营养 Joel Greene

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Thank you for listening to the Boost Your Biology podcast. My name is Lucas Owen. I uncover the most cutting edge health information on the planet, ranging from hormones, nutrition, supplementation, fat loss, biohacking, longevity, wellness, and a whole lot more.

02:34

Welcome to the Boost Your Biology podcast. Today, I have a supremely special guest who's actually already featured on my podcast before. Today, we have Joel Green joining me on the show. And Joel is an absolute wizard when it comes to functional nutrition, fat loss, optimizing the immune system, and so much more. In fact, I look up to Joel in so many ways because he shares information that is truly original and

03:02

And so Joel, welcome to the show. Well, thank you. Thank you for that overly kind, glowing, very, very kind. Thank you so much, Lucas. It's great to be here. It's great. Just great to hang out and talk again. So it's been a while. Yeah. Yeah. Awesome. So Joel, maybe for my listeners, I mean, my audience has grown quite a lot since we first spoke. Did you want to share a little bit about your journey and how you got interested in optimizing human health? Yeah. Yeah.

03:29

probably at the highest level, the foundational aspect was I don't come from great genetics. So my mother had issues with hypoglycemic, just hypoglycemic her whole life, died of cancer. My dad was a diabetic.

03:43

Died from kidney related issues from diabetes. Health was always really important to me. Then my mom really stressed it from a very young age, really young. About five years old, I got into fitness just through Jack LaLanne on television. I grew up with it. It was just always around me. I just happened to be in the right place at the right time.

04:06

with respect to a lot of different movements that just hit. And, and because I was always pushed at such a young age, I was just always into it. So the, uh, the running craze hit, um, it's why I'm, um, massively old. This was in the seventies and the running craze hit, uh, in, in when I was in the fourth grade. And, and, uh, I just thought that was cool. So I started running around the block and running and I saw it on a TV show and it was just, you know, kind of a thing. And,

04:32

And the more I ran, I saw I started getting quads and I was like, that's kind of cool. What are those? So then I started sprinting in fifth grade, like literally every day, just trying to get faster because a 50 yard dash was kind of a thing back then. And I was really into bodybuilding at a young age. I just, just watching it. So about the time that I was, I think it was probably fifth grade, I

04:56

they had this show called wide world of sports and they'd show the mr olympia every year and i remember frank zane winning and arnold going you know what was that like and frank going almost as good as the time i beat you arnold

05:08

So anyways, I was an athlete in track and field competing in high school and then college. And I just always, I was just always, you know, consuming and really just to get that. Honestly, I'm nothing more than a consumer who just, that's what I've done my whole life. And I went to work just in the work world. I wasn't like a, you know, dedicated fitness person. And right about early nineties, Metrex came out.

05:38

And I went on Metrex and actually a guy you should have on your show eventually would be a guy named Yemeni Mesa.

05:45

He was the first Metrex guy. And he worked at Quest. Is this MetRx? Yeah, MetRx. Yeah. And for those of you who don't know, so Metrex was – before Metrex, it's kind of a history of fitness. There were what were called metabolic optimizers. And this was at the time a bunch of pasty goo that you'd stick in a pouch and tell your –

06:10

tell your consumers it did something and they would, you know, give it to bodybuilders jacked up on steroids and go, look what it did to him.

06:16

So Metrex came out, which was by Dr. Scott Conley and was really promoted by Jeff Everson and Bill Phillips and blew up. And the first iteration of that stuff was insane. And we'll talk about this later on today. But I'd never really apart from athletics, like in athletics, I'd reached super low body fat levels, like lower than anything else I've ever done. But that was just, you know, from competitive track and field, you get really ripped.

06:44

But I'd never prior to that really used diet. And so I was on Metrex for a while and just got peeled to the bone on that stuff. I mean, ripped. And everybody was like, what's your secret? And I was just your typical gym rat, working out, doing sprints and all that. And yeah.

07:04

So the interesting thing was about four or five years later, I started just eating uncontrollably. And that has dictated my entire existence in the realm of health and fitness, really, that one event. Because I had done something, I didn't know what I did, but I just knew that I'd never had issues eating. And I was just eating a lot. I couldn't stop eating. And later on, what I eventually know now is I just dysregulated all of the hormones that govern food intake.

07:31

And so that led me to a period of just a lot of trial and error where kind of by the time 2000 started, I had done the whole clean, fresh, everything raw, everything fresh. And I'd done that phase. Then I'd had the macro counting, everything phase, grams, everything. I had that phase. And it all always kind of led to the same point, which was, you know, getting really peeled and then, and then just regaining the body fat. And, and,

07:56

Right about 2003, I went to work in technology for a technology company. And it turns out a lot of people that are prominent in different ways now were in the exact same industry. We all, you know, we're customers of each other. We all knew each other. Some names you'd be pretty surprised at. So anyways, the interesting thing during that period of time, and it really shaped me a

08:25

I got fat because I had been doing the fitness thing my whole life. I was 42 at the time and I had 30 plus years of doing that stuff. Then I was in the situation where I was working 14 hour days and it was a startup and it was incredibly stressful. When you're in a startup and your revenue is really growing very fast, every day is a fire. Every day you show up, there's something wrong. You just have to fix it.

08:50

So anyways, the stress and age and all that kind of hit me by about 2006. And so I had come into that job fresh off of my latest tinkering foray into nutrition. And I'd come into that job, ripped abs and everything. And I left nutrition.

09:06

35, 40 pounds overweight, 260, just fat and big, tons of muscle because I'd been working out. I was like a 3X in my shirt. I'm a 1X now. So I was much bigger, but just fat, no endurance, no cardio.

09:24

And one of the seminal things that changed that really got me on a different path was the kids in the neighborhood used to come to our house. And one of them wanted to wrestle because they always want to wrestle the big guys. And so I was wrestling with this 16-year-old kid, and I got gassed after about a minute. So I was just like, okay, I'll be with you just one minute, one minute. And I was like, okay, that's it.

09:47

I'm making a radical change, you know? So, so I really started emphasizing just getting back to being lean, but figuring out how to get there in a way that would have survived the crush of a full-time real world gig. And that changed everything. So long story short, I wound up creating the number two site on the web for weight loss. I was only behind WebMD and,

10:09

And then I created a software that was based on the gut biome. It was based on the microbiome. In fact, the very first article that I know of written to the public about the microbiome and weight loss, which you can still go look up today, was written and published by me in 2007.

10:28

And I did some experimenting. Long story short, I kind of found some diet patterns that were really geared at recolonizing the gut microbiome. Incredible results, incredible energy. I mean, it really changed. I got my body fat measured after about seven days of going on this diet. And I was 6.7% body fat measured in water. Mark Bell challenged me on it. He was like, I don't believe it. So I sent him the document. I'm like, here you go for the original document.

10:57

So that period of my life, I created this software and we began selling it to corporations and to hospitals and to cities. And that changed me a lot because up until that point, if you'd asked me, why are people overweight? I would have said, well, because you have no self-discipline and you like to eat.

11:21

And then what happened was we started doing these corporate wellness engagements and I would, and literally there were thousands of people at any given engagement. I mean, literally I've got video that you can see to this day, literally 500, a thousand people in a room. And what hit me was, Oh my gosh, I finally understand weight loss. I never understood it before. And it's, it's people that can't work out. That's what weight loss is for because they can't work out. And if you could, in fact, um,

11:48

I'll send you a video when we're done with this. You can kind of look at what I'm talking about. They were basically desk workers. Everybody was overweight. Everybody was in their 40s and 50s. And, you know, like there's a reason Dan Marino is selling diet because he can't really do the fitness thing. You know, his body's so busted up from years of football. And I saw that. I saw that firsthand. And so it just it changed my perspective completely.

12:12

And I developed a lot of really good, let's call it IP during that time because I had so many thousands of people coming through this software. I was able to kind of harvest which protocols worked best. And so by about 2013, I had over 15,000 people who'd been through that software. And this, it just helped me a lot. It helped me to see what worked and what didn't. And out of that came…

12:35

Was the tracking software itself, was that anything like chronometer or like calorie counting, anything related to that? No, it was actually the reverse. So it was just based on visually identifying foods on a plate. So no calorie counting. But the internal stuff that I could see, I could kind of see like results and who was on what protocols and because there were a lot of variables in it. There were like different variables for food protocols based on, you know, if you said I have inflammation, then we would take tomatoes out of the diet and

13:04

And so I was able to kind of figure out protocols from there that worked. And then it led to a lot of stumbling and bumbling. I didn't really understand corporate wellness. And we had a few hits. We had some misses. And more than anything, it was like a…

13:20

a period in my life where I kind of just figured out what worked. And then that led to a consulting deal, just very brief with Quest Nutrition. And I was able to meet a lot of really amazing, incredible, brilliant people at that, not the least of which would have been Ron Penna, the founder of Quest. I was sitting in a round table one day and I was like, okay, everybody kind of had their shtick and I had my shtick and it would take too long to explain. I'm like, I'm writing a book. I need to write a book to explain this. And so my first book came out of that.

13:49

And in that book, I just put all the protocols that I figured out over about the previous 10 years. The one that really…

13:57

really took off was the gut protocol and that basically involved feeding very specific bacteria to replicate the immune system that we had when we were young just simply based on the interplay between a couple of species acromantia muciniphila and then the family of phytobacteria which are innately involved in immunity and so if you could feed those species you could literally reset the immune system we had when we were young and so that protocol just took off like gangbusters and

14:24

And that kind of more or less catches us up to today. So yeah, that's me. Yeah, it's incredible. I mean, quite the journey. And I think the one thing that caught my eye early on was the information you provide about functional foods, Joel. And before we get into that, I want to actually hear more about your athletic career because that's something that I've started incorporating a lot more again, which is sprinting.

14:52

And I feel like sprinting is by far the most effective exercise to drop body fat. But, you know, tell us about like when you were doing that sprinting protocol or when you were training yourself, like you said you felt like you literally dropped so much body fat. Do you still do any sprinting today or like how has that evolved?

15:14

Yeah, no, it's been part of my life going back to really my teens. So I was a pretty good high school track and field athlete. And then I ran in college as well for one year. And I ran the decathlon and yeah,

15:29

Uh, it just sprinting just became something that I did, um, my entire life. So even as a workout in my twenties, I would just go to the track and I would run two hundreds and, um, it was just what I always did. I've got like film of me, like in my thirties, just going to the track and just running hundreds. And, um, in fact, on my,

15:48

my 46th birthday, I did this thing called the, I called the man tathlon where you take a, you take two, five gallon water jugs, weighs 90 pounds. You go a mile up a hill, um, a thousand feet vertical, come back down holding them. You do that and then run a, uh, all out 200 after doing that. And, um, I ran a pretty good time too. I mean, I was 46. So, um, it's always been there. And I, I, in my first book, the immunity code,

16:15

Essentially, I put it out there that the real longevity test, or rather the real test of your age is just simply the ability to sprint. You can take a biological test and it can tell you, oh, I'm 10 years younger, but if you can't sprint, you're not young. I hate to break it to you. That's the difference between old people and young people. Young people can sprint and they can usually, especially in your teens, you can just do it at a moment's notice. You don't need to warm up. I put this thing out in my book, which got

16:45

copied and just now it's everywhere, which was no warmup sprinting. And, um, so yeah, it's just, it's just been part of what I do, you know? And, um, I mean, I'll go through periods where, um, especially at this age where something will happen, I'll get hurt or something. And then, you know, you gotta take a few weeks off and then, and then you just,

17:04

It's like you go back to the back of the line and it takes, you know, weeks to build back up just to being able to do it. But I'll probably, I'll never, I'll never get away from it. It's, it's the most effective way to,

17:17

to do a lot of things it's the most effective way to elevate your hormones elevate your mood it's amazing for body fat it's the hardest single thing you can do for the body like if you want to go to a track and run 200s there's nothing harder than doing that there's no workout that's harder than if you go around six 200s and try and shoot for under 30 for all of them that's a workout that's a real workout so yeah yeah i love that

17:44

Awesome. So let's sort of switch gears into some of the interesting content you posted recently, Joel. You've spoken about a specific flavonoid that naturally occurs in honey called pinose sembran. So do you want to sort of elaborate, you know, what piqued your interest with this flavonoid?

