach, supporting the gut microbiome and also overall health and wellness. I know because I feel it myself. What I love about AG1 is that it has a commitment to research and furthering the science around nutrition and gut health. AG1 uses research backed ingredients and they even take it a step further by conducting multiple research studies on the complete formula. They continuously publish their findings curated across many disciplines and are deep in the research, testing, validation. Now. It's a great first step to investing in your health and that's why I'm so excited to be partnering with them. Try AG1 and get a bottle of vitamin D3K2 free and five free AG1 travel packs when you first subscribe@drinkag1.com lion that's a $48 value for free if you go to drinkag1.com DrLion check it out. As a mom of two kids, I have always had major concerns with what we cook on and how we store our food. I felt a ton of relief when I started using Our Place cookware and appliances because they are made without Forever chemicals. These products do not have PFAS or Teflon in it. In comparison, most of today's nonstick pans contain pfas, also known as Forever chemicals and I will tell you the EU plans to prohibit PFAS use by 2025. Now most cookware brands continue to use these Forever chemicals because because they are at a low cost. That is why our Place came out with non toxic appliances. They have been integrated into our family's life. I strongly recommend that you try them. If you are not using them, go to fromourplace.com and enter my code DRLION at checkout to receive 10% off storewide. That's from Our Place and use the code drlion. They also offer a hundred day trial with free shipping and returns. I will also mention this it makes a fantastic gift. These are beautiful pieces and they can be used safely. Again, I believe that chemicals used in cooking ware are going to be like what we thought about smoking. We thought smoking was benign and then we figured out it causes cancer. This I think is going to be the same thing. We think that Teflon is benign, but in fact I think it is going to cause major health problems. So do not be a victim for being behind in knowledge just because the general population and science may have not caught up. Check out our place. On occasion I like to ask yes or no questions which is very difficult for you. It's gonna be very difficult. You're not allowed to say it depends. It's only like yes or no, blah blah blah Fasting. No ketones, Beta hydroxybutyrate ketones.
- [100:20]
B
Can't ask me yes or no on this for what purpose? And fasting for what purpose?
- [100:28]
A
We're not doing that and it's only yes or no. So fasting I the reason I chose fasting is because you and I both believe there's a tremendous Amount of hype and has been very much taken out of context. The. I'm just gonna put words in your mouth. We believe the fasting is great, allows for calorie control, may help with gut rest, which is how. Okay, so this is the only reason. It's just very controversial and people are really. I think there's. For autophagy purposes, there's multiple ways to gain autophagy, like calorie restriction exercise. Have I appeased you? Okay, so fasting, yes or no?
- [101:00]
B
No.
- [101:01]
A
Okay, ketones. Beta hydroxybutyrate ketones. Okay, fine. I will do something I've never done on my podcast. I will preface this thank you by saying beta hydroxy be the fifth butyrate for cognitive function.
- [101:18]
B
I actually don't know. I haven't looked in that research enough to form an opinion.
- [101:22]
A
Dom D. Agostino and I both agree and use it for our operators and ourselves at between 10 and 12 grams.
- [101:28]
B
You guys would know more than me.
- [101:29]
A
You know, but like no one wants to hear about. From me today, all about you. Okay, Sweeteners. Oh, wait, sucralose.
- [101:37]
B
Yeah.
- [101:38]
A
Okay, see, probably. Can we just touch on that? Even though it's kind of out of cadence?
- [101:43]
B
Sure, sure.
- [101:44]
A
Just.
- [101:45]
B
Yes, Sucralose.
- [101:46]
A
People are very upset about sucralose in general. Yeah, they are very upset about what? Aspartame. I don't even know what people are upset about.
- [101:52]
B
Yes. If you look at the non nutritive.
- [101:54]
A
Sweeteners, which is non calorically contributing, is that correct?
- [101:58]
B
Okay, so you've got things like sucralose, not erythritol.
- [102:02]
A
Right. Like not erythritol. Is that.
- [102:04]
B
I mean, erythritol is. I mean it has a little bit.
- [102:09]
A
Of calories, but it's in the non nutritive sweetener group.
- [102:13]
B
Okay. We'll say no, probably not non nutritive, but it's very low.
- [102:16]
A
Okay, so we have sucralose. Let's talk about this. Sucralose. Give me the other ones.
- [102:20]
B
Aspartame.
- [102:21]
A
Aspartame. That's the blue. The blue pack.
- [102:24]
B
Saccharine.
- [102:25]
A
Ooh, saccharine. That's an oldie wickety.
