[00:00:00] Hey, welcome back to another episode of super human radio. A today show today is January 30th, 2020. For those of you listening to the show a hundred years from now, and just realizing how far ahead we were, uh, from everybody else. And, uh, I have to thank our title sponsor. This show is powered by legendary foods, and if you haven't tried that new tasty pastry, you are really missing out.

[00:00:26] One of the greatest snack creations in the world. Think of a pop tart, but think of a pop tart improved to have nine grams of protein and only three to four grams of impact carbs in one gram of sugar. I mean, it's, it's amazing. They taste amazing. They are amazing. I had some, but they will literally gone in a day and I wasn't the only one who ate them.

[00:00:52] Elisa. Also ate them. He couldn't believe how delicious they are. Go to eat legendary.com [00:01:00] today and show them some love. Uh, my guest today is none other than my brother from another mother, Joe Green beat. Be kind to me. Joel, I'm here. You want to see a universal chuckle from the entire audience? I'm giving up caffeine again.

[00:01:15] Oh, Carl, please just stop. I just, I just. You know, it was up to two bangs a day and you know, I just, then all of a sudden I don't feel the caffeine and I'm like, why am I even drinking this? What I have to start drinking a third one now, so I have to stop. I don't feel good. I don't feel good when I have too much caffeine now.

[00:01:36] I wonder the same thing that problem is, uh, there is this, there's this, uh, cycle off period where your brain just doesn't work. Dude, I'm, I'm, I'm sitting here wondering why it feels so horrible. I'm thinking like, gee, what's wrong with me? Is there something? And then I'm going, Oh, wait, I'm giving up a drug.

[00:01:52] Right, right. Cold Turkey giving up a drug. Yeah. And it's noticed. It's so notice. Okay. [00:02:00] I haven't, uh, I haven't had caffeine in a while and I just. My brain needed it for today. Right. Just do this interview and Elisa doesn't get it. So Elisa will say to me, why do you always do this to yourself? Cause she's right.

[00:02:15] Like I always abuse myself. I, it starts off with, I'll have coffee in the morning only and then it's a, well, I'll have a bang energy drink after the workout. So then I'm alert for the show and then it'll have a bang energy drink in the morning. Literally I was buying them and keeping them in the refrigerator and drinking them when I got up and then one after the, after my workouts for the show and she says, why do you do this?

[00:02:39] And I say, because I have the kind of job where I can't just show up and not be on, like if I'm just working at my desk, yeah, I can be like, yeah, I don't feel good today, but I'll get this work done. But I have like an hour and a half to make all these connections in my brain when we're talking and I can't go, [00:03:00] Oh yeah, I forgot about that.

[00:03:01] I just can't. So I'm on the same, same page with you, like the same page, like every now and then, uh, for something like this, um, it just, when the brand really needs to be on, you know, like nothing works quite like a cup of coffee. And you know, if I hit the lottery tomorrow. I would go lay on the beach for five months and like not have coffee at all, and just get it out of my system and soak up the sun and relax and chill and read good books, and I need the, I need that.

[00:03:34] I'm 61 years old. I'm gonna be 62. I really need a frigging reboot. Yeah. Let's start. Uh, let's start. Uh, let's start a reboot. Carl. Uh, like Kickstarter. Yeah. Nobody's gonna everybody's in the same boat I am. They're going to be like, why am I going to help Carla help myself? I don't think, I think there's so much love for you.

[00:03:56] I honestly think that, you know, we did it. Let's reboot Carl [00:04:00] Kickstarter. I'll find out that I'll find out the day after I die. How much love there is for me. That's true. I actually asked I in anticipation of my death, which I have no idea when it's coming, but today, uh, last half hour of the show, and you're welcome to stay if you want to.

[00:04:16] I'm doing these new segments where I things I'm digging. I got some blood work done recently. Made me literally freak out until I started digging and finding out why I am the way I am. But it's like I told Anthony Roberts, I says, when I die, will you write my eulogy? He said, absolutely. You know, so he, cause he's been, he goes, Anthony's brutally honest.

[00:04:37] He won't sugar coat anything. And he's been with me since the beginning of the show. He was one of my earliest guests. So, you know, it's funny, the longer we've known each other. And the more that I've seen you do, I have this, I'm trying to turn to put my finger on what it is. It's like this, a [00:05:00] lot of them respect for you and what you've done, and like you just, you're so consistently, consistently, like I'm breaking new ground.