18:04

Yeah, well, so I just published a new book called The Way, The Immunity Code Diet. And one of the objectives of the book was just to end confusion on different topics. And so I took different food topics like oxalates and oats and honey and, you know, phytates and several other things, several other topics that are

18:27

really kind of vilified by food tribes. And then I just kind of went through these exhaustive sort of inventories of those things. And I even, I even, there's one section of the book where I even take, um,

18:39

I even argue both ends. So it's like, I'll take meat and I'll go, okay, the best argument you ever heard for me. And now here's the best argument against me, you know, and I kind of argue both ends just to kind of show that, you know, I can, it's possible to argue convincingly on either side. So one of the, I think kind of interesting ones that came out of this was, um, there's, there's the criticism that honey is just sugar, you know, and it's, that's all that it is. And

19:04

It's quite fascinating when you dig into honey. Like, what's in honey? I mean, it's really, really fascinating. Like, honey is, you know, I just describe it as a unique entity. It's a unique whole, and it can vary dramatically based on varietals of honey, but…

19:23

There are specialized sugars in honey that run a very long list, things like trellis, things, you know, all kinds of different kinds of sugars. And then there are specialized flavonoids in honey, and this one in particular. And the interesting thing about this one is its application as a drug target. Like when you begin to look at the research,

19:46

like what aren't you making a drug for with this stuff? Like it's a flavonoid and it seems to impact just about every area of human biology, um, in some positive way. And so when you, when you inventory like what it does, well, it's anti-cancer seems to help with depression, seems to help with, you know, obviously inflammatory issues seems to help with so many things. Uh,

20:11

It's very interesting that the drug companies are all over it. I mean, there must be 30, 40 different drug lines coming out of this, just one single flavonoid in honey. So it just speaks to these reductionist arguments, trying to make everything a macro, trying to look at something like, oh, it's a carb, it's a macro. And I think what's interesting about that is that…

20:36

We are in this age of semantic mind control to a degree where we are so powerfully controlled by the words we use that we kind of miss things sometimes, you know, is how I would put it. Definitely. I think, you know, I'm fascinated by some of the flavonoids that are found in these foods. And yeah, you know, Simbrin is definitely one of them. You were actually the first person that introduced me to Trehalose, which was an incredible, versatile, functional sugar.

21:07

which I'm sure you're still probably leveraging till this day and have found new applications for it. But I think

21:14

Going back to what you said before around, you can find arguments really pro consumption of meat versus no, let's not consume meat. And have you applied that same lens or application to the argument between poofers? So these canola oil, safflower oil, sunflower oil versus like these saturated fats at all? Boy, that is such an interesting topic. Boy, where do we start there?

21:45

Yes. So high level, a few ground rules. So the first thing to factor in on this one is that you're not going to see the same effects at all points in time. That's completely missing from the spectrum of diet today. In other words, we are under this assumption that the same thing is going to always work the same at all points in time.

22:13

That's just a myth. That's not how, well, first of all, it's not how anything works. Like you talk to doctors, they'll tell you that. No, the drug's not going to really work after about five years. You know, you talk to bodybuilders and the steroids don't work as well later. You know, it's, it's also true of, it's true of foods. And so there are, there are basic forces at work in the body. There's four, there's accumulation,

22:35

There's degradation, there's compensation, there's attenuation. And all four of these forces change how things work over time. So when we look at like, you know, the pros and cons of, you know, some of these types of oils versus saturated fats, the first thing that we have to start with is that we have to get out of the good bad paradigm. We have to get out of the, because that's just going to mire us in a non-reality. The non-reality, let's take saturated fats.

23:05

The non-reality is, oh, well, saturated fats are good. All the studies have been debunked. You can eat butter and eggs till the cows come home. Or the other end, which is, oh, no, no, there's an overwhelming weight of evidence that shows saturated fats are bad. No, no, no, no. You're in that.

23:20

Well, if you just apply the variable of time and those forces, what you come up with is that the exact same saturated fat, for example, can have wildly different effects on you at one point in your life. Like in your 20s, 30s, you can eat eggs and butter and meat till the cows come home. When you get to your 50s, there are differences in things like the state of your vasculature where the same saturated fats can be pathological.

23:47

So we're not dealing with this black or white proposition. And that's true of all of these things. So let's just lay the ground rules there. When we get to looking at different types of oils, the first thing is that

24:03

If you just look at the research, you can find a lot of benefits for oils that are vilified. You know, like you look at, for example, like the worst of them all, let's say canola oil. There's a lot of, there's a lot of benefits in the research for canola oil, like that you can look at. I'm not a fan of canola oil, but I'm just saying if we were just to be pure empiricists. What are they usually, what are the research studies usually focusing on with canola oil? Is it mostly around

24:27

the fact that they don't raise, I don't know, blood levels of triglycerides? How are they justifying the use of canola oil? Yeah. Yeah. So let's take the vasculature first. So something that's super underserved with the vasculature has to do with the interplay between what are called the NOX enzymes. These are the NADPH oxidases.

24:52

And these are the body's only known enzymes that produce free radicals. And they line the endothelium, they line the vasculature, and they perform a number of functions. Probably the most important is that they throttle free radical production in very specific timing and ways and related to mechanisms so that they maintain glucose homeostasis. I mean, that's, and nitric oxide production.

25:20

vessel mediated vasodilation so when we're young they work perfectly they work the way they're supposed to work and they so they produce hydrogen peroxide that interfaces with um phosphatases that nerf turn turn off um the glucose transport pathway um and so they inhibit these phosphatases there's one in particular uh pt i think it's pt forget the number on it but anyways um

25:47

And so they essentially work as a feed forward mechanism helping glucose transport. And that's great. What happens though as we get older is they fall apart and they basically start hyperproducing free radicals. They make too much hydrogen peroxide.

26:04

That's a disaster because in the endothelium, the net of it is that glucose transport becomes impaired. And more importantly, they change the way the body handles saturated fat significantly. And so saturated fats where once they really had no effect can be very, very detrimental once the NOX enzymes go. And that typically happens in conjunction with the decline of what's called the glycocalyx hormone.

26:27

So the glycocalyx is this furry mechanism that's a tension sensor inside the vasculature. It's these hairs. And what the glycocalyx does is sort of senses tension based on blood flow and vasodilation. And you can kind of think of it like the shock absorbers in your car. You know, it's very important mechanically speaking. And imagine driving your car with no shock absorbers, you know, I mean, that would,

26:51

not be good for the car. So what happens is as we get older, you, you hyper express knocks enzyme free radical production and interferes with proper production of nitric oxide in the endothelium. At the same time you lose the glycocalyx. And so what happens is the vasculature opens up and it potentiates basically cardiovascular disease. And so, so when those mechanisms are not functioning properly, properly, then saturated fats can become a real issue.

27:20

you know and so it's not this black and white of our saturated fats go to bad it's not so much that it's where at what point are you at in life and what's the condition of the of the vasculature and the endothelium and the the the activation state of the nox enzymes that changes the whole picture dramatically so

27:35

you know, what we've seen a lot of is these sort of polarized tribes arguing with one another about the black or the white or the good or the bad of things without taking into account time and taking into account, you know, how the very same thing can affect us completely differently at different points in time. So then you get into, you know, these arguments about, you know, puffers and saturated fats and are they good or bad and more food tribe wars and

27:59

I think, I think the point I was making was one of the things I tried to do in my book was just kind of show that I could, I could argue either end really well if I wanted to, you know, and it might make me, it might make for an interesting thing. It might create, create a following, but it doesn't necessarily make mean that I'm revealing the greater truth. So if, and again, don't get me wrong, I'm not a fan of canola oil. Okay. But if I wanted to make a pro argument for it, I could just go to the research and go, ah, you know, there's a lot of research that shows it really helps life profiles, you

28:28

seems to really help the vasculature, seems to help on and on with cholesterol-related issues and all this stuff. I could make that argument probably pretty convincingly, and then I could pick the opposing argument and just say, yeah, well, most of that stuff is sort of married in one way or another to glyphosate and does this and that. So I could kind of argue either end of it really well. What gets lost in that is just the bigger picture, the bigger truth, which is that we've all missed –

28:56

the impact of time and how time changes the equation. So these things by themselves, let's just refer to whole foods for a second, not, not manufactured foods, but whole foods. But generally speaking, there's a very important reality that is lost in it's in it. Once you get this, it, it eviscerates the food tribology of this era and,

29:19

And it's this, it's that the opposing food groups, the ones that you're demonizing, like let's say I'm a meat guy and I hate plants and I'm demonizing plants. It's the plants that protect me from the toxicities in the meat. And in reverse, it's, it's meat that rounds out the equation, protecting me from the, the, the, the, the lackings of plants per se. So they work together in very synergistic ways and,

29:45

And so, you know, that's a rant. I mean, I can go on for hours on that. No, but I actually really like that sort of perspective. And I'm glad that you're looking at it from that angle because I'm similar to you, Joel. Like I have been very open-minded with nutrition and I think it's a sign of a good scientist, someone who's not dogmatic. You know, that's an important trait of a nutritionist.

30:11

well-informed, educated researcher, it's actually critical just to think critically about nutrition. In terms of some of the elements associated with meat itself, I know you've also been interested in some of the peptides that are now being discovered in meat that probably confer major health benefits that we've never really considered before. Yeah.

30:42

I'm sorry. Go ahead, finish your question. Just with those peptides that are found within meats, I mean, what have we uncovered so far in terms of what they may be doing to our health or how they may be impacting our metabolic functioning? Well, probably one of the most important aspects that maybe doesn't get enough play just has to do with –

31:07

It has to do with angiotensin converting enzyme and the renin-angiotensin system, so blood pressure management. And so there are peptides in meat. I think it's like APPV4. It escapes me the exact nomenclature top of my head, but just suffice to say,

31:24

There are very powerful antihypertensive peptides in meat, and they have an extremely beneficial effect, not just on things like blood pressure, but also on management of the renin-angiotensin system, which historically it was believed that this was just concerned with fluid balance. And now post-COVID with the whole ACE receptor thing, we know that metabolic health itself is

31:52

relies to a large degree on, you know, the, the ACE receptor and these things working properly. And there, there are peptides in meat that are very beneficial for, for that particular aspect. Um, and, and there's, there's quite a few others. I mean, there's, there's a number of different types of peptides in meat. The, I mean, the one we all know about is, you know, BPC one, five, seven, and, you know, some of those different types of peptides, but, um, suffice to say that

32:19

Meat is essential. We need it. And we need it particularly for the intestines, the upper gut. And it's the optimal food for the upper gut in every way. It's the optimal food for the upper gut. That being said, plants are the optimal food for the lower gut. And they work very synergistically together. More synergies than not. One good example is when you look at just the – there's no real and lasting health

32:49

without accounting for the commensal bacteria because they are so entwined with the immune system. Just for listeners, just to give you a quick overview,

32:59

You have the family of bifidobacteria, a very specific species in there. They're intimately entwined with antigen sensing. They potentiate antigen sensing in the gut. They potentiate the uptake of antigens into dendritic cells or dendrites. You have the gut lining commensal acromantia, which is very much entwined with regulating T cells and different ratios of T cells, cells of bifidobacteria, and they are very, very synergistic.

33:26

So it's very difficult to make an argument for health without the presence of these bacteria because they're so entwined with the immune system.

33:33

And so then what you get into is this thing of like, well, when you look at these extremes, like, well, just, you know, I'm going to, I'm just going to do the all meat carnivore thing. What you wind up with is you're going to get some spillage into the, into the colon every day. You're going to get, um, 10, 15 grams of amino acids reaching the colon. And when you look at the bacteria that ferment amino acids, there's nothing good. They're all cancer promoters. Okay. You have bacteria like, um, you have bacteria like Fusobacteria nucleatum. That's a cancer promoter.

34:03

Well, what happens is when you have synergy in the diet of mix between plants and animals, the locus of fermentation shifts away from the protein fermenters and shifts more to the sacrolytic, more to the carb fermenters. And you get a balance. You don't get the negative aspects. So you get the negative aspects nerfed and then you get the benefits of meat. And they work very synergistically together. Yeah.

34:28

this is a, an interesting discussion because, um, you know, over the years I've also been very selective with, with, uh, which vegetables I'm consuming in my diet. And nowadays I've landed on like carrots, onions, uh, white button mushrooms. Um, I definitely try to avoid like kale and spinach, like the ones that are generally speaking higher in oxalates. But what is your stance and what have you seen with most people nowadays? Like,

34:57

their tolerance factor for these vegetables. Well, there's a massive hole running through the oxalate issue. And that is that, so the, the, the, the incorrect thing we've all been shown or taught is that, you know, you shouldn't eat these foods. They have oxalates, oxalates are bad.

35:15

There's a reality that's been left out of the picture. The reality is that there are over 761 species of bacteria that detoxify oxalates in the gut, and they are mostly in the commensals. So there are your species of lactobacillus, your species of bifidobacteria. It's a big list. The old, the outdated notion was that it was just one bacteria, O-forma genes. Well, that bacteria, it turns out, doesn't even detoxify oxalates. It's actually a network of bacteria.

35:45

And so what you find is that the way nature has set things up is that, you know, just go do a survival course, a ton of them out there.