- [102:27]
B
Yeah. So if you look at the research data and there's several meta analyses now, so some of the claims out there is, well, you don't want to have these. These spike your insulin and it's going to cause you to store fat. Or the other ones is it's going to make you hungry or it's going to cause you to gain weight. No, no and no. So if you want to like hack together a story of, well, when you.
- [102:53]
A
Take wait time out. So non nutritive sweeteners like sucralose, aspartame, what else? We say saccharin do not spike your insulin. Do they make you hungrier?
- [103:06]
B
No.
- [103:06]
A
Do they cause cancer?
- [103:09]
B
No, not based on the research literature. So here, here's okay. So here's okay.
- [103:13]
A
Wait, we have more. I'll take it. Yeah, I'm ready for it.
- [103:16]
B
Recent meta analysis looked at the glycemic responses in terms of not just insulin and blood glucose and I think like.
- [103:23]
A
Gut hormones, that was the other thing. So our friend Suzanne Devkota, I always ask her about that is their influence on the gut microbiome.
- [103:32]
B
Yeah. And she's her, her take is that maybe, but it's pretty far down the list of things that I worry about is what she said. So the, and I'll touch on the gut microbiome stuff real quick. But no effect on glycemia. Basically the conclusion of this meta analysis was all these markers. The effect was as the same as water. Right now, weight loss, appetite. In cross sectional studies that look at people who are obese, they are more likely to use artificial sweeteners or non nutritive sweeteners. And so people have said, well see those make you fat. Well, as we know, correlation is not causation. So if we look at the randomized control trials where they instruct people to consume non nutritive sweetened beverages in place of sugar sweetened beverages, people lose weight and significant weight and they actually lose a little bit more weight on average than if they tell them to drink water.
- [104:33]
A
Oh, that's interesting.
- [104:34]
B
Yeah. So it equates to about a kilo kilo and a half of body weight difference.
- [104:39]
A
Okay.
- [104:40]
B
Now it's not because they're fat burners, it's because people are eating less. So again, there's the appetite portion of it. It's obviously not increasing appetite because if it was, then what you're saying is these, are these non nutritive sweeteners must be fat burners if you're saying it increases appetite and they're consuming more. So again, I'm not saying people should have them. If you want to drink water, that's totally fine. But for some people, I think especially people who are coming from drinking a lot of sugar sweetened beverages, you have something else to fill that sweet taste. What possibly is happening in these groups that are drinking water is they're seeking out that sweet taste somewhere else. Whereas if they're getting it from, say, diet soda or whatever, it's fulfilling that. Now let's talk about the gut microbiome. So some of them appear to affect the gut microbiome, some don't. Sucralose does appear to have an effect on the gut microbiome. Now here's where we. I disagree with a lot of the scientists out there because they say, oh, they call it gut dysbiosis or whatever.
- [105:41]
A
Gut dysbiosis? Yeah.
- [105:43]
B
Okay. What they've shown is that there can be a. Some of the studies have shown no change. Some studies have shown a change. Okay, there's a change. But one of the studies where there was a change, I looked up to some of the species of gut microbiota that were increased by sucralose. One of them, oh, Blaudia cocoides, I probably mispronounced the hell out of that because it's a Latin name, actually has been shown. So that was increased with sucralose intake. That's a bacteria that produces more butyrate. It is associated with less body fat and better insulin sensitivity. So based on that, couldn't you make the argument that sucralose actually improved the gut microbiome? I'm not saying it did. What I'm saying is we don't know if this is a good change, a bad change or neutral. And if somebody can loot. And every time I post about diet sodas, people will comment and say, yeah, all I did was switch to from regular soda diet. So I lost £50. You have a hard time convincing me that some small change in the gut microbiome makes them worse off than if they lost £50. Right. As far as the cancer claims, this is where negativity bias really comes in. So I'm a, I'm on the scientific advisory board of a company called Consensus and they're basically think about like chat GPT coupled with PubMed. Right. So search function on PubMed is kind of garbage.
- [107:10]
A
No, come on guys, get that together.
- [107:12]
B
You can go to Consensus, it's consensus app and you type in a question about research and it will do basically the AI crawls the, the, the research literature and comes up with a consensus and will show you what percentage of studies say what.
- [107:30]
A
That's really interesting.
- [107:31]
B
If you ask it a yes or no question, it'll say yes, no, maybe if you put it on synthesize. If you type in does aspartame cause cancer? 80% of the studies say no. But you wouldn't know that from watching the News, Right. Why? Because if a study comes out showing no effect, it's not newsworthy. But if a study comes out saying. But let's take. So for me to be convinced that something is carcinogenic, there has to be a viable mechanism. There has to be human data, there has to be cohort data which.