[00:05:15] That no one else has done, and it's a body of work, man. It really is. And I used to have it in my head that I was doing that, but I read the more I, the more I've come along, I'm like, you're, you're, you're more ahead than me. Saw your, your, you know what? You're patronizing me now because you're so brilliant.

[00:05:34] Uh, and, and that's why I keep bringing you on the show. The fans, the audience loves you because they're like, wow, like today's question. Today's question actually came. Uh, from a listener named Gabriel Shaw. And it was from the last time you were on the show. And we talked about a variety of things, which people love when we do shows, because we just go over, you know, we, we hit so many different targets.

[00:05:59] And, uh, [00:06:00] and you did mention that there are three distinct points where the body ages. Early thirties early sixties late seventies as indicated by the presence or absence of certain proteins in the blood. And Gabriel was like, Joel needs to like dig into that. What? What's that about? Well, it is a, so there was a study, brand-new study, 20 2019 that came out of Stanford and there were 15 researchers on the project.

[00:06:33] And they were, they examined roughly around 4,000 people, I think it was, um, yeah, right around that number. And they were able to examine the plasma protium. Okay. In biology, there's only Dolans. There's, there's the, uh, there's the glycone the home that Della theory, Yom probing alone there. They're just talking about [00:07:00] like basically an umbrella.

[00:07:01] So they're talking about and what was it? And this actually made the cut in my book. Uh, just write up a wire, but, um, I wish that I had had an extra month because I would have really, really delve into this fascinating study, fascinating study, and it, it connects some dots out there to other things, but high level, long story just kind of abbreviated.

[00:07:25] There. What these researchers were able to identify is there are three distinct periods of aging in our lifespan. Uh, one is right around 34. Another one is right around 60. Another one's right around 78 and I, I've spent a lot of time dissecting their work and I had some pretty interesting takeaways that I, that I'm going to speculate on.

[00:07:49] Because it relates to what's falling apart and when and what to do. And that's, and it really ties in a lot of other things that, um, that [00:08:00] I personally, for me, I wrote about, um, immunity and aging, uh, macrophages. But it also, I think more than anything, and I think the fun part will be throwing these things out to the audience and letting everybody kind of, um.

[00:08:14] Uh, do them and see what happens. I think that's what's going to be interesting. So high level, it's this, right around age 34 there's a, there's the first major shift of aging, the first major fall off the cliff, and it seems to be characterized all of this, by the way, it comes out of parasitosis, which is a, we can accelerate aging by putting old blood into young subjects.

[00:08:38] And the reverse is true too. You can. Slow aging by putting a young blood into old, old subjects, particularly in the brain. So that's where all this comes from. But what made this really interesting were the specific proteins that were identified. So at age 34, what seems to be the case is there are two really, uh, noteworthy, [00:09:00] indistinct, um, sets of proteins that characterize what's going wrong.

[00:09:04] The first has to do with structural integrity. So it has to do with, um, specifically matrix Malana protease 12. So matrix Milena, protease 12 is an enzyme and it is produced by, uh, immune cells, macrophages in your fat mass. And I, ironically, in my book, I had a, uh, kind of last minute decision to make. There were two key enzymes.

[00:09:31] I was deliberating on which way more. One was matrix when a protease 11 and the other was matrix. Tomorrow Proteus, 1211 was a little more involved in, uh, in, in chronic weight cycling. So I kind of went with that one. But both are equally important for different reasons. Sometimes do is they allow enzymes break things down.

[00:09:51] That's what enzymes do. So, matrix amount of praise, 12 is very, very interesting. It's involved with, um, it's a double edged sword. [00:10:00] So on the one hand it promotes insulin resistance, and on the other hand, it prevents excessive fat storage because it sort of limits the amount that the extracellular matrix in your body fat can remodel.

[00:10:11] So what this gets to, and now I'm going to speculate what this gets to speculation wise is there seems to be a key shift right around age three, four. It has to do with the body's ability to rebound and adapt to, um. Fluctuations or changes in in skeletal mass, particularly body fat. And I was so geeked up when I read this because in my book, I make this very long case that body fat actually is a key driver of aging, a key mechanism driver of aging.

[00:10:46] And that one of the effector factors are changes in stiffening of the extra cellular matrix. And this study seems to, in my mind at least, maybe I'm [00:11:00] making it more important than it is, but the study seems to point out that that's very true. That a lessening of the ability of the extra cellular structures to change and adapt.