35:54

You'll see that nature actually has a very specific meal plan that is provable and repeatable to whoever does it any part of the world. And it's you throw someone in nature, immediately they start foraging. So in the middle of foraging, they're just going hungry. We call that fasting. Okay. Some people call it famine, but you're foraging and foraging is this pattern of getting less preferential foods, you know, not things that you prefer to eat. Like you might eat some green leafies, you might eat some things with oxalates, but

36:20

Well, it turns out that the foods that contain those very often stimulate the bacteria that detoxify the oxalates in the gut. So the old picture of, you know, you eat oxalate containing foods, you absorb them.

36:34

That can be true. That can be true if you have the wrong enterotype or the wrong profile of bacteria in the gut. But then it cannot be true if you have an optimized microbiome. So if you have lactobacillus represented well, you have bifidobacteria represented, you have acomanceria, you have all these commensal species represented. Well, then for the most part, on a bell curve, we're going to be detoxifying the oxalates. But here's the really important thing that's been left out of that.

37:01

We absolutely have to have, no debate, must have nitrate-reducing bacteria in the mouth. Have to have it. The reason is, particularly as you age, without the nitrate-reducing bacteria, which are fed by nitrates in the diet, dietary nitrate, green leafy vegetables, things that contain oxalates, without those in the diet…

37:24

Then as you get older, the conversion from nitrate to nitrite is not happening. And when we begin to think about cardiovascular health, probably the biggest single imperative as you get older is keeping the cardiovascular system working optimally. And so the problems that you're going to run into, you're going to run into loss of the glycocalyx, you're going to run into hyperactivation of the NOX enzymes. Guess how you fix that dietarily?

37:48

You fix it with things like berries and nitrate-containing veggies. Those are the things that nerf that problem. The very things you're told to avoid actually solve the bigger problem you have to face. So the sort of the silo of the oxalate foods are bad, avoid them, you can – and there's good research for this. This is just not me making this up. In my new book, I list I think probably about 20 bullet points –

38:12

from the research of study after study and expert after expert, guys like Aaron Miller from the Cleveland Clinic out of Harvard saying, yeah, we need to look more seriously at detoxifying oxalates through the diet, meaning creating the optimal gut microbiome enterotype profile that detoxifies oxalates. Now, when I say this, again, we're in this era of black and white thinking, right?

38:40

a lot of people will jump on this and just think that's an either or proposition. And it's important to say that everything happens on a bell curve. Okay. So in a bell curve, the middle is going to be the first and second standard deviation. It's going to be 94% of the people. Okay. So in that middle, you're going to have a range of effects. You know, nobody's going to be a hundred, very few, you know, maybe someone at the top, but we're going to be in that range somewhere. So that's to say that,

39:08

If you took a million people and you optimize the microbiome, you loaded the commensals that detoxify oxalates, most of them probably would have not too much issue eating them in moderation and they would actually get the benefits without the negatives.

39:21

Now, you're always going to have that third standard deviation. You're always going to have people in there that they've had issues, they have pathologies, and they're sick, and then that advice would not apply. But that same argument holds in the reverse. It holds for the argument of, oh, no, oxalate foods are bad. Don't eat them. Same argument holds. Actually, no. We have a bell curve. Yeah.

39:39

Yeah, I'd love to see a debate between yourself and, you know, I'm talking about Paul Saladino. I don't know if you've ever been on his podcast or done sort of any rebuttals to his content and also Sean Baker, but they are very prolific and prominent in their stance of, yeah, we need to avoid all oxalates and minimize their consumption completely. Yeah, anytime, anytime.

40:08

Anytime, anyplace, anywhere. Hey guys, if you're watching, let's do it. Yeah, I'd love to see that happen. Maybe I'll have to try and coordinate that. But definitely, yeah, it's an interesting perspective in terms of these foods. We know, both you and I understand some of the amazing pleiotrophic effects of how they can affect the microbiome, how they can affect humans.

40:31

One of our favorite gut bacterias, which is Acomansia. I mean, do you want to maybe just remind our listeners about the importance of Acomansia? I know you've covered it in your books, but do you want to sort of just remind them about the importance of Acomansia? Yeah, well, so suffice to say that this one bacteria was discovered about 2004. I first glommed on it about 2007.

40:54

There's really two. There's acromantia, and then the other one is fecal bacteria prosnitzi, but really the major player is acromantia.

41:05

It is the primary bacteria responsible for the health of the gut mucus layer. And the thing to understand is that it eats the gut mucus layer. So its food is mucins. So in the gut mucus layer, you have these glycoproteins and that's its food. So it eats those. So it actually thins the gut mucus layer out. But in the process, it's creating metabolites and doing a number of other things that activate genes in the gut mucus layer that produce a thicker, more robust layer.

41:34

So generally that's good. Generally that's what we want. And, uh,

41:40

It's very much involved in the immune response. It modulates the human body's immune system in a number of different pathways. I think I mentioned T cells, but it also modulates IgA and sensing of antigens and a whole bunch of things, and it works in concert with bifidobacteria. So when these two are present, you have an optimized immune system by optimizing the

42:05

Which is really kind of a cool proposition that you can actually selectively feed a couple of bacteria. And then the net of that is that you can really optimize the internal immune environment in the gut. Iggramancy is interesting because it does a number of things. One of the things that's interesting about it is that it primarily prefers…

42:33

endogenous nitrogen as its food source, meaning exogenous nitrogen in the diet

42:40

actually can reduce populations of it. So it prefers endogenous, meaning mucus secretions. That's what it feeds on. And so it lives in the lining of the gut, not so much in the lumen. And when you flood the lumen with nitrogen, you can actually suppress acromantia to some degree. So what we see with acromantia is that it thrives on a few things. It thrives on phenols from berries. Phenols seem to feed it. It thrives on fasting.

43:09

because it thrives on endogenous nitrogen, meaning nitrogen secretions. So when you essentially are fasting, you actually can replete acromantia to a degree. And it's a bit of a double-edged sword. So what can happen is if you're doing too much fasting or too much of a thing, you make too much acromantia, it can actually wear the gut lining out. And so you see this with starvation. What you see in starvation is that the gut lining is just completely worn out.

43:36

And it's because you're actually feeding too much of this thing. So, like all things, it requires balance. But what's cool about it is it's involved in glucose control. It's intimately involved in helping blood sugar, helping insulin work effectively. It's a GLP-1 agonist. So, when you have acromance, it actually triggers GLP-1 in the gut.

43:58

And so what's cool about it, I think, I think the takeaway from the immunity code, my first book was that you can a selectively target this thing through some feeding techniques and then B it confers a lot of benefits. So there's a lot of simplicity compounded into just understanding what this bacteria is and understanding how to feed it. You know, you mentioned a GLP one agonist. I mean, this is definitely a trending topic at the moment in terms of a Zen pick a semi-glutide and some of these other compounds in terms of, um,

44:28

assisting with weight loss via shutting off tiredy, but they do deep down work on many other pathways. It's not just appetite signaling. It actually helps with many other pathways. But over the years, Joel, I'd imagine you've come across some pretty unique, naturally occurring GLP-1 agonists or ways to actually stimulate the production of GLP-1. So do you want to sort of elaborate on that? Yeah, sure. I mean, the first thing to understand, I think, is that

44:58

With the GLP-1 agonist, you're dealing with a synthetically manufactured form of GLP, so it's got a much different half-life. Food is never going to work the same as the drug. The drug is just going to be more powerful. But that being said, understanding how to target GLP-1 from food, I think, is a skill that's definitely worth inventorying how to do.

45:18

And so the first thing to understand is that, you know, these gut hormones or rather these receptors in the gut for GIP and GLP-1, the incretins, kind of a funny story. In 2012, I landed a hospital for my nutrition software.

45:35

And we were nobody, like nobody. So to get this deal, it took a year. And they kept parading like this round of deal busters in front of us, you know, how to explain how the system worked. And a lot of it was based on GLP-1 on the incretins.

45:51

So they would parade these doctors and stuff in front of me. And I'd be like, well, see, a lot of it works on Ingrid and targeting. So what we're doing is we're targeting GLP one and GIP. And they were just like, look at me with these blank stare. Like, what the heck are you talking about? And now it's mainstream. You know, now, now everybody's like, oh yeah, well, it's an Ingrid and you target the Ingrid. Yeah.

46:08

But now this is something I've been doing for quite a long time. The first thing to understand about GLP-1 is that lots of different foods can activate GLP-1 and GIP and that they are opposed in different ways. So they work together, but they are also opposed. One can turn fat burning on, one can turn it off. And

46:29

What you see in diabetics is that it's GIP that's the bigger player. GLP-1 seems to be maintained, but GIP seems to have the bigger effect on blood sugar control. And that's why Manjaro seems to work so much better than the other ones, than Wagovi and Somagutide. But your go-tos that I use, that I've used for a long time, are things like eggs, things like… Interestingly, when you combine proteins with fibers that ferment in the gut, you get a synergistic double effect with it.

46:58

So if you take things like… This kind of sounds ridiculous. It sounds obvious. But if you take steak and potatoes, you get a much more powerful effect on GLP. And it's because when things ferment in the gut, it's going to activate GLP. And then protein also activates GLP-1. And so those two things together work really well. Another one is…

47:22

Honey and Stevia, both of those work very synergistically together. In the new book, I actually have a GLP-1 shake where I combine honey with whey protein, with Stevia, with a few other goodies, all of which target GLP-1. And then the really important thing to understand is the timing.

47:43

So the sequences are just as powerful as the foods. And we tend to ignore the sequences and focus on the foods. But the sequences have as much power as anything else. So when you time something like that, let's take the shake. So whey protein.

47:58

Weight protein has a number of beneficial effects on insulin function. It will activate GLP-1, and then you combine that with, like, nut butter. So the fat in nut butter is going to activate GLP-1 and stevia and then honey together. Now you've got this massive GLP-1 activator. Throw in some resistant starch.

48:15

The combination of whey protein and resistant starch has been shown to increase fat oxidation while activating GLP-1 and then time it correctly. So you back it off 20 minutes before a meal. So that's called a preload meal. And now what you get is this very, very powerful, as powerful as you can get with food, GIP GLP-1 activation tool set. And it's just understanding how to combine and time things. It's that simple. Now, again, it's never going to be powerful as the drugs, but just using food, it's pretty effective. Yeah.

48:43

And this is something you can use anytime. Yeah, I love that approach. And I think it's a pretty easy to implement strategy for people looking to regulate satiety. I mean, both you and I understand the importance of even the order in which we eat foods. Ideally, you want to eat the protein portion first to stimulate the satiety signaling. But even like, for example, you said steak and potatoes, most people that eat a steak

49:11

don't really feel nourished and full. Like they're looking for some sort of carbohydrate component to actually make them feel like, oh yeah, that was a beautiful meal. Like I just had a great meal. I'm actually full. I'm full now is what they say. I'm actually full now. So yeah, it's definitely an interesting pathway to look into the incretins and even like specific gut bacteria that are now being shown to help with that.

49:36

satiety signaling. It's just Joel, I think the next five to 10 years is going to be a very interesting space. Just having a look at, yeah, where things are heading. Yeah. Yeah. I think the stuff, you know, I've been talking about for a while now is catching on and it's kind of a new cool party. Like I want, I mean, don't you notice this? Like whenever you're at a social gathering, all anybody's talking about is biohacking and food combining, you know, it's kind of like the news. It's the new stocks like talking about this stuff. I mean,

50:05

I was in a sauna the other day at the gym and these guys are in there just talking about, yeah, well, the thing is if you use TB500 with PPC157, then it works better, bro. It's bro speak now. It's hysterical. Yeah, yeah. What's on the horizon for you, Joel? I mean you're spending a lot of your time, I guess, with continuous –

50:28

continuous education, you know, probably a bit of mentoring, maybe a little bit of coaching, writing books, like what's on the horizon for you, Joel?

50:37

Yeah, I think we were talking a little bit about this before the show. So me, I've spent since 2006 just creating what to me was the solution to the problem that I ran into, which was how to control the body under real life circumstances. And everything that I've done has been towards that one end, which is

51:00

you know, if I worked a job 14 hours a day, you know, I don't have time to work out and do this. I mean, what am I going to do to not get fat and not age fast? And so, so my last 16, 17 years was devoted to that. And now, now I'm really just focused on getting the message out there and, um, you know, just promulgating that I just, I just finished a new book. And so making the podcast rounds, just, just growing the, that basic nugget that I've done now. Now it's the

51:24

Yeah, I didn't really worry too much about the marketing piece. It kind of took care of itself, but now I'm probably just going to switch gears and focus more on that end of the business and just kind of keep doing what I'm doing, I think. Yeah, keep doing what you're doing. I mean,

51:39

You're definitely one of the best in my eyes when it comes to understanding nutrition from a much deeper lens and also like understanding things from a very unique perspective. And like you said before, being open-minded, not being dogmatic is what I respect the most about what you do every day. So yeah.