- [108:07]
A
Which is what?
- [108:08]
B
So basically like they track people for a number of years, there's no intervention, they show like difference in rates of cancer development. So one study, that nutrisante cohort came out probably like five years ago that got a lot. It was a 100000 person cohort out of France. I believe it was done over 20 years. And the big headline was aspartame increases the risk of cancer. Okay. So I looked at the data and they had like low or never consumers, moderate, low to moderate consumers, and then moderate to high consumers of aspartame. So they showed an increase from the. The non to the moderate, which then decreased in the high consumer group. I'm not aware.
- [108:53]
A
I love, I love those.
- [108:54]
B
I'm not aware of any carcinogenic compound that in a low dose.
- [108:59]
A
Yeah.
- [109:00]
B
Is carcinogenic, but in the high do is not.
- [109:03]
A
Yeah.
- [109:03]
B
So to me like it as. I'm not saying it's a bad study, but if you measure enough things. Not saying if you measure enough things, this is like p hacking. You will find something as. As Don used to say, if you torture the data enough, it will confess what you want it to say.
- [109:25]
A
It's so true. It's so true. You know, I. I feel like you personally have paved the way for a whole new generation of influencers. Okay, so hear me out. People cringe. Well, I, I just, I think this is important because some may find you aggressive. Just some. Some may find you. Yeah, okay, fine. We are in Texas. Things are spicy here. But I do want to point out it's not to do it for attention. It's not to do it because you are trying to raise visibility on yourself or something. And I find that right now the majority of people, believe it or not, get their health information from online, whether it's TikTok or Instagram or YouTube. And you are the first, to my knowledge, the first PhD to come out in a way to say, you know what? No man, these claims are not true. And this person is saying this. And part of that I think has paved the way for a very unqualified, extremely rambunctious group of non scientists or people that have no clinical experience or are just finishing Ph.D. that is maybe not as Rigorous because in the real world, in the academic world, people that have earned their keep. You would never go to Don and do a video about him, would you? Do you understand where I'm saying I think people have to. And I'll just leave it at this because I love that about you and I think that you created a pathway forward. But I want people to understand that there's a huge responsibility why you do it and that everyone is not qualified to do that.
- [111:23]
B
So I really try to save my vitriol for the worst offenders of stuff, you know. Now I have on occasion done videos on like, I'm thinking about. There's a gal who had a channel food science babe and I think overall her stuff was really, really good. But there was something specific I disagreed with her about and I did a video on it. But, but I couched everything with, hey, I agree with most of her content. I think it's really good. Here's why I disagree with this. Right. So it wasn't like an aggressive like debunk sort of thing. And I really, if somebody has like strong academic chops, they haven't said a lot of crazy stuff over the course of time. I really do give a lot of leeway to that. Like, I don't. I'm not going to say I've, I've never acted out of pocket before because I probably, I definitely have.
- [112:16]
A
But with Mike's. I mean Mike is. Mike has. Shout to Mike Fox, who we love is Been a really good. Yeah, yeah.
- [112:25]
B
But you know, I think, I think there is, there's, there's evidence based and then there's. I won't believe anything you say unless you give me a PubMed citation, which I, I understand where that comes from, but I think I have. People send me videos all the time of stuff where I go, I'm not gonna do a video on this like this. This person said it's their opinion. They're allowed to have their opinion.
- [112:51]
A
But why has it now become that? Because that was not your, you know, your intention is very clear from my perspective. You are here to protect people.
- [112:59]
B
Yeah, I mean, so I think you have to understand like how this whole thing started with me doing debunks is I had never been afraid to call out BS and I had never been afraid to like speak my mind. And again, I think credit to Don Layman, but when I was getting into coaching, I saw kind of on a like a like battlefield level how some of this bad advice really negatively impacted people, like, and just saw it in their lives. You know, a lot of it in the form of, like, food anxiety or, you know, eating disorders. They know those sorts of things. And I just. I really saw how much it was harming people. And for a long time I kind of had the perspective of. So I would, like, call things out, but I wouldn't do people by name. You know, it was always like, boy.
- [113:55]
A
Times have sure changed.
- [113:56]
B
Yeah. Well. And what I found was people found it kind of disingenuous because they're like, oh, you're creating this. Nobody. Or nobody saying this, or you're making this up, or, you know, I'm like, no, this is real stuff. You know, And I just hated seeing how it negatively impacted people.
- [114:17]
A
Yeah.
- [114:17]
B
And I. I do have a very strong sense of justice and what's right and WR especially. And again, because I went through a PhD where I was wrong so many times.
- [114:32]
A
Yeah.