[00:11:11] In other words, ages, rigidity, youth is supplements. So when you're young, for example, you can do reductions in body fat and body seems to snap back just fine as you get older, things don't snap back. Okay, so take away from that first protein. Is that really you want to, you want to get a handle on your body fat, younger versus older, because the body's ability to adapt to fluctuations of structural rigidity, meaning.

[00:11:41] Uh, you lose fat and your body has to reshape to the new shade. Seems to slide off the cliff. You know, we don't even think about that, right? We just, we just assume that this, uh, this casing that covers us. So, you know, our skin is, we don't realize that it takes energy for it to [00:12:00] retract. Yes. I mean, you know.

[00:12:03] That's amazing. Like we don't even consider that. And take a guy like me at 39 years old, 330 pounds, that skin doesn't retract completely because, because the network, the under the scaffolding of tissue that holds it all together, just tears right now. Here's the facet. And by the way, thank you for suffering through that very long winded explanation of the.

[00:12:26] That was on Mark Bell last week, making fun of myself over my long winded. Oh, no, no, no. This is, this is, no, no, no. I, I'm thinking, wow. You know, there's so many things that we don't think take energy. We think that, Oh, well, when the skin is, is, is, doesn't have things push, it gets, it's resting. No, it's actually working harder to get back to where it was.

[00:12:46] Okay. So this is where the really fascinating part kicks in. So I'm a primary reason. In my book, I had to kind of introduce this idea of rethinking body fat. [00:13:00] Is that remodelling the extra cellular matrix is extremely energy intensive. It's so energy intensive. In fact, the mechanisms that allow or that are necessary to remodel the exercise matrix are the exact mechanisms involved in cancer.

[00:13:17] So cancer. Oh, wow. Yeah. So here's where this gets interesting. The energy required to remodel the extracellular matrix. So in other words, you shrink fat cells, okay. And then covering them as the extra cellular scaffolding, and it has to shrink as well. Okay. The problem is it requires massive amounts of energy to do that.

[00:13:41] The energy involved is a Warburg like process. Okay. So it relies heavily, heavily, heavily on glycolysis to do that. So during active fat loss, very often the extra energy. Required to do that may not even be there. To do that, which leaves fat cells with only one choice, which is to refill [00:14:00] in order to match the scaffolding to the fat cell.

[00:14:03] Now, where it gets super interesting is in repeated remodeling of the extracellular matrix, uh, in very specific tissues like breast, for example, you can follow what's called a cancer adjacent adipocyte cancer addition. Adipocyte is a fat cell that feeds cancer cells. And the reason why wait, a fat cell that eats cancer cells feeds, feeds cancer cells.

[00:14:26] Okay. Okay. Okay. Yeah, yeah, yeah, yeah, yeah. So a cancer, Jason adipocyte is a fat cell that you find these a lot in. For example, breast tissue. It's a fat cell that feeds cancer cells, the substrate, they need to grow and proliferate. What's driving part of the equation? Driving the proliferation of a cancer patient.

[00:14:49] Adipocyte are fluctuations in the remodeling of the extracellular matrix using a Warburg like effect. Interesting. Yeah. So [00:15:00] when it gets to is how closely related fat cells and cancer cells are so, so tangentially. If someone is fighting breast cancer and they are overweight. And a lot of that fat is stored in breast tissue.

[00:15:17] That fat is going to make it harder for them to combat combat that breast cancer because the breast, the cancer cells literally have a bag of groceries attached to them that they can just feed off of whenever they want. I mean, is that, is that  do, do lean breasts tend to eradicate, you know, using the standards of care today, eradicate cancer better than fat breasts?

[00:15:44] There's some truth to that, but the the point that I'm in my book, I did vote for those of you who haven't heard anything about it yet, I devote four chapters to fat specifically for this reason. What it gets to is the precise [00:16:00] makeup of your fat in terms of collagen fibers, the types of collagen fibers, the types of immune cells.

[00:16:07] Um, and the repeated history of remodeling the extra cellular matrix as a result of fat loss. All of these things, you're going to have a cumulative pole on the extra cellular matrix and body fat in general. And what they do is they actually, depending on a number of factors, the specific configuration of fat as a system can be altered sort of into a pro cancer phenotype.

[00:16:35] That's amazing. So what's really important is to put simply getting the fat off of one and done. That is what's most of that. And that's exactly the opposite. The antithesis of what most Americans do, where they lose a bunch of weight, they gain it back, then they lose a bunch of weight and they gain it back.