51:58

Definitely keep doing what you're doing, man. You're making strides in the health optimization space. I'll make sure to leave all of the things you mentioned in the podcast show notes. But do you want to remind my listeners where they can connect with you or they can check out your books?

52:15

Yeah, so you can go to my website, which is veepnutrition.com, or an easier URL is theic.health, T-H-E-I-C.health, or veep, V like Victor, E like Edward, E like Edward, P like Paul, nutrition.com, either one. And so we got it all. We have the immunity code gut reset there, the original. Actually, I've souped it up. I've added NAC glycine and some other things to it.

52:45

Um, and then the new book is there and all kinds of goodies. And then my Instagram is real Joel green. And my, I just started a, um, I just started an x.com Twitter. So that's real Joel green. And then my Tik TOK, I just started to, that's real Joel green. So, and yeah. And then I think by the time this airs, the new book will also be on Amazon as well. So, um, that was, that was me.

53:07

That's incredible. Yeah. Well, thanks again, Joel, for coming on the podcast. It's a, it was a absolute pleasure chatting and I'm, I'm sure there might be a, you know, round three in the future. So yeah. Thanks again. Yeah. Thank you. Thank you so much for having me. Awesome.

53:26

I can't tell you how often I hear, oh, I'm a little OCD. I like things neat. That's not OCD. I'm Howie Mandel, and I know this because I have OCD. Actual OCD causes relentless unwanted thoughts. What if I did something terrible and forgot? What if I'm a bad person? Why am I thinking this terrible thing? It makes you question absolutely everything, and you'll do anything to feel better. OCD is debilitating, but it's also highly treatable with the right kind of therapy.

53:56

Thank you.

54:16

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D:2025.07.10<markdown>

卢卡斯・欧文欢迎乔尔・格林再次做客播客，介绍乔尔在功能性营养、减脂、免疫系统优化等方面是 “行家”，并表示自己很敬佩乔尔，因为他分享的信息极具原创性。

乔尔・格林分享了自己的健康优化之旅。他表示，自己的健康基础并不理想，母亲一生受低血糖困扰，最终死于癌症；父亲是糖尿病患者，因糖尿病相关的肾脏问题去世。因此，健康从小就对他至关重要，母亲也从他很小的时候就强调健康的重要性。大约 5 岁时，他通过电视上的杰克・拉兰内接触到健身，从此健身就融入了他的生活。 70 年代跑步热潮兴起时，他正在四年级，觉得跑步很酷，就开始绕着街区跑步。后来在五年级开始短跑，每天都练，想跑得更快，因为当时 50 码短跑是件很流行的事。他小时候还很喜欢健美，会看《体育大世界》节目，里面每年会播放奥林匹亚先生大赛，他记得弗兰克・赞恩获胜，以及阿诺德和他的互动。 他在高中和大学都是田径运动员，参加十项全能比赛，短跑成为他一生坚持的事情，即使在二十多岁时，也会去田径场跑 200 米。46 岁生日时，他还进行了一项名为 “男子十项全能” 的活动：提着两个 5 加仑的水壶（重 90 磅），在 1000 英尺垂直高度的山坡上往返一英里，然后全力跑 200 米，而且成绩还不错。 他坦言自己本质上就是一个 “消费者”，一生都在不断吸收健康相关的知识。90 年代初，MetRx（美瑞克斯）问世，他开始使用该产品。他提到，在 MetRx 出现之前，市场上有一些所谓的 “代谢优化剂”，其实就是一些糊状的东西，装在小袋子里，商家会告诉消费者这东西有效果，还会找一些使用类固醇的健美运动员做宣传，声称是产品的功效。而 MetRx 由斯科特・康利博士推出，杰夫・埃弗森和比尔・菲利普斯对其进行了大力推广，其最初的产品效果显著。 大约四五年后，他开始出现无法控制的暴饮暴食情况，这成了他在健康和健身领域探索的一个重要转折点。他当时不知道原因，后来才明白是自己调节食物摄入的激素失调了。这之后的一段时间里，他不断尝试不同的饮食方式，2000 年左右，他尝试过全生食、新鲜食物，也试过计算宏量营养素，精确到克，但结果总是相似：先是变得很瘦，然后又重新发胖。 2003 年，他进入一家科技公司工作。那段时间，很多现在很有名的人也在同一个行业，他们彼此是客户，互相认识，有些名字可能会让人惊讶。这段经历对他影响很大，因为他在进入公司前，刚刚完成了一次营养方面的尝试，当时身材很好，有腹肌；但在公司工作期间，由于是初创公司，业务增长很快，他每天工作 14 小时，压力极大，每天都有各种问题需要解决。到 2006 年左右，年龄和压力的影响显现出来，他离开公司时，体重增加了 35 到 40 磅，达到 260 磅，虽然肌肉量很大（因为一直在锻炼），穿 3X 的衬衫，现在穿 1X，但身材肥胖，没有耐力，也无法做有氧运动。 一个重要的改变发生在他和邻居家的孩子摔跤时。一个 16 岁的孩子想和他摔跤，他只坚持了大约一分钟就气喘吁吁，这让他决定做出彻底的改变，重新变得 lean，并想办法在全职工作的重压下保持这种状态。这一决定改变了一切。后来，他创建了网络上排名第二的减肥网站，仅次于 WebMD，还开发了一款基于肠道菌群的软件。2007 年，他撰写并发表了第一篇面向公众的关于肠道菌群与减肥的文章，至今仍可查阅。 他进行了一些实验，最终发现了一些饮食模式，主要是通过喂养特定的细菌，来重建年轻时的免疫系统，这基于 Akkermansia muciniphila 和参与免疫的 phytobacteria 家族之间的相互作用。如果能喂养这些细菌，实际上可以重置年轻时的免疫系统，效果显著。通过这款软件，他能看到不同人的结果以及他们所采用的方案，因为软件中包含很多变量，会根据用户的情况（比如有炎症就从饮食中去除西红柿）提供不同的食物方案，这帮助他总结出有效的方案。 到 2013 年，已有超过 15000 人使用过这款软件。卢卡斯询问这款追踪软件是否类似 chronometer 或热量计算工具，乔尔表示并非如此，它是通过视觉识别盘子里的食物来实现的，不涉及热量计算，但他能从后台看到相关结果，从而总结方案。不过，他当时不太了解企业健康管理，期间有成功也有失败，但这段经历让他明白了很多有效的方法。 之后，他与 Quest Nutrition 有过短暂的咨询合作，在那里认识了很多优秀、聪明的人，包括 Quest 的创始人罗恩・彭纳。有一天在一次圆桌会议上，每个人都有自己的见解，他也有自己的想法，他觉得需要写一本书来解释这些内容，于是他的第一本书就应运而生。书中收录了他过去大约 10 年总结出的所有方案，其中 “肠道方案” 尤其受欢迎，大致内容是通过喂养特定细菌来重建年轻时的免疫系统，这一方案大获成功，也让他一路走到了今天。

卢卡斯提到自己现在更多地开始进行短跑训练，觉得短跑是减少体脂最有效的运动，询问乔尔当年的短跑训练情况，以及他现在是否还进行短跑，训练方式有何变化。

乔尔表示，短跑从他十几岁起就成为生活的一部分。他在高中时是不错的田径运动员，大学也跑了一年，还参加过十项全能比赛。整个生活中，短跑都是他会做的事，二十多岁时，他会去田径场跑 200 米。他甚至有自己三十多岁时去田径场跑 100 米的视频。46 岁生日时，他还进行了一项名为 “男子十项全能” 的活动：提着两个 5 加仑的水壶（重 90 磅），在 1000 英尺垂直高度的山坡上往返一英里，然后全力跑 200 米，而且成绩还不错。 他在自己的第一本书《免疫力密码》中提出，真正的年龄测试是能否短跑。生物测试可能会显示 “年轻 10 岁”，但如果不能短跑，就不算真正年轻。年轻人能随时短跑，甚至不需要热身，他在书中提到的 “无热身短跑” 后来被广泛传播。 现在，随着年龄增长，他偶尔会受伤，需要休息几周，之后又得重新开始，需要几周时间才能恢复到之前的状态，但他可能永远不会放弃短跑。他认为短跑能有效提升激素水平、改善情绪、减少体脂，是对身体最具挑战性的运动之一，比如在田径场上跑 6 个 200 米，每个都努力跑进 30 秒以内，这是非常高强度的训练。

卢卡斯提到乔尔最近发布的内容中谈到蜂蜜中一种天然存在的黄酮类化合物松属素（pinose sembran，推测为 pinostrobin），询问是什么引起了乔尔对这种黄酮类化合物的兴趣。

乔尔表示，他的新书《The Way, The Immunity Code Diet》旨在消除人们对不同食物话题的困惑，其中探讨了草酸、燕麦、蜂蜜、植酸等被某些饮食群体诋毁的食物，并对这些食物进行了详尽的分析，甚至在书中有一个章节从正反两方面进行论证，比如分别列出支持吃肉和反对吃肉的最佳论据，以此展示从不同角度都能进行有说服力的论证。 在研究蜂蜜时，他发现蜂蜜是一种独特的存在，其成分因品种不同而有很大差异，含有多种特殊的糖类（如海藻糖等）和黄酮类化合物，而松属素就是其中一种。研究表明，这种黄酮类化合物在药物研发领域有广泛应用，似乎对人体生物学的几乎每个领域都有积极影响，如抗癌、改善抑郁症、缓解炎症等，有 30 到 40 种不同的药物研发都与这种单一的蜂蜜黄酮类化合物有关。这也说明，那种将食物简单归结为宏量营养素（如认为蜂蜜只是碳水）的简化观点，可能会让人们忽略很多重要的东西，而人们在这个时代容易被用词所 “语义操控”，从而错过事物的本质。 卢卡斯表示自己对食物中发现的一些黄酮类化合物很感兴趣，松属素就是其中之一，还提到乔尔是第一个向他介绍海藻糖的人，这是一种用途广泛的功能性糖类，询问乔尔是否仍在使用，是否有新的应用。随后，卢卡斯将话题转向植物油（如菜籽油、红花油、葵花籽油）与饱和脂肪的争论，询问乔尔是否从正反两方面对此进行过研究。 乔尔认为这是一个有趣的话题，首先需要明确一些基本规则：同一种食物在不同时期对人的影响可能完全不同，不能认为某种食物永远好或永远坏。这是因为人体内存在积累、降解、补偿、衰减四种力量，它们会随着时间改变食物对人体的作用。以饱和脂肪为例，人在 20、30 岁时，可能可以大量食用鸡蛋、黄油和肉类而无不良影响，但到了 50 岁左右，随着血管状态的变化，同样的饱和脂肪可能会产生病理影响，所以这不是非黑即白的问题，所有食物都是如此。 谈到不同种类的油，从研究来看，即使是被诋毁的油，也能找到很多益处。以菜籽油为例，虽然他个人不喜欢菜籽油，但纯粹从实证角度看，有研究显示菜籽油有诸多好处。 乔尔进一步解释，血管中有一种叫做 NOX 酶（NADPH 氧化酶）的物质，这是人体已知的唯一能产生自由基的酶，它们分布在内皮细胞和血管中，有多种功能，其中最重要的是在特定时间和方式下调节自由基的产生，以维持葡萄糖稳态、一氧化氮生成和血管介导的血管舒张。年轻时，这些酶能正常工作，产生的过氧化氢会与磷酸酶相互作用，从而有助于葡萄糖转运。但随着年龄增长，这些酶会失调，过度产生自由基（过多的过氧化氢），这会损害葡萄糖转运，更重要的是，会极大地改变人体处理饱和脂肪的方式，一旦 NOX 酶功能失调，原本可能无影响的饱和脂肪就会变得非常有害，这种情况通常与糖萼激素的下降同时发生。 糖萼是血管内的一种类似 “毛发” 的张力传感器，能根据血流和血管舒张感知张力，就像汽车的减震器一样重要。随着年龄增长，NOX 酶过度产生自由基，干扰血管内皮中一氧化氮的正常生成，同时糖萼减少，血管状态改变，从而增加心血管疾病的风险。因此，饱和脂肪的影响并非绝对的好或坏，而是取决于人的年龄以及血管、内皮和 NOX 酶的状态。 在看待不同种类的油时，即使是那些被诋毁的油，也能在研究中找到其益处。比如菜籽油，有研究显示它在血脂、血管健康、胆固醇相关问题等方面有帮助，他虽然不喜欢菜籽油，但如果要为其辩护，可以引用这些研究；反之，也可以从草甘膦等角度提出反对意见。但人们往往忽略了时间的影响，时间会改变一切。 对于天然食物而言，那些被对立的食物群体其实是相互作用、协同增效的。比如，喜欢吃肉的人所诋毁的植物，其实能保护人体免受肉类中的毒素影响；反过来，肉类也能弥补植物的不足。这种协同作用在共生细菌方面体现得尤为明显，因为共生细菌与免疫系统密切相关。例如，双歧杆菌家族与抗原感知密切相关，能促进抗原被树突细胞吸收；肠道内的 Akkermansia 与 T 细胞调节等有关，它们之间协同作用，没有这些细菌，就很难实现真正持久的健康。 当饮食中同时包含植物和动物食物时，发酵的场所会从蛋白质发酵菌转向糖分解菌（碳水化合物发酵菌），从而达到平衡，避免负面影响，同时获得肉类带来的益处，两者协同作用显著。