- [114:32]
B
And I had my PhD advisor tell me I was wrong so many times. And also.
- [114:37]
A
But did he ever say to you, wow, that was stupid?
- [114:39]
B
No.
- [114:40]
A
Well, he said that to me, Don.
- [114:42]
B
Oh, really? I mean, he. He probably said it in more words than that.
- [114:48]
A
Yeah.
- [114:48]
B
You know, like, he. He did. He. He's had some hard conversations with me as a PhD student, but I just got okay with being wrong. And I think for me, what I tell people is like, listen, I don't usually plant my flag super strong. I mean, you talked about the word choice I use and how I'm very careful with my words. So I tell people, I don't. You very rarely hear me plant my flag super strong. So when I do, you should probably pay attention, you know, And I think that just got beat into me with being like, the amount of rigorous. And honestly, I think. I think there's been a big shift after Covid. Sorry. I probably should have like, X you got. You'd have to bleep that out so we don't get knocked down, you know. But, you know, I was explaining this to the guy I was talking to last night. I said, you know, this created a lot of distrust in science. And, you know, when, as it was happening, I said, this is going to be a real problem because people are going to watch the scientific process, which is messy, play out in person. Right. Which is science. Before that was a very behind the curtain thing. It was scientists got together at conferences.
- [116:05]
A
Really good point.
- [116:06]
B
And argued in journals and politely. And 30 years later, we emerged from behind the curtain and go, we think, meh. Right. Instead, you got to see every time a new study come out. Well, this study said this well, the study said this. Well, the study and I think the, the take home people have. Well, I don't trust any science. It's all bought and paid for, you.
- [116:29]
A
Know, so far off base based on those individuals that have done it.
- [116:35]
B
And that's why I tell people replication is the mother of all science. Right. If something's legit. But layman and I say this like, yeah, we don't really get excited about single studies anymore. Like wake us up when there's, you know, like when it's been done in three different labs in different countries across a period of time in multiple different populations, you know, then we'll start getting excited. Right. But unfortunately we were kind of like trying to build the ship while we're trying to sell the ship. And it just looked really messy and it made people have a fundamental distrust and that's why so many people on social media now can say crazy stuff. And I'll say, no, here's the data.
- [117:15]
A
Yeah.
- [117:15]
B
And they'll say, well I don't trust that data. It's all bought and paid for by big whatever insert thing you don't like, you know.
- [117:21]
A
But I also think, and you know, some listeners may disagree with me is that I think that you've earned your place to be a bit on the aggressive side. I mean you've I think, earned that position where we're starting to see a pop up of all these people, quote, debunking. And it's so ridiculous because they don't have the chops to stand on. This is not a decade or two decades of work or in the field. And I just want to call attention to their. I'm hoping that the pendulum swings for this younger generation to be a bit more respectful and that to understand that kind of like the big dogs like you come from a place of aggressive knowledge. Even if the tone is aggressive, it comes from a very noble place to be able to protect people that would not know the difference. Would you say that that's fair?
- [118:18]
B
Yeah, I mean I think I have a lot of empathy for people who I say, I'm like, man, it's one thing for me navigating this stuff as somebody with a PhD who'd done extensive research in it, but it's another thing for like the average person. Like it's, it'd be really hard. You know, there's a lot of noise out there and it's hard to know who to trust. And I guess what I would say is like scientific studies are not perfect for sure. Now science is perfect. The Scientific method is perfect, but it's done by people. And people are fallible. They have their own insecurities. They have their own personal beliefs. They have their own biases. I have those. In fact, I had somebody the other day say, you know, I just like that I can trust everything you say and take to the bank. I said, no, no, you. You know, stop, stop. Don't do that. Don't turn your brain off. Don't turn your brain off. Now, I'd like to think that I have consistently shown that I will be willing to adjust my position based on data, even if I got. If I felt like I got something wrong. And so I felt like that creates a little bit more trust. But I'm still a human being, and I'm like, I'm prone to the same mistakes. In fact, one of the big things I think is a. Is a real problem is people don't realize that expertise does not transfer across disciplines at all, not even a little bit. Okay? So, like, don't get so invested in one person that you just believe everything you say. Like, that's. They're not God. Okay? And I see this so much with, well, this person is. Is this engineer for. Okay, where'd they get the nutrition training? Right? Like, you think I'm qualified? I have Dr. In front of my name. Should I go and, like, walk into a cardiac surgeon's office and be like, hey, guys, I got this. You know? And all you need to do is look up Nobel Prize syndrome, and you can see a laundry list of unequivocally, some of the smartest, most intelligent human beings in history who believed in absolute buffoonery and nonsense in other areas of science. To know that being smart does not protect you against cognitive dissonance. And believing in. The only protection against that is. Is constantly questioning what you believe to be true and trying to disprove it. And I think, again, full credit to Don Layman. He said, I just want. We just weren't afraid to be wrong. You know, we just didn't put an ethical. Like, we weren't afraid to be wrong. And I think that level of, like, I think what really upsets me about people who make these strong claims is I'm like, you are so arrogant with nothing to back it up.