[00:16:54] So what you're saying here is that's actually hyper [00:17:00] aging. The body. That whole process of losing weight, gaining it back, losing weight, gaining it back, because every time you dip into that energy to remodel you, you're, you're actually kind of accelerating the aging process. Ah, yes, yes, yes. It's a very long explanation as to all the mechanisms in that, and I, I go into my book, but essentially fat aging and cancer are.

[00:17:27] Very closely related for a number of different reasons, and the best thing you can do is to be one and done with that loss. A worst thing you can do is repeat it and chronic weight cycling. So there is, there's an emerging view that that normality for the extra cellular scaffolding may just be that it over time just stiffens that.

[00:17:50] That may be. Business as usual. Now, up until now, the belief has been that that's just the case with obesity that only in [00:18:00] obesity do we see stiffening of the extracellular matrix. But there's newer papers now that are starting to take a a point of view that it may be. That the more you mess with the extra cellular scaffolding, making it contract, making it expand, expand contract, over time, it begins to get stiffer.

[00:18:15] And there's, there's sort of common sense reasons to believe that may be true. And there's also a mechanistic empirical evidence that it also may be true. I want to know, I want to answer dr Nigel's question here real quick. Hold on. Hold on Stacy, cause this fits nicely with this. He says, fat cells feeding cancer cells.

[00:18:33] A valid reason why suffers cancer sufferers. Uh, lose weight and struggle to gain. Is this part of the  mechanism of cancer? Um, that particular answer, I don't know. I don't want to S we don't want to, we don't want to guess. Right. Okay. With respect to, um, why cancer sufferers lose weight and struggle the game, those are, those are probably different reasons.

[00:19:00] [00:19:00] We thought that, I always thought that cancer cells, uh, they. Capitalize on everything that healthy cells capitalize on, but they do a better job of it. So they literally eat everything they can, leaving very little for the healthy cells that have to also do their job as well. That's what I always thought it was.

[00:19:21] Well, the, um, they wrote the, there obviously the Warburg effect, they rely on what causes a lot, but they have the ability to shunt on energy production into other pathways and derive. Uh, such as glutamate and things like that, they can get their energy via a lot of different things. The, the cancer adjacent adipocyte is sort of a perfect example of that where, um, you have this kind of like, um, uh, look like an aunt calling, you know, you're the queen bee, which is the cancer cell.

[00:19:49] And then the worker cells, which are the normal cells around it. And, and what happens is, so here's your cancer cell, here's your normal cells. They begin to. Influx free fatty acids into the cancer [00:20:00] cells so the cancer cell can grow, right? So cancer cells are Wiley. They have a lot. They are actually the highest evolutionary cell.

[00:20:09] I mean, I did a show probably 10 years ago about how cancer cells are actually, they, they switch on an evolutionary mechanism to not only survive but to thrive. They don't realize they're killing the host, but they are like, when they switch. It's evolutionary driver for them to survive. It's amazing. Um, well, go ahead.

[00:20:31] I'm sorry. I was just going to add to that. What's interesting is how closely fat and cancer parallel one another. Um, if you think about it, they're really the only two tissues that have an unlimited capacity to expand. That's not true. Buckle such a brain's not true of any other tissue except cancer and fat.

[00:20:47] Wow. They are several mechanisms and which is one of the reasons why a lot of cancers begin and adipose tissue. Um, so rethinking adipose tissue in terms of the old paradigm, it's, you know, fats, just fat. You [00:21:00] just lose fat. The new paradigm, which is how things have always worked, is no fat, is highly involved in immunity and aging.

[00:21:06] And one of the takeaways of this new research on the distinct periods of aging seems to validate that, that contention as well. What, why? Why 34 do you think this is evolutionary? You think it's epigenetic? I mean, I was thinking, why 34 you know, we know that evolution is driven by culture and part of culture is a, getting married, having children and raising children and people get married, have children, and they become really fat.

[00:21:39] When they're raising their children, they stop training. Everything becomes focused. All their energy is focused on nurturing and raising the children and launching the children. And they become an unhealthy, let's say. I mean, could, could it, could it be that a hundred years from now? Because, um, you know, we seem to be able to, the, the [00:22:00] reproductive period is getting longer.

[00:22:03] Along with a health span. And so there could be a time when people put off having children till they're in their forties will we then see this first wave of aging pushed further out because of epigenetic effects of lifestyle? That's really interesting, and I wonder as you were saying that, I was wondering if there's a correlation between drop off in fertility.