卢卡斯提到乔尔对肉类中现已发现的肽也很感兴趣，这些肽可能带来我们从未考虑过的重大健康益处，询问到目前为止，在这些肉类中的肽对健康的影响或对代谢功能的作用方面有哪些发现。

乔尔表示，肉类中的肽在血管紧张素转换酶和肾素 - 血管紧张素系统（与血压调节相关）方面的作用可能未被充分关注。肉类中含有非常有效的抗高血压肽（如 APPV4 等），不仅对血压有积极影响，还对肾素 - 血管紧张素系统的调节有好处。过去认为该系统仅与体液平衡有关，但在新冠疫情后，随着对 ACE 受体的关注，人们发现代谢健康在很大程度上也依赖于 ACE 受体及相关物质的正常运作，而肉类中的这些肽对此有很大益处。 此外，肉类中还有多种其他肽，比如众所周知的 BPC 157 等。肉类对人体至关重要，尤其对 upper gut 来说，是最佳食物；而植物是 lower gut 的最佳食物，两者协同作用显著。 卢卡斯分享自己多年来对所吃蔬菜很挑剔，现在主要吃胡萝卜、洋葱、白蘑菇，尽量避免羽衣甘蓝、菠菜等高草酸蔬菜，询问乔尔对人们对这些蔬菜的耐受度有何看法。 乔尔指出，人们对草酸的认识存在一个很大的漏洞，即普遍认为含草酸的食物不好，应该避免，但忽略了一个事实：肠道中有超过 761 种细菌能分解草酸，这些细菌大多是共生菌，如乳杆菌、双歧杆菌等，而以前认为只有 O-forma genes 能分解草酸，事实并非如此，而是一系列细菌共同作用。 自然界中存在一种可验证且可重复的饮食模式：当人处于自然环境中，会立即开始觅食，所吃的食物中可能包含含草酸的绿叶蔬菜等，而自然界的设置是，这些食物会刺激肠道中分解草酸的细菌。 随着年龄增长，保持心血管系统的最佳状态至关重要，而这需要口腔中存在硝酸盐还原菌，这些细菌依赖饮食中的硝酸盐（如绿叶蔬菜等含草酸的食物中的硝酸盐）。如果饮食中缺乏这些，随着年龄增长，硝酸盐向亚硝酸盐的转化就会受影响。而含硝酸盐的蔬菜等正是解决 NOX 酶过度激活、糖萼减少等问题的关键，这些被认为应避免的食物实际上能解决人体面临的重大健康问题。 克利夫兰诊所、哈佛的亚伦・米勒等专家也认为，应更重视通过饮食（即培养能分解草酸的肠道菌群）来分解草酸。但需要注意的是，一切都呈钟形曲线分布，中间 94% 的人在优化肠道菌群后，适量食用含草酸的食物可能不会有太多问题，还能获得益处；而处于曲线两端的少数人，尤其是有健康问题的人，则可能不适用。不能用非此即彼的思维来看待这个问题。

卢卡斯提到自己和乔尔都了解阿克曼氏菌（Acomansia，推测为 Akkermansia）的重要性，让乔尔提醒听众这种细菌的重要性。

乔尔介绍，阿克曼氏菌于 2004 年被发现，他在 2007 年开始关注它，另外还有 Fecalibacterium prausnitzii 也很重要，但阿克曼氏菌是主要的。它是负责肠道粘液层健康的主要细菌，以肠道粘液层中的粘蛋白（糖蛋白）为食，在分解这些物质的过程中，会产生代谢物并激活肠道粘液层中的基因，从而促进更厚、更坚固的粘液层形成，这通常是有益的。 阿克曼氏菌与免疫反应密切相关，能调节人体免疫系统的多个途径，如调节 T 细胞、免疫球蛋白 A（IgA）、抗原感知等，与双歧杆菌协同作用，通过选择性喂养这两种细菌，可优化肠道内的免疫环境。 阿克曼氏菌更喜欢内源性氮（即粘液分泌物）作为食物来源，饮食中的外源性氮可能会减少其数量，它主要生活在肠道内壁而非肠腔中，当肠腔中氮过多时，可能会在一定程度上抑制阿克曼氏菌。 阿克曼氏菌的生长得益于浆果中的酚类物质和乏食，因为乏食时能为其提供内源性氮。但它也是一把双刃剑，过度乏食或某种因素导致其过多，可能会磨损肠道内壁，就像在饥饿状态下，肠道内壁会被严重磨损一样，因此需要平衡。 此外，阿克曼氏菌还与血糖控制有关，

继续

能帮助胰岛素有效发挥作用，它还是一种 GLP-1 激动剂，当体内存在阿克曼氏菌时，能刺激肠道产生 GLP-1。总之，了解这种细菌并知道如何喂养它，能带来很多益处，这也是《免疫力密码》一书传达的要点之一。

卢卡斯提到 GLP-1 激动剂是当下的热门话题，如司美格鲁肽等化合物，不仅能通过抑制食欲帮助减肥，还能作用于许多其他通路，询问乔尔多年来是否发现一些独特的天然 GLP-1 激动剂或刺激 GLP-1 产生的方式。

乔尔表示，合成的 GLP-1 激动剂半衰期与食物不同，效果更强，但了解如何通过食物激活 GLP-1 很有价值。2012 年，他为医院提供营养软件服务时，就涉及到 GLP-1 和肠促胰岛素，当时很多医生对这些概念并不了解，而现在已成为主流。 多种食物都能激活 GLP-1 和 GIP（葡萄糖依赖性促胰岛素多肽），它们既协同作用又相互拮抗，一种能开启脂肪燃烧，另一种可能关闭。在糖尿病患者中，GIP 对血糖控制的影响更大，这也是曼吉妥（Mounjaro）比其他药物效果更好的原因之一。 他常用的天然激活 GLP-1 的食物包括鸡蛋，以及蛋白质与肠道发酵纤维的组合，这种组合能产生协同效应。例如，牛排配土豆，因为肠道中的发酵物质会激活 GLP-1，蛋白质也能激活 GLP-1，两者结合效果很好。蜂蜜和甜叶菊的组合也有协同作用，在他的新书中，有一款 GLP-1 奶昔，将蜂蜜、乳清蛋白、甜叶菊等结合，都能靶向 GLP-1。 时间安排也很重要，食物的食用顺序影响很大。比如，乳清蛋白对胰岛素功能有多种益处，能激活 GLP-1，搭配坚果酱（其中的脂肪也能激活 GLP-1）、甜叶菊和蜂蜜等，效果更佳。再加入抗性淀粉，乳清蛋白与抗性淀粉的组合已被证明能增加脂肪氧化并激活 GLP-1。将这样的组合作为餐前 20 分钟的预加载餐，能产生很强的 GIP 和 GLP-1 激活效果，虽然不如药物强效，但通过食物也能达到不错的效果。

卢卡斯表示未来 5 到 10 年，关于肠道细菌与饱腹感信号等领域的研究将会很有趣，随后询问乔尔的未来计划。

乔尔说，自 2006 年以来，他一直在努力解决一个问题：如何在现实生活中控制身体状态。对于每天工作 14 小时、没时间锻炼的人来说，如何避免发胖和快速衰老，这是他过去 16、17 年的研究重点。现在，他主要致力于传播这些知识，刚完成一本新书，正在参加各种播客活动，希望推广自己的研究成果，接下来可能会更多地关注业务的营销方面，继续自己正在做的事情。 卢卡斯认为乔尔在营养学领域有深刻且独特的见解，且思想开放，不固执己见，值得尊重

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00:00

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02:31

Hey everyone and welcome to the Boost Your Biology podcast. My name is Lucas and I am the founder of Ergogenic Health. Together in this podcast series, we will go underground to explore cutting edge health and human performance insights that you simply cannot search on Google to help you upgrade your existence. So without any further ado, let's jump into today's episode.

03:03

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03:24

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03:38

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04:01

Hello, everyone, and welcome to yet another episode of the Boost Your Biology podcast. Today, I'm joined in with a very special guest joining me in all the way from the US. Today, we have Joel Green joining me in to talk all things biohacking, intermittent fasting, a little bit on fat loss, and some other very novel concepts. So Joel, welcome to the show, man. Thanks, Lucas. It's good to be here. Thank you for having me.

04:31

Awesome. So maybe you want to give my audience a bit of a background into, I guess, your story and your mission. Yeah. So I'm very old. I'm 56. So I've been doing this a long time. And I've had… I had the…

04:53

probably a good 30 years doing, doing the fitness thing, you know, that, uh, we've all done it. You know, you just, you're in your teens and twenties and you want to look good and you know, you, you watch pumping iron and you know, you did that thing. So I did that for like 30 years. Um, and, uh,

05:11

going into the 90s, the early 90s, when the modern era of nutrition really began. A lot of people don't know this, but MCTs were introduced in the early 90s and a lot of other things, keto diets and stuff like that. So I was an early adopter for those things. And I read an article by Jeff Everson in 1992 about

05:38

about where he said that he was just eating one meal a day in the evening. And I'd already known that like Herschel Walker, this like a guy who was this amazing athlete, like back in the 80s was doing that. And I was like, wow. So I started doing that and just taking Metrax.

05:58

And this was like probably '92 and it was like in two cans. And I was peeled. I was probably four or 5% body fat. I was ripped. And I had everybody asking what I was doing and, “Tell us your secret.” And what happened to me is what actually nowadays I get a lot of people coming to me, which is after several years of doing that, you basically break your metabolism.

06:25

You know, your hunger is out of control. Your insulin sensitivity is wrecked and all these different things that you'll do if you go down that path. So that happened to me in the 90s. And it was a wake up call for me. And I didn't know what I had done.

06:42

I knew that I did something, but I didn't know what it was. And so the gut hormones at that time hadn't even been discovered and they were just sort of in the research phase. And so I really kind of started what you might call a biohacking. There wasn't a word for it. I was just trying to figure out and experiment with different things. So that led me down a road or probably…

07:07

through 2006 of just trying one protocol after another, trying things like what you would call time-restricted feeding or just clean eating, fresh whole raw, everything fresh whole raw, that phase. And then I had my clean macro phase. I had all these different phases. And what was notable about this thing, two things. Number one,

07:30

I was a regular person. I wasn't getting paid to be fit. So that was number one. And then number two, what was sort of interesting about that was that I was in the real world, I was getting older. Okay, so I was I had passed out of being kind of carefree and single, moved into like my early 40s by 2005. I think I turned 40.

07:55

And so I was just sort of seeing the cumulative effects of all these different things that I'd been doing over the years. And notably what, what I really noticed was that, um, it all broke down, um, under pressure in real life. Like, like it, like,

08:08

And I realized what I was trying to do, same thing everybody else is doing. You're trying to import into a very distinct ecosystem, a bunch of strategies that weren't born in that ecosystem. You're trying to import into the ecosystem of real life where time constraints essentially dictate what you can do with your time, strategies that are born out of an ecosystem where everybody's paid to be fit. And they broke down. It all broke down. So I was…

08:37

I was in a startup company. We became pretty successful. The company, we went from like zero to $2 million a month here pretty fast. And I was working, just working, working, working 14 hours a day. And I had come into that job in probably 5% body fat. I was really in shape. And I left it being 257 pounds. You know, kind of like that, really fat.

09:05

but big, big, big, but fat, you know, like a big arms, big chest, big gut, you know, the whole story. So, uh, coming out of that, uh, it was a big change for me. And I, I, uh, I kind of ran into the problem everybody's going to run into, you know, which is, um, uh, time kind of makes a prison out of the body. And it really kind of formed the core of what I'm doing today. Kind of what I would say my mission is. And that is, um, uh,

09:31

Really, everybody has the same problem with the body. We all face the same problem. It's a problem that time will make a prison out of the body. Time makes a prison out of the body. And it's a prison made from where the bars are invisible, but you feel them. It's declining energy. It's restricted mobility. It's…

09:50

increasing body fat and it's a risk of disease, like cancer and things like that. So that's what time does to the body. And the solution really is to keep the body young. It's just, that's the solution. And what I really have come to realize is that, and this is the premise of my book, “The Immunity Code.” The premise of the book is that real health is missing.