- [121:13]
A
Yes. Or haven't earned it. Just haven't earned it.
- [121:17]
B
Like, yeah, yeah. And so, like, I know how easy it is to be wrong even when you're smart. Okay? So imagine how easy it is to be wrong when you're stupid, you know?
- [121:29]
A
Yes.
- [121:29]
B
So.
- [121:30]
A
Well, I think that there are a handful of us that really stick together and support each other, and there is a community that, I'm sure you would agree with this, that, you know, we all know who's vetted and who we trust and what their strengths are and what their weaknesses. And I, I think we're going to start, Start to see an increase in that kind of like a community. Yeah, Yeah.
- [121:55]
B
I mean, I think, again, like, I, I, There are certain people who I never turn my brain off, like I tell people, but, you know, there are certain people who I obviously like, hey, if Brad Schoenfeld's talking about hypertrophy, I'm gonna shut the hell up and listen. You know, if Jeremy Lineke's talking about blood flow restriction, I'm gonna shut the hell up and listen. If Brett Contreras is talking about glute growth, I'm gonna shut the hell up and listen. Like, this is that narrow sliver of what they do. But I'm never going to turn my brain off because, again, everybody's a human being and is prone to their own biases and whatnot. But again, that is why replication is the mother of all science. That's why we start with the consensus of the data. We start with the meta analyses, we start with the. What does the, the big picture say versus getting into, like, really individual studies. You know, we. It takes time, and unfortunately, people don't realize that it takes decades for scientists to come to a consensus. And even then, even when data is as clear as it can possibly be, you'll have people on the fringe, even scientists, who will argue against it. So I think people, it's just, they're so exhausted with all the information that's out there, and they really do want to be able to turn off their brain and just, oh, I picked this expert. I listen to what they say, and I wish I could tell you that I could be that person for you, but I'm not, because in other arenas, I'm just as big of an idiot as everybody else. Well, like, dates and calendars and stuff.
- [123:38]
A
Well, those aren't that important. Dr. Lane Norton, thank you so much for coming on the podcast. And I just have to say, as a friend and as someone that has watched you over almost two decades, I couldn't be more proud. And it really, really, I'm so proud of you.
- [123:55]
B
Well, I am proud of you as well, because I remember, like, six years ago, I don't read a phone call, and you were like, I think you had, like, 3,000 followers on Instagram at the time, you're like, I just don't know how you do it. You know, I'm thinking about getting more into social media and now you're like approaching a million followers and crushing it. So obviously you've done a phenomenal job as well and you're had a bestseller. You're disseminating a lot of really good information to a lot of people. And you know, you and I are very similar personality wise. I think, you know, we have really big hearts. We're very spastic and sporadic.
- [124:29]
A
Speak for yourself. I am not spastic and sporadic.
- [124:33]
B
If you say so. Mike jokes. He was like, I'm glad I met you first because you warmed me up for Gab.
- [124:39]
A
Well, I just have to say I am so honored to know you and I feel like we're family and I'm really excited to take the position as Director of Women's Health at Carbon, which is pretty amazing that we get to work together.
- [124:55]
B
I am so excited that you're going to take it as well. I think this is like in some ways coming very full circle.
- [125:00]
A
Isn't it amazing?
- [125:02]
B
I think that you're going to bring a really awesome perspective to what we do at Carbon, and I'm excited for you to introduce it to your community and give them even more tools to improve their body composition and get in more protein.
- [125:18]
A
Yes. And I will include a link. I'm sure that Lane is going to give me some kind of discount for my community or something for you guys. And I'm going to hold you to that. Protein powder.
- [125:27]
B
Sounds good.
- [125:28]
A
The Dr. Gabrielle Lyon podcast and YouTube are for general information purposes only and do not constitute the practice of medicine, nursing or other professional health care services, including the giving of medical advice and no patient doctor relationship is formed. The use of information on this podcast, YouTube or materials linked from the podcast or YouTube is at the user's own risk. The content of this podcast is not intended to substitute for professional medical advice, diagnosis or treatment. Users should not disregard or delay in obtaining medical advice for any medical condition they may have and should seek the assistance of their health care professional for any such conditions. This is purely for entertainment and educational purposes only.