[00:22:31] At the same time, um, with some of these sexual way to changes in aging, which by the way, one of the defining characteristics of the study that we're talking about was that men and women age for very different reasons, and the sex hormones play a massive part in that, which was something you kind of really got me thinking about probably about three years ago.

[00:22:54] And, uh, you were, you and I were just off air talking on a phone convo, and you were mentioning. [00:23:00] The viability, uh, you reproductively has a lot to do with keeping you young. And I remember that stuck in my thought. Well, if we will, if we all agree from an evolutionary perspective, job number one is to procreate.

[00:23:11] Everything else doesn't matter. Maslov doesn't even come into the picture when we discussed this. And if we think that the number one driver is to procreate, then the longer your body thinks you're a viable procreator. Then the longer you will live. I think that once you start to see those dips in sex hormones where fertility becomes a little iffy, then the body goes, uh, you know, we really don't serve a purpose much any longer and we probably should start winding down.

[00:23:41] That's always been my very feeble idea. That's not really backed by science. Obviously. Let me surprised, put a pin in that. When we get to age 60 there's one more image 34 but we're going to come back to that. That's actually very, very interesting. Well, [00:24:00] and so, so age 34 and I'm thinking of myself by heroine gray in my thirties, which now we say is probably from stress.

[00:24:08] Some people, I think it was early signs of iron overload for me. Um. But my hair went gray in my thirties prematurely. My, my father's hair wasn't gray when he died at 86. So I mean, that was like something that I was doing and that was an outward sign to me that I was aging.  so I agree with you on the 30s Mark.

[00:24:33] Uh, okay. So that brings up the other, another really noteworthy takeaway from this particular study was. Just put it under one bucket. It's energy production. So there is a, uh, is a very key enzyme. Um, it's called ADP ribosome, Alation, uh, relating factor. Uh, . And that seemed to be [00:25:00] state seem to really stand out at age 34 that begin fall off the cliff.

[00:25:04] So when you, when you look at, well, what the heck is that? You know, other than a big word, what does that, so this is an enzyme, uh, that is a kind of, uh, uh, control protein. But what stands out about it is the words, ADP, ADP, right? Both solution and ADP by both Alation reactions are. Essential to life there.

[00:25:25] They're involved in virtually anything you can think of that makes energy, they all will be in common. They all require NAD. So we know that with age, NAD begins to drop off. It begins to spill down. You have less of it. Um, and there's a number of reasons why that's true. But, and now I just want to be clear, I'm speculating here, but a takeaway for me from this was that NAD is kind of a hot topic right now.

[00:25:51] And. Yeah, there's a lot of, a lot of chatter, a lot of noise in the marketplace about that. Um, in my book, I made the case that, uh, we've got to get away [00:26:00] from thinking of things as good and bad and insanely talk. I love it. I have no idea how many times I've said to people about Joel green and baby, especially with nutrition, you know, this is bad.

[00:26:12] That is good. And it's not. And in fact, I hope that we are at the precipice of time now. Where people stop making generalizations in nutrition. I had some guy the other day look at a post of mine and said, lose the broccoli, you'll, you'll feel better. Trust me. And I didn't want to be like, dude, do you know who you're frigging talking to?

[00:26:33] Like I've been studying this shit for 14 years now. And I said, I said, cause I was eating a lot of chicken breasts. It, Oh, well he said, Stan efforting says eat more red meat. Well, stay on effort. Dan would probably ask me, are you an iron overload? Because you don't want to eat red meat when you're trying to get your iron levels down.

[00:26:50] We have to stop this generalization. I understand that generalizations create tribes and that's the new thing today. Are you a carnivore [00:27:00] or are you a vegan? But start to start to become more of an end. Are you an individual? Do you figure stuff out on your own breeze right. Yes. Couldn't agree more. Well, you, you're, you've always been an independent thinker, which I love.

[00:27:13] Um, funny. Um, Ron kinda commented on my Instagram under a cup of thing about baby talk, and Ronald was like, I'm really liking this. I use it. It's great. I had this guy the other day, he made this comment that I said, you'd, you're talking in baby talk. Oh, a red meat is good. You know, broccoli is bad. It doesn't work that way.

[00:27:37] It doesn't work that way. I was going with that was to say that, um, I get asked a lot, is this good? Is this bad? And my answer is always, well, what's the goal? What's the goal? What's the goal? Are you an athlete, a hard training athlete? Are you an elderly person trying not to lose weight? What's the goal if people don't ask you that [00:28:00] question first, but just start spitting out their nutritional advice, run as fast as you can.