10:17

that we have this endeavor everybody's chasing after. We call it being fit or different words we use on it like weight loss or biohacking. It's all the same sort of thing. And if you look at it and you look at kind of just get out of the selfie, the before after selfie and just kind of track long term what happens, you get a completely different picture of what's really happening. What's really happening is that

10:45

you're over time, you just see that by following most of these strategies, trying to import these strategies out of that ecosystem into the real life ecosystem, what's happening is that, um, it just doesn't work for most people over time. And when you look at their bodies, they're doing this with weight over time. But more importantly, like a lot of the people that you think know what they're talking about are just as cast cancer prone, if not more, uh, just rate of heart attacks is just as, just as frequent, if not more. And so, um,

11:13

When you study it, you see very clearly real health is missing. And there's a long, long list of names of people that I can think of from the past 30 plus years, 40 plus years that are dead, that were once really famous and really fit and famous for being fit.

11:27

And they're all dead, all of them. So they're not living longer. They're not any less cancer prone. So real health is not there. And when you start to peel back, well, why is real health not there? I give the analogy in my book of

11:43

a real guy. I used a pseudonym. I called him Simon. And Simon was a meathead who got on the juice and got super fit. And next thing you know, was running a big supplement business and everybody wanted to know, what's your secret, dude? What's your secret, man? And I knew the secret. The secret was the same secret it's always been. It's a whole bunch of time and a whole bunch of drugs. That was the secret. But I saw a funny thing happen. And

12:11

as the years rolled by, like Simon tried to get off of the juice and he couldn't because when he started getting off the juice, he's like, ah, man, I'm just getting that old man body, you know? And he didn't have the power to control his body. He couldn't get his body to do what he wanted it to do. And that's the problem everybody faces over time. You can't get your body to do what you want it to do. And you'll hear that story more often than not. And the story you most often hear is,

12:38

Well, I tried this program in my 20s and it worked for a while. And then I did this for a while in my 30s and it worked for a while. But now nothing's working and I can't lose weight. It's the power to control the body and to get it to do what you want it to do. And there's really no solution that has ever been proposed to solve that problem. And that's kind of my thing. That's what I'm working on. Because all the solutions that have been proposed…

13:04

they never they never take into account the real world ecosystem see it's like it's one thing to propose some solution that um you know uh takes a whole bunch of time and a whole bunch of energy and often a whole bunch of drugs it's another thing to do it without time and that's the trick is in the real world you have to there's you have these periods where there's no time there just aren't and you have to make it work when there's no time and that's that's

13:27

It's a whole other layer of difficulty. So that's kind of a long-winded what I'm doing. Yeah, really well put, Joel. There's one concept there that I really would love to expand upon, and that is the idea around performance versus longevity. Like this sort of trade-off that was sort of, you know, the quick results with this, you know, steroids, drugs versus, oh, what's the trade-off for longevity and things like that. Yeah. Yeah. Yeah.

13:57

we can we could do an entire show on just that if you wanted to because it's you know there's a lot to that so the first thing to understand is that um

14:11

We get into things like, we want the benefits of things like fasting, for example. We want the benefits, but what are those benefits? And what are the mechanisms that drive those benefits? What are they? Well, it's the only proven model to ever extend lifespan is starvation or just eating less, caloric restriction. Okay, well, that's a huge benefit, right? Well, what's the mechanism? How's it work? Why does it work? Well, when you break that down,

14:40

It gets down to signal pathways, really. And it gets down to the activation of very specific signal pathways that either trigger the body to run through its allotted cycles of growth or put the brakes on one of the two. And so the inherent cost of pushing growth into the body is that you're using it up faster.

15:04

So, now that's fine as long as it's an individual choice, as long as you know what you're doing and you understand that it's very much like a car. It's very much like, you know, let's say the average engine has 100,000 miles in it and you just want to take your car to the track all the time. Well, that's cool. You can do what you want with it. You got to understand that pushing the car…

15:27

in that way is using the life cycle of the car up a lot faster. And the body works very much the same way when it gets down to looking at the way signal pathways work. And there's very good science on this. And I put it in the book in terms of a, it's called the IIS, Signal Pathways Paradigm of Aging.

15:48

And in a sense, aging is somewhat linear with respect to inputs down the insulin, insulin-like growth factor pathway. And in order to grow, we need that pathway to fire. So from a performance aspect, in terms of putting on muscle or things of that nature,

16:09

That requires growth from the body. And there's a balance between too little growth, just enough and too much. And so it's a very interesting topic to think about versus longevity, which is sort of the inverse pathways, things like the AMPK pathway, the sirtuins and different processes like ubiquination and all that stuff.

16:27

So, these things sort of exist, kind of opposed, but also complementary. They work together, but they're also opposed. And it's a big discussion in a big universe to dive into. Yeah. Well, let's sort of segue into a bit about fasting because I know you talk quite a lot about various types of fasting, things like that.

16:52

Firstly, I want to ask you, what can people do to amplify the benefits of fasting?

17:02

Fast less. That would be the first thing. Fast less, yeah. So the first question that I can tell people is, “Well, why are we fasting? What's your purpose in fasting?” And your purpose is probably, “Well, I want to induce autophagy. I want to do all these things.” Well, almost all those things happen during sleep.

17:25

They just happen much better during sleep because that's why we call it break fast. Sleep is fasting. But sleep is fasting done in a way where it syncs to circadian rhythms and it syncs to signal pathway activation. So optimizing sleep is sort of the first level.

17:45

of amplifying fasting, making sure that your sleep is really tracking in all cylinders. That's kind of the first level of it. But beyond that, what I talk about a lot in my book, maybe kind of the core focus is

18:01

there are things that are complementary to fasting. And when we look at what those things are, there's something very interesting that pops up. It's that

18:18

You see that, just to use an ancestral narrative, which by the way, narratives are helpful. They're not facts. They're just narrative and story. They're helpful. I use them. But we always have to remember when we're using narrative that it's just a narrative. Let's see if it correlates to the data. But a very helpful narrative is to understand that historically speaking, when we were starving, pretty much the last thing on the menu is going to be roots.

18:44

Okay. Like it's, I mean, you'll eat them. You'll, you'll dig up roots and eat them if you have to. It's just not your first pick. Your first pick is, you know, probably like a steak or, you know, something else. That's your first pick. But it turns out that, um,

18:58

the way nature has sort of partitioned the economics of starvation, that there's a benefit to roots in a starved state. And it's that roots in a starved state feed bacteria that mimic the effects and enhance the effects of both exercise and fasting.

19:16

So certain types of bacteria proliferate with certain types of food inputs, and those bacteria are commensal, meaning that they're extremely beneficial to their human hosts. And when you look at like, if you were to just draw out a spreadsheet, and how about a selection of checkboxes and compare exercise to certain bacterial metabolites,

19:40

You'd see one-to-one as they're doing the same thing. One is exercise-produce of lactic acid. Certain bacteria, check. Exercise activates the AMPK pathway. Certain bacteria, check. Exercise induces mitochondrial biogenesis. Certain bacteria, mitochondrial microbiome cross-talk, check. And so what we see is that that's very interesting, that in a starved state, certain roots potentiate certain bacteria, which…

20:07

essentially mimic exercise and amplify fasting. And if you can time that to best of all worlds, to the maximum signal induction, diurnally speaking, in other words, during sleep, what you're doing

20:21

is you're inducing um essentially more cells more signal strength for all the things that that make fasting work so that then coming into a fast you don't have to fast as long you just don't have to fast as long and there's and there's good reasons to not fast as long um we see that um

20:42

It's becoming pretty common now because we're getting into year two, three, four for people who've been doing fasting. A lot of people are having a lot of problems with it. The longer that they do it, they're getting into just uncontrollable eating. And those are things to be expected when you look at how leptin works over the long term. So there's very good reasons to want to economize fasting so that you can do it on a regular basis. And then every now and then you want to do an extended fast, you can do that. But in terms of like…

21:09

you know kind of having this unchecked um sort of uh binge on fasting uh there's there's negatives to that and one of those one of those could be sleep disruption so it's something that um there's some very good reasons to want to get as much bang for the buck out of fasting as you can amazing amazing points just uh just mentioned there one of them um one of them really excited me and that is looking at um how yeah obviously how fasting can manipulate

21:37

certain gut bugs and these gut bugs can elicit some of the same effects that fasting has downstream. So I want to discuss one of the key bacterias that we have quite a lot of research around and that is the Accomansia species of bacteria and specifically Accomansia

21:58

I mean, I personally use metformin twice a week. I have certain criteria for using metformin. It's a bit of a weird setup that I have. It's like if I've had a single night of very bad poor sleep or sleep deprivation, I'll use metformin the next day.

22:16

or a day that I don't train, I'll use metformin. And one of the reasons why I'm excited by metformin is the fact that it can increase the akkermansia growth. So do you want to talk about this particular bacteria and why it's so beneficial? Yeah, well, so in the gut, the gut barrier, the gut junction, you have a layer of mucus

22:46

And that layer of mucus is very thin, and it is the only thing separating you from the outside world. So every day, you bring the outside world into your body, and it stays the outside world. It doesn't become part of you. Okay, some of it.

23:01

And so there's kind of a selection process in order to see who gets in the door, who gets into the body. And so when you look at the actual epithelial barrier, you'll see there's this little layer of mucus that's just essentially protecting you from the outside world. And that's no small thing. I use the example in my book of a…

23:20

a piece of salami and just digging and just cutting, if you just cut a square patch where your flesh was exposed and put some salami on that, you'd have a real problem in about an hour or two, like a very big problem. But if you covered that with a layer of mucus,

23:42

we had some protection there, it would be a different story. So that layer of mucus is what protects us from the outside world. And the way that layer is maintained is by a very select, very few number of bacteria. The principal player in that picture is Ackermansia mucinofa. And Ackermansia mucinofa is what's known as a mucin forager.

24:05

These are bacteria that really like olink glycans. They feed on them and they forage for mucin in the gut. So the net effect of these bacteria is that they are probably the most commensal bacteria known in many respects. In other words, that

24:24

our health is so inextricably linked with acromantia and a couple others, fecal bacteria, prosodensia, and beta-bicron, that our health is so linked to these bacteria that we could probably make a list and say, wow, these are really at the top of the list of the most commensal bacteria. And acromantia does a number of things. One of the things it does, well, first of all,

24:48

It just seems to correlate very well to body composition. What you see in obesity is that people who are obese, they just tend to have less acromantia. And then people who are lean and thin just tend to have optimal levels of acromantia. It's not 100%, but it correlates very, very well.

25:11

And there's some good reasons for that. Acromantia seems to have the ability to contract the surface area of the gut. So actually, actually can help, help us absorb fewer calories, simply contracting the surface area of the gut. Yeah. It's also seems to be involved in cold induction. So cold and acromantia seem to work and seem to work together. And it's,

25:36

Basically, it maintains the integrity of the gut barrier. It's very, very much involved in maintaining a healthy immune system. So the way the immune system typically works is that in the gut junction, in the epithelial barrier, we have dendritic cells that will sample antigens and sample the gut lumen. And acromantia does a number of things to sort of keep that whole

26:01

optimal and keep our immune system working. So it's extremely important. We also see it in autoimmune disease. So curiously enough, I mentioned this in the book, I mentioned the case of MS, but you can see it in other autoimmune disease as well, where you get too much achymanthia and it becomes a problem. And it's probably a case where…

26:24

there is an over polarization of immune signals coming from things like interferon gamma, which is stimulating populations of acromantia. But it's just an extremely fascinating sort of field of study. Yeah. Fascinating. Interesting. So what about, let's sort of segue into, I guess, maybe

26:48

We touched on metformin. I'd like to hear your stance on this particular, you know, medication for, I guess, longevity, performance. Yeah. Things like that. Yeah. You know, I think metformin is one of those wonder drugs. You know, there are a number of drugs out there that are wonder drugs. I mean, we're lucky to have them. And I think metformin is probably one of them. Yeah.

