63. Alcohol Enhances Fat Loss? How Fasting Changes Your Gut Bugs & More Biohacks With Joel Greene
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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.

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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.

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...

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,

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

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.

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.

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.

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...

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,

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.

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,

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...

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.

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,

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...

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.

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

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,

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.

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

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

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,

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...

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

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.

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

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,

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.

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...

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.

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,

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.

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.

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

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.

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.

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

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

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.

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,

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.

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,

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...

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

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

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...

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

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

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.

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

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.

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...

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,

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.

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

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,

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.

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,

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

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...

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

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.

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

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

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,

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,

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

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...

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

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.

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.

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.

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.

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

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.

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.

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.

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...

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

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

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

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,

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...

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.

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

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...

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

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

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

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.

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?

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.

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

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...

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

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.

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.

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

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.

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.

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...

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

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

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.

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.

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.

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.

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

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.

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.

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?

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.

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

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.

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,

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.

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

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.

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.

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.

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.

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.

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,

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.

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

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...

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.

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.

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,

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,

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.

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.

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...

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,

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

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.

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

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

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...

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...

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...

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

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.

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?

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...

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...

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

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

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.

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.

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

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.

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.

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.

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?

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

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

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...

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

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,

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

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.

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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