[00:28:08] Oh, amen. I would agree. Uh, so with respect to NAD, the question of what's the goal? I think this is a really good example of implementing that, because once we say, what's the goal, then we have to say what, when, and how, and what's the goal and what, when, and how really parses down into, and now we're really talking.

[00:28:31] Now we can get to function. So when it comes to any ed, uh, in my book, I. Like lay out this case that even if you're older, you don't want to jump on that right away. You've got to get inflammation down for a number of reasons. But again, I'm speculating, but if you are early thirties it, it may be the case that this is the first onset of the spin down of energy production mediated by NAD and which case I think we're now getting into what's the goal and what, when and how, which [00:29:00] is so one of the ways we can perhaps begin to.

[00:29:04] Offset some of the age related decline in energy production is the, what would be NID? The when would be early thirties and the how would be a cluster of things, but, but you would not need to jump on the inflammatory aspect. You could go straight into supplementing with NAD because at that point in lot in life, senescence hasn't kicked in.

[00:29:23] You don't need to spin down. Immune cells and all these other things I talk about in my book. And so I think that, I think potentially this makes a really good case for the use of NAD in your early thirties to push back the age related wave, the first one around age 34 and again, I'm just speculating, but I think it's an interesting question.

[00:29:41] I'm injecting a NAD three times to four times a week at 25 milligrams per injection. 25 NAD plus. Yeah. Yeah. I figured, you know what? I read enough about it. I know there's still a lot of discussion about intracellular versus extracellular and [00:30:00] what you supplement. Where does it end up? There's that whole discussion.

[00:30:03] So I'm not taking mad amounts and not going in for like these crazy IVs that make you feel like you're on fire. I feel like 25 milligrams three or four times a week. Uh, you know, ongoing. I'm going to get something. I'm not going to get mad amounts of it, but it, hopefully it'll do something good for me.

[00:30:20] Very interesting. Um, when you did your blood work, did all this, this is really interesting. So w what are the, what are the issues you get into with NAD supplementation? Is that, um, inflammatory macrophages use it as a substrate to. Just to proliferate. They need it for energy. So some of the newest science papers are cautioning sort of an order of operations.

[00:30:48] And I talk about this in my book, which is, um, you really want to get into San Alysis and spinning down senescent cells and all that stuff before supplementing with NAD because you may be, uh, inadvertently [00:31:00] fueling immune reactions without realizing it. And I'm just kinda curious, uh, what you did or I know you do.

[00:31:07] Why don't you start? I'm do. I'm doing a few different things right now. I'm not doing near as much as I used to because I, cause I'm, I don't want to, I want to feel like I can figure out what's working. I'm using, I'm using a brain peptide right now called FGL L, which is supposed to increase a synapses and functionality in the neurons and memory and all that sorta stuff.

[00:31:29] It's actually in a second phase, all's Hymers study right now. The first phase was excellent. Um, I'm taking NAD plus 25 milligrams three or four times a week. I use McConnell growth factor now more than I do IGF one because I want recovery, but I don't want necessarily a, it's still an IGF, but if the one E C version and it doesn't tend to drive blood sugar out of the blood and [00:32:00] it doesn't do a lot of the things that IGF one is responsible for, but it does something that I'm interested in.

[00:32:05] Because I'm flirting with over-training right now. In fact, we're going to talk about that in the last half hour of the show. I'm training three days on and I'm training a lot of volume, a lot of weight, and then I'm taking three days off to recover. But, um, I'm trying to recover faster because I'm sick.

[00:32:23] I'm going to be 62 years old. I'm adding muscle. That's the beauty of it. I'm doing something that people say, Oh, you can't do that at 62 but I'm adding muscle. But we have, we have some questions that we need to get cleared up for the audience. So, uh, Matthew Watkins is saying, what's he saying, ATP or, and I'm not sure what he, you must've said something, ATP and then something after that.

[00:32:46] I don't know. Oh, I think he was asking. Oh, okay. I Matthew, I think what you're asking is, when I referred to ADP, ribosome collation reactions. It's just guess [00:33:00] maybe that was it. Yeah. Maybe that was, if not post something else. Matthew, with the, with a little clearer question and we'll get an answer and I promise you.

[00:33:08] Uh, yeah. So ADP rivals is an intermediary in the process of making energy from ATP, and we need NAD to fuel ADP, ribosome, Alicia, and reactions. And so these are enzymatic reactions that are involved in energy production for virtually. Everything we can think of in the body and the motor oil of that reaction is NAD.