27:15

I don't take it personally, but I will eventually. I'm saving it for the finish. But yeah, I think metformin is best used sort of intermittently and strategically. So it's not something I would use every day. It's not something I would use on a continual basis. But I do think that there's a very good case for seasons of metformin and using it very strategically, like the way you're using it for

27:43

it for example yeah um i think in that case it's a wonder drug i mean you know it it helps us age slower um probably keeps the mitochondria in better shape uh as long as we're kind of not overdoing it and you know just as a number of really fantastic things yeah awesome awesome yeah i tend to with the the metformin usage um yeah again like i said very strategic about when i'll

28:08

you know, deploy it or rotate it with other insulin sensitizing agents. Um, but ultimately like nothing will be, you know, I mean, I, I aim to get 20,000 steps in a day. So there, there was a study where they compared, you know, um, 15 minute brisk walk versus metformin, you know, post, uh, postprandial glucose levels and walking out performed metformin. So I think I'm getting the best of both worlds there. So, um,

28:37

Yeah, I would agree with that. Yeah. That gets to another fascinating topic, which is exercise-induced glucose transport. And what's interesting about that is that it can work locally as well. So, kind of the myth of spot fat reduction and all that. Well, when you look at exercise-induced glucose transport,

28:59

uh you can get sort of insulin resistant pockets in the body particularly in adipose mass and exercise or just muscles contracting uh works as a works as a sort of an insulin pneumatic so

29:13

when you have problem areas and you have things typically in the belly or things like that. What you'll see very often with very specific areas in the belly is you'll see hypoxia and you'll see insulin resistance. And so glucose transport's impaired. And just muscle contractions. When you look at people who are…

29:32

move their muscles, move specific muscles a lot. They're always lean in those muscles. And I believe it's because exercise and muscle contraction is so good at keeping glucose moving, shuttling back and forth and mimicking insulin. Yeah, that's fascinating. That's something worth exploring more of. So Joel, let's sort of segue and discuss a little bit around

29:56

I know there's one video on trending quite well. They're talking about the metabolic fate of alcohol and how we can biohack that. So let's talk about, yeah, let's talk about alcohol and how we can just work around that.

30:10

Yeah, that's a big one. People want to know that. Yeah. Well, first thing, alcohol does not make you fast by itself. It actually helps you get lean, if anything. It's thermogenic in nature. So anybody who's ever woken up in the middle of the night with sweats knows that alcohol is thermogenic. So in fact, there's been some very interesting studies with heavy drinkers where they replace carbs with alcohol and they get lean.

30:35

Based on that thermogenic response, is that the mechanism? Interesting. Oh, yeah. In fact, I hate to say this because I know people are going to do it, but just lean protein, like lean anti-inflammatory protein like cod, something with a lot of omega-3s, something that's by its very nature anti-inflammatory, together with alcohol, you'll get lean.

31:04

But everybody knows heavy drinkers, people like winos. Everybody knows that wino in the back of the supermarket who just ripped the bone, right? Yeah. Yeah. Yeah. Well, it's because of the thermogenic nature of alcohol. Yeah. So by itself, it doesn't make you fat. But what it does do is that when you look at the conversion pathway to clear alcohol from the body, you have to convert it eventually into acetate to get rid of it.

31:33

And in order to do that, carb metabolism and fat metabolism takes a backseat. So carbs and fats will get stored in the presence of alcohol. And that's

31:43

That's where you get in trouble. That's where it gets skewed. A lot of wines now are really sugary and so you have an inherent problem because it's a high sugar wine, you got alcohol. And wherever you find carbohydrate together with alcohol, that's a problem. And fat too. But lean protein sources together with alcohol aren't really the problem that we think they are.

32:06

So that's one of the ways you begin to hack it is when you're going out and when you're drinking is just understanding what foods are complementary with alcohol. And so very lean protein sources, typically fish work really well. And then there are certain vegetables that also are very complementary. So asparagus and broccoli are the two that really stand out. Asparagus increases alcohol dehydrogenase.

32:32

and another enzyme. And then broccoli, actually, the sulfur-fermenting broccoli activates certain genes that detoxify alcohol, and you'll actually get an increase in the cytosol for alcohol enzymes. So broccoli is very good and very complementary with asparagus. And so those two together with lean proteins, and then it depends on the type of alcohol that you're taking in. So basically, the hard stuff is kind of more the go-to.

33:01

So, because it doesn't have any carbs or anything with it. Beer is kind of like a much harder road to hoe because you're dealing with all the carbohydrates in it. Although I'm sure the people at Guinness would argue differently. So, go ahead. I was going to say, I was thinking of one potential benefit of alcohol that I don't know if it's really explored or researched is the effect on…

33:25

gastric acid production like is it going to help with protein degradation through gastric acid secretion like is that one is there research around that at all or hmm trying to think

33:42

i'm trying to think if i've ever read that i i don't know i don't know that i've actually looked at that i guess it has this region and alcohol protein degradation i don't know i couldn't answer that one yeah yeah yeah a big big good thing to study up on yeah like ethanol itself like is it a

34:00

a secretor of gastrin or gastric acid and then potentially that's why you know people say drink have a bit of lean protein with your alcohol help that actually stimulates digestion i'm wondering if if there's a link there if it's influencing other gut um stomach hormones things like that well um what's interesting and what's interesting about it is you know you're getting you're getting um

34:32

you're getting short chain fatty acid production out of it. Uh, and so you're, um, you're getting, it's, you're going to get a couple of things out of alcohol. You're going to,

34:46

Number one, you're getting sort of the cousin of a ketone body and you're getting sort of these alterations in short-chain fatty acid production. And how those play out as a result of alcohol, I don't know that it's been totally studied. But those are things that get very interesting because it affects the liver and it affects…

35:09

It just affects things sort of in a different way. So yeah, that's a whole topic we could kind of get into, like, you know, whether or not you're getting like acetate in the liver and all that junk. Yeah, yeah. With, from my listeners, they may not know the three types of short-chain fatty acids, butyrate, acetate, and propionate. Most of the research, correct me if I'm wrong, is conducted on butyrate.

35:33

um or in terms of promoting beneficial effects on human health but i haven't actually personally explored any around acetate or propionate so you offer any like insights around those two short chain fatty acids

35:47

Yeah. Well, there are benefits to all three short-chain fatty acids, but the most important thing is sort of the ratios of the three. You kind of optimally need them in certain ratios. You don't want too much acetate. Too much acetate will give you fatty liver. And then with propionate, if you have too much propionate, you can get things like certain autoimmune issues. So it's…

36:14

There are definitely benefits to both the PNA and acetate, but…

36:20

probably the bigger picture is to look at the whole and it's really the ratios of all three that you want to be optimal. And when you get into that discussion, there are a number of different metabolic pathways to create the short chain fatty acids. So one metabolic pathway is fermenting fiber, another is fermenting proteins. And then within fermenting proteins, you have a couple of different pathways. You have a ketogenic pathway where you can ferment

36:47

uh short chain fatty acids from and so the various different pathways will produce different end products um and the best thing to say probably is that ultimately there needs to be a balance in the way that you're producing short chain fatty acids like like you don't want to do it exclusively too much in one thing although the optimal home is probably fermenting them from fiber um

37:13

But that doesn't mean that you can't prevent them from proteins and different meal patterns in protein. So you can use keto meal patterns or you can use like kind of overfeeding patterns, carnivore patterns, things like that. But it's just that ultimately that they have to balance out. You don't want to get too much of like acetate or propionate relative to butyrate would be the way that I would answer that.

37:34

Right. Awesome. Okay. So let's sort of delve into a little bit around fat loss. I know you've covered a little bit on something known as FGF21. So do you want to explore this as an enzyme? What is it?

37:51

Yeah. So I can never say this word every time I try and think. It's fibroblast. My tongue like ties up on it. Fibroblast growth factor 21, FTF21. Yeah. FTF21 is a, it's a hormone.

38:08

And we used to think that it was primarily a starvation hormone, a hormone involved as a reaction to starvation. But then it turns out that you also make it when you're feasting too. So really what it is, FGF21 is a stress hormone. And it's produced and it does a number of things. It helps in a starvation state. FGF21 does a number of things in terms of like

38:34

The way that fat is released in partition and drives feasting and drives hunger, it can drive a lot of things. It can make insulin work better. It does a whole bunch of things. What's notable about FTF21 is that when we shrink fat cells, we get a reduction in FTF21. And so I have a course that I've released called Immune-Centric Fat Loss, which deals one of the aspects of…

39:01

of fat loss that's ever really been dealt or accounted for is that when fat cells shrink, there's a whole list of mechanisms that are activated. And nobody's ever bothered to actually inventory what they are. And that's a problem because the vast majority of people that take any, it doesn't matter what it is, any program, they all regain it within five years. And it's because to a large degree, we're not inventorying what the mechanisms are that happen when fat cells shrink. We're not dealing with what's true

39:30

And so as a result, we're not getting the results that we want. When you begin to inventory what's true and you start to see that there's all these different hormones and mechanisms and genes, all these things are happening post-fat loss, just from the act of shrinking fat cells down. Well, one of those is FGF21, and that we need to increase FGF21 post-fat loss. And it's just something that really has… And when I ask that, I have no idea why that's never been accounted for. It just seems ridiculous to me. Yeah.

39:58

We should do things based on how things work, right? So anyways, FGF21 plus fat loss is something that we probably want to look to stimulate.

40:10

If we want to prevent weight regain, and there's some decent research on this too, like on basically getting FGF21 stimulated in the post-fat loss phase or in the maintenance phase. What a lot of people don't understand is that post-fat loss, you have a maintenance phase. And in that maintenance phase, there are very distinct sets of genes that turn on

40:29

And there's some good research that showed there's a cluster of genes, several dozen that activate in the post-fat loss phase. And they can very much dictate whether or not you're going to regain the weight or not. And that's just the genetic components. There's a number of other components. So the maintenance phase is a really critical piece of the equation that's never been accounted for ever, anywhere.

40:51

And FGF21 is kind of a big player in that. Interesting. Do we have any research around any botanicals, drugs, supplements, compounds, anything that can actually stimulate FGF21 at all? Well, metformin, one, but also berberine would be another one. Awesome.

41:13

Yeah. Bourbon and metformin, how odd. Yeah. And it's funny because they both share so many similar… This is what I find really fascinating. So many of these supplements and ergogenic aids and things, they all seem to…

41:27

tickle the same sort of pathway or they might like scrape the same sort of a lot of overlapping pathways which i find really fascinating so yeah that's that's that's new that's brand new to to me i've never heard of yeah this fibro fibroblast growth factor 21 um is is there much i was about to say is there research around this that you're excited to see more of or

41:51

Oh, yeah. It's a continuing field. Like FTF21 is…

41:58

has very much an evolving understanding on it. Like I said previously, just a few years ago, it was just thought to be the fasting hormone. But now we know that's not true. It's a stress hormone, which brings up a really good point that fat loss is inherently stressful on the body. It's stressful on the body. And so the body has a number of different stress responses.

42:22

because stress itself, particularly in fat loss, is coming from the fact that you're injuring the body at a cellular level. When you look at like, so here's your adipocyte, here's your ECM. What you're doing is you're ripping it away from the ECM when it shrinks.

42:42

Well, that's essentially like a tear. And so it's got to repair that. The ECM has to deform, has to try and, you know, has to pull this thing back, has to reach out to the out of the site, pull it back, has to shrink it. So there's all this stuff that's going on that mechanically speaking falls under what's known as mechanobiology. And under that, there's another sort of thing going on called mechanotransduction, which refers to signals and how signals propagate from mechanical forces.

43:09

And this affects body fat. It affects fat cells. It even affects whether or not they can release fat. Like literally, whether or not cells can release fat has a lot to do with the tension, tension within the cell. And you mentioned something, actually, you mentioned a really good point, which is how all these signals, these signal pathways converge.

43:33

What it really gets to, kind of big picture, is that growth…

43:41

Growing, perpetuation is the business of life. That is life. Okay? So there are things like the Hayflick limit where cells have 50, 60 allocations per cell. Well, growth is tightly, tightly, tightly regulated in the body. It has to be fine-tuned and tightly regulated. And it's like a road. It's like a toll road where every mile down that road, you're paying a toll to go down that road.

44:10

And kind of at the high level is really insulin and insulin's effect on a couple of key pathways, notably one called MATHK, mitogen-activated protein kinase.

44:25

And really, this is a pathway that controls the decisions that cells make about should we go forward and replicate and divide or should we not? Should we just kind of chill for a while and stay here?

44:40

And the big takeaway is for the listeners to begin to understand you can control that. You have control over that. You can turn that switch when you want to, and you can turn it off when you want to. So once you understand what turns that switch, which is the production of insulin, you can decide how fast you want to age. Yeah.

45:04

Yeah. I mean, that's, it's a great point there. And I'm glad you're really emphasizing this role and function of insulin outside the scope of just managing blood sugar, because it really has so many broad spectrum pleiotrophic effects that seem to be modulating aging, as you mentioned. So, yeah, I'd like to quickly touch on the AMPK versus mTOR

45:31

Yeah, because explain to my listeners how AmpK, AmpTor, and fasting and growth are all linked. So the best way to understand it is to understand two big concepts. It's that the production of energy and growth are one. They are the same thing. We think of them as different things, but they're not.

45:57

They're the same thing. So the body's ability to make energy is life itself. If every cell in your body stopped making energy right now, you'd be instantly dead. Instantly. Okay. So the body's ability to grow requires energy. It has to have energy to do that. In fact,

46:20

I make the point in my book that cells, we use the word cell, but really what you're looking at are computers. That's what they are. They're just a form of computer that's much more advanced than something we can associate as a computer because they incorporate energy production, they incorporate a 3D printer, and they incorporate information processing, and then structural integrity all into one thing. It becomes a single thing. But what they're doing is they're making decisions.