[00:33:36] So I think that's, that's what I was talking about. Okay. Hope that helps. And if not, just just continue with another question. So the 34 is the first point, and where should I take a break now? Okay. Because when we come back, we're going to talk about where I am in my early sixties I see, I see myself aging now.

[00:33:58] I look in the mirror. And there's a [00:34:00] vast difference from my fifties, my city and in my face. And, um, you know, I've, I've, I've had a hell of a few years here between two surgeries in 2018 not being able to really train my legs at all for two years. Um, I also, you know, I, I'm not discounting the effects of anesthesia for those two surgeries back to back.

[00:34:23] Uh. I buy sleep went haywire for a couple years. Um, really bad. Like I S I sleep good three days, three nights, and then one night I, I wake up at three o'clock in the morning and I just can't get back to sleep. But there, it's not simple with me because I got a lot of things going on. I have iron overload going on that I really think that once I get my iron levels low enough, a lot of this stuff is going to start to subside.

[00:34:50] But let's talk about the 60s when we come back. If you want to be the smartest kid on your block, you have to go to V E P nutrition.com [00:35:00] and buy Joel Green's new book, peak human. Because what Joel has done in this book has taken him years. He's condensed and connected all the dots for us and gives you one.

[00:35:13] This is one thing that frustrates the crap out of me when somebody says, Oh, this is the problem. They give you no actionable steps. Joel gives you actionable steps to correct these things. If you suspect that you are falling prey to them. Again, the hardcover is available now, right? Oh yeah. Yeah. We're, we're catching up with an order backlog, so we're, I think about a week delay right now catching up to will, I think in about a week we'll be caught up in at day one.

[00:35:44] We've been doing anyways. Yeah. So if you go to Veep, nutrition.com and order the book. Oh, order the bundled package where you get the hardcover and the ebook. You'll get the ebook right away, and when the hardcover comes, you can put it out on your coffee table and impress [00:36:00] everybody in your neighborhood.

[00:36:01] We're going to take one quick commercial break. We'll be right back, and by the way, this picture that I'm going to put up is called the endoplasmic reticulum. We're going to start to talk about that in this next section too, as we talk about proteins. Uh, present in the blood stage. This is the superhuman channel.

[00:36:19] Evolution. Just got kicked up a notch

[00:36:25] back.

[00:36:29] So we talk about proteins. We're going to talk more about the presence of these proteins and what they mean. Um, and when we talk about proteins. We talk about a favorite little, is this considered an organelle? Is the NFL, okay. We talk about a very favorite little organelle of mine when I learned about the endoplasmic reticulum.

[00:36:51] This thing that looks like it looks like a cranberry surrounded by tripe. If any of you have eaten tripod menudo you [00:37:00] know what I'm talking about and in Joel's Joel put it great. I used to say. This is the Telegraph office that sends messages from cell to cell and it uses amino acids and punctuation and syntax, and that message gets to a cell and the cell goes, Oh, I need to repair something.

[00:37:20] But, but Joel put it even better. Every one of your cells has its own three D printer. That's it. That's the three D printer in your cell. That really is. It really is. Um, the, uh, it, it is, I don't even, I'm trying to find words to adequately convey like what, what this is and all of the mechanisms surrounding this thing.

[00:37:45] But, um, uh, from my book, there was a, an area of research that I just didn't have a face to include and it was just too much. But, um, it had to do with, uh, the way that proteins are put [00:38:00] together. And it also had to do with, um, what's called the glycone, which are like, like constellation, uh, reactions and the manufacturer of glycoproteins.

[00:38:13] And it's not generally known, but half of the proteins are, half of, half of the proteins in the body are sugar proteins. They're, they're, they're black hands. They are bound to long, long chain oligosaccharides. And when you get in and you look at how, first of all, the proteins are manufactured, it's, it's my bottom line.

[00:38:36] Essentially what you have is a miniature three D printing manufacturing plant that has all these automated robots that do all these things like 3d, positioning, maintenance, folding, uh, quality control, quality checks. They got the, obviously, if you're type setting a book back in the 18 hundreds. And you run out of W's, you're in [00:39:00] trouble.

[00:39:00] Yeah. And, and it just, uh, someday, someday, uh, we'll either have to do a video or show on like all of the, just, just for the sheer wow factor of how all that works. Cause it's, it's beyond, uh, incomprehensible the, the level of complexity that that goes on. And you know, what, and, and I, I would be derelict of my duties.