46:48

And they're making decisions on a regular basis, not just from computer code, but also from their environment. And so they're constantly making decisions about how to partition things. Well, the most important decision that a cell can make is to live or die. That's the most important decision. And that decision is based on energy production and power output. So within the cell, there's all these meters that essentially are always measuring power output. The power output in the cell gets too low

47:15

There are some backup measures. One of them is a protein that sits in the wall of cells. It's what's called a heterotrimeric protein, meaning a three-pronged protein.

47:28

And so one head is ATP, the next is ADP, the next is AMP. And so when energy gets down and hits this prong and this prong fires, a signal pathway fires. It sets a cascade of events in motion. And that cascade of events we call AMPK.

47:51

And what that does is it turns on a number of measures that change the way that we get energy. So it's very much like being on a ship.

48:03

and we're low on coal, so we're just gonna burn the deck chairs for a while, okay? We're gonna take all the spare furniture, a little spare part, let's just throw those in, okay? And in the process, the ship's lighter and it's cleaned up, kinda looks better. So, hey, there's a benefit to that, right? Well, that's kinda how AMK works. AMK is, it's a signal pathway when energy is low that turns off the process of growth.

48:31

Now, what we call mTOR really is a signal pathway and it is really referring to a series of kinases. That's what it's really referring to, serine 309 kinases. And this signal pathway is a pathway that essentially is tied to all of the body's signals to grow.

48:56

for cells to continue to advance down their cell cycle allotment and all these other signals that impinge upon growth. So the thing about what we call mTOR is that, again, kind of at the center of all this, you see energy and you see insulin driving all this. So that when energy is abundant,

49:21

Meaning when ATP is abundant, the mTOR and growth and all those things can go down that road. We can use up our primary fuel source. In other words, let's use the analogy of a car. The pistons can only go up and down so many times in that engine before there's wear and tear.

49:41

When we are activating amp K, that's like the electric drive on the car, the backup drive. And so the engine's not wearing out. But once fuel's abundant again, we can use the piston, and that's great. We can do a lot of things. We can really go for performance, but there's a cost. The cost is we're wearing out the engine when we use it. So all of the body's growth-centric pathways impinge upon these kinases that help release energy. And

50:07

and drive all the body's growth factors. So life and death, energy and growth, they're all kind of linked. And in that is…

50:19

In that, the body's sort of starvation pathways, which are AMPK and activation of very key proteins called the sirtuins, and salvage sort of pathways and cleanup pathways like ubiquitin, proteasome pathway, and autophagy, and all these things. All these other things activate when we're in a starved state. We use these words like fasting and time-restricted feeding. Our body doesn't understand what you're talking about. All it knows is just that starvation.

50:48

The body has defenses against starvation, but starvation serves a benefit too. It stops aging in a sense. So AMP-K and M4 are kind of these two ends of the seesaw. And kind of the cool thing is once you understand, once again, how to flip the switch, you can kind of, what I talked about in the very beginning, the power to control the body, you gain the power to control your rate of aging by understanding how to pedal these things.

51:15

Sorry, long-winded explanation. I hope that… No, that was beautifully summarized and very concise. Hopefully that makes sense to my listeners because I think they're critical points to understand. They're really critical energy sensors in the body. They mediate so many downstream biological functions. And for my listeners, just remember like, you know,

51:40

Stimulating mTOR is going to be achieved through high protein diet, increasing your caloric intake, whereas stimulating the mTA side of things is when there's a shortage of food supply, the body will stimulate that side, that pathway to preserve, maintain, and promote longevity. So really well put, Joel. I'd like to wrap up with one final question around the carnivore diet. Now,

52:09

I don't know if you've personally experimented with it. I'd just love to hear your opinions around, you know, maybe some pros and cons around the carnivore diet.

52:19

Yeah, I think the carnivore diet, first of all, there's a lot of, I think it's extremely useful. And I'm just after, I'm like a martial artist. I'm just looking for new techniques. Okay. So if you've got a way to kick that is fantastic, I want to learn it. Okay. But at the end of the day, I'm not relying on any one thing. I'm mixing them all into one thing so that whatever I'm presented with, I have a response for. Okay. That's the way that I'm approaching this.

52:49

So that being said, the carnivore diet kind of fits under the aegis of something I talk about in the book, which is the era of imbalance. And I make the point that we have gotten away from what's really true. We have, as a whole, believed something that's not true. We believe that we can obtain…

53:13

uh, health through imbalance. And that's kind of something to really think about because every school of thought today is telling you to imbalance your health inputs, you know, like, and they all fight with each other. So on the one hand, it's like, you know, meat's bad, meat's murder, uh, meat sucks, you know, uh, just eat plants and, you know, and then, and then keto and all these different schools. But when you look at it, when you look at the thing that we call disease, uh,

53:38

The one consistent thing that you find is that you cannot describe a disease without using the word imbalance or homeostasis, loss of homeostasis. All diseases are just an imbalance of something. And so we believe something that's not true, which is that we can obtain health through imbalanced inputs. And that's just going against the laws of physics in terms of how the body works. So there's always a short-term and a long-term

54:07

The short term is that you'll probably see a lot of benefits in the short term. And the carnivore diet is great. It's great for adding muscle. It's great for fat loss, probably heal your gut if you have issues temporarily. But over the long term, that's where things really play out. And what you're probably going to see over the long term, I would just begin by asking yourself, are there any known disease states that can come from an excess consumption of meat or protein? That's what I would ask.

54:35

And the answer to that is, yeah, absolutely. Yeah, colon cancer probably top of the list. Yeah, 100%. Well, are there any mechanisms that would substantiate that? Yes. I talk about them in my book. You have to understand that, you know, do bacteria like meat

54:54

Yeah. Right? Yeah. Leave a piece of meat out and watch what happens. Right? But the kind of bacteria that like meat are some of the nastiest bacteria known. I mean, the type of bacteria that want to ferment meat are some very nasty players, some very pro-carcinogenic players. And not just that, but

55:16

There are all kinds of mechanisms you can see, particularly when you get into the colon, where you can see an increase in pH, you can see things like N-glycol, neuraminic acid, you can see all these sort of oncogenic things that happen. If you do it too much, you need to do it too long. And then there are ways to offset that. So you add a little bit of fiber in with meat, you can push the pH of the colon back down, and you just see those risks go away. So I would say that…

55:41

over the long term that a lot of people would probably see, could in fact have a chance to see some health related issues from imbalancing too much, too much meat in the diet, too much protein in that way. Where in the short term, you'll probably see a lot of benefits. And it just gets to how the body really works. And the truth is that you can…

56:04

There isn't anything I can think of that if you do it to an imbalance that won't make you sick in some way. It's true of water. It's true of fiber. And yeah, it's true of meat too. So the highest truth of health is that balance…

56:19

uh rules the body and the imbalance inputs eventually will produce imbalance in the body this doesn't matter what it is you could take anything and imbalance it and eventually it's going to cause a problem so uh that's the way to explain it i think in 10 years we're going to look back on this era and kind of see like wow

56:36

yeah, how did we buy that? We were just kind of in balancing everything. And that really the real truth is that a healthy balanced diet always was the best answer. It's just, we'll be at a new level. We'll be at understanding that it's really meal sequencing and it's really like using foods functionally in these sequences. And that's kind of the next thing. So time will tell. Time will tell with the carnivore community.

56:56

Yeah, I think… I know, I mean, you've got a bunch of haters now. Yeah, but I think, like you said, like anything to an extreme is going to have some downstream consequence. And I think the one thing that they pull from is that, is there like literally one or two studies that they keep on drawing upon? Have you seen those like long-term carnivore diet studies? I think there's like one. What are they finding by long-term?

57:25

It was only conducted in like the sample size, I think it was like two participants. I'm not exactly sure. I'll have to double check. But yeah, I mean, it was basically illustrating zero effects on ill health. Like it just had no deleterious effects. What was the duration? What are they calling long-term? I think it was at least 30 years. I'll have to… Yeah. Well, first of all, that's…

57:54

I mean, that's just gibberish. I mean, there's been no formal… That's purely anecdotal reporting just put into or dressed up as science. That has nothing to do with anything. Look, I'm a fan of the carnivore diet as a protocol. There's a lot of great…

58:16

What I've been doing for a number of years is something more close to what I would call martial art. And it's just that when you begin to factor in what, when and how into anything, you'll find that there's a use for just about any eating protocol at a certain time in a certain way. And so carnivore diets are great. They're very functional. I just don't do them

58:39

I just don't do them long term and as a way of life. That's the only difference. But there's a lot of utility to it. So that's probably where we differ. Or rather, I would differ from a strong adherent. In fact, I'll probably call it Mark Bell. Yeah, I share a very similar stance in that regard. The one thing that really just frustrates me about what people say about

59:04

eliminating these polyphenols and oxalates. I understand that. I understand that can be toxic. But what about all the research that we have that demonstrates the beneficial effects of these polyphenols on these pathways we've just spoken about, like improving endothelial function, improving ENOS, like modulating ACE enzyme. These polyphenols are definitely having these biological effects that meat on its own just does not address.

59:34

Well, okay. In 2006, I wrote an article on grass-fed beef in an era when beef was vilified. And I referenced all the available literature which is coming out of Northern California, talking about the benefits of grass-fed meat. So I've been a long time adherent of meat as a superfood. And I still am. And it's part of my diet on a regular basis.

01:00:04

I think there is a… I'm speaking right now as a consumer who has done things for a lot of years. And…

01:00:14

What will happen is when you get to the end of a road, it takes a long time to find out what was really healthy. And you may not be happy with the answer doing something that you thought was healthy and it really wasn't. And the only person who's going to pay for it is you. But when you make a list of the 10 or 12 greatest superfoods, almost every one on that list comes from a plant.

01:00:39

Now, I would put salmon in there, I'd put grass-fed beef in there, but the majority of those are going to be plants. And that's because they're highly functional. And I don't get into this, meat's bad, plant's good. To me, again, I talk about this in the book and I just explained that that's one-dimensional baby talk from a generation or from an era that's dying.

01:01:02

It's from an era when we looked at these hyper-polarized extremes and we're really just doing simplistic talk about things. What I'm seeing is a new generation forming of people that are much more interested in a much more nuanced, more accurate conversation of how things work versus just getting into debating narratives and things like that. There are mechanisms that we can look at and identify that are highly beneficial in polyphenols and they're just healthy.

01:01:32

Yeah. So why ignore it? Yeah. I love meat. I love a good ribeye by itself. I mean, I love that. I'll do that several times a week. But so what? I mean, polyphenols are healthy. Yeah. Yeah. Joel, for my listeners, if they want to learn more about these books you keep mentioning and some of your other resources, where can they delve into all of your amazing resources?

01:01:56

Oh yeah. So the book is The Immunity Code and Veep Nutrition, veepnutrition.com. And then we have also the Immune-Centered Fat Loss Course there and other goodies. So yeah, I'd love to come on by. Awesome. Well, for those listening in, I'll make sure to link those in the show notes. You can check those out. That Immune-Centered Fat Loss Course, that to me is such a novel concept that really excites me that you're

01:02:24

tackling sort of addressing fat loss from such a unique angle a unique perspective I'm sure they've been green food would be very very proud of that concept because you know we both love that novel novel pathways which is cool yeah but Joel thanks so much for coming on the show man I've got one final question and that is basically

01:02:49

Just out of curiosity, is there one area within research that you're really excited to see more of? I think it probably has to do with, yeah, I'd like to see more on…

01:03:10

the long-term effects of ECM dynamics in different collagen proteins post-adipose remodeling. So when we remodel

01:03:25

our fat mass, um, different kinds of collagen fibers get, get put back in to the ECM. And, uh, it's, it's really difficult to appreciate what these things really are because the words don't describe, we use these words, collagen and fibers, but they're, that's not what they are. They're,

01:03:44

I can't even really… Just find an analogy for what these things are. It's like they're sort of like computational construction materials that talk back and forth to the cell. It's like a smart building where you have this ongoing dynamic sort of tensioning and all this crazy stuff happening. And I think it's a thing that's just in identity right now. So I think it's going to be really fascinating to see what

01:04:12

what comes down the line with that. Awesome. Okay. Well, hopefully once you find out more about that, you can probably share some educational content around that. So Joel, thanks so much. Thanks for letting me know it up today. Yeah, it was a lot of fun. I know my listeners are going to absolutely love this episode. So it'll be on across all platforms. I just want to say a massive thanks again, Joel.

01:04:39

Hey, thank you. This was fun. Sorry. And thanks for letting me just babble. I can see you coming back for a second episode. That's for sure. That would be fun. Awesome. Thank you everyone for joining in to today's episode. For in-depth show notes and lessons learned, visit nofilter.media forward slash boostyourbiology.

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