[00:39:23] To not identify this time, this moment to say, but those of you who think that there's any one thing, any one thing that you could do to change your body, heal your body, you're so foolish because the complexity of the human body is in comprehensible. We're so fascinated with space. We don't even really know.

[00:39:49] We don't even know 30% of what our body does and how it shows it. That's the truth. Gosh. Yeah. You gotta call, uh, when I was researching my book and I was diving into [00:40:00] ly cans and the way the play cans are made and all of the steps and quality control checks to making some of these sugar chains are a million units long.

[00:40:09] I mean, they are very large structures and. This is actually is a, it's, it's a related segue so I won't spend too much time on it, but there's an another lesser well-known study that came out in 2014. It's been a very large, uh, came out of China. We looked at about 5,000 individuals and they looked at glycans in the serum, and what they found was that, um, serum, why cans?

[00:40:36] Well, first of all, these sugar proteins are direct modulators of immunoglobulin. Okay. Which is another way to say yes. So they are direct, um, signatures of how the immune system functions. And in my book, I took a, I took a stand, I took a position and I said that, um, uh, there's a lot of reasons why we age.

[00:40:58] No one's got the market cornered. [00:41:00] Uh, there are different researchers that have different ideas and, and very well spoken and, and very compelling. Um, but they don't agree with one another. On all the big points. And so it's all that to say was that, uh, w aging isn't one thing. It's no matter who wants you to think it is, it's not.

[00:41:20] And one of the, uh, one of the schools of thought that's not very well known has to do with, um. The role that immunity plays with aging in a sense of that, and I kind of, I kind of parked myself in that corner in my book, which is to say that aging and immunity are closely, closely related because aging in one sense is like an injury and the body is trying to heal this injury, but it's everywhere.

[00:41:46] And so the immune system gets provoked in ways that, um, in essence, uh, over sensitize the immune system and exhaust it. Well, serum glycans play such an important role in that, [00:42:00] that this study was able to show that measures of serum glide Cannes, very specific, um, uh, proteins involved in glycosylation.

[00:42:10] Actually measured with much greater specificity, real biological age than, than measuring DNA methylation and telomeres and all that stuff. Cause that, cause telomeres are so 1984 now, people are still talking about telomeres. And we know there was so much contradictory information and research show that there are people that live to be a hundred and they got tiny little short telomeres.

[00:42:32] There are people that are in horrible shape. That's at 40 and 50 and they've got long ass telomeres. So it, you know, and, and this is why I love what you just said. You know, you drive a car and your car ages from use, but some of you, because you live in New York and you drive over the BQE, it's your suspension that gets whacked out.

[00:42:58] You know, your, your, your tires [00:43:00] don't point straight anymore because that's what's being abused. Other people who live. In salty by the ocean. Maybe they end up with Russell over their car. That's the sign of aging for the car. This aging is not just one thing. It's a, it's a, it's a multitude of things.

[00:43:17] Thank you for that. Yes. Thank you then. And that, that message really needs to spread because, um, you know, God bless him. There's some incredible researchers out there that have advanced our knowledge, uh, along certain silos about why we age. But you have to understand that those are silos, that, that they represent one aspect of aging, and there's a very compelling research in completely different silos.

[00:43:39] Um, one, you actually brought something up. Uh, I think in chapter two of my book, I talk about, uh, studies with sanitarians very long Luke humans, and there's new research coming out that basically tell them our length was not the driving factor. Instead, it's [00:44:00] inflammation and inflammatory related issues and that and that.

[00:44:03] And that's what I wanted to talk about, right? So one of the things that everyone agrees about is that as you age, chronic inflammation seems to become a problem. And I've said it's you class. How many times did I said this? When you hear the word inflammation, think about the army of the immune system.

[00:44:20] Yet when you hear the immune system, think of your gut. So when we talk about aging, one of the hallmarks of aging. Is inflammation. Well, guess where that's coming from? It's coming from your immune system, which is actually housed in your gut. Now, I'm not saying anything conclusive, but what I'm saying I'm saying is everyone agrees that inflammation is a problem with aging.

[00:44:44] Everybody, no matter what silo you were in, it's probably the problem. It's probably the problem, and that means that the immune, but that means that the immune system that the problem, yes, 100%. Again, you know, not to, not to [00:45:00] hit my book out too hard. No. Do what people need to buy this book because they, they'll, there'll be heads and shoulders above the rest of the people out there.

[00:45:09] There it is. Peak human. Yeah. But to your point, um, if we go tissue by tissue and we look at why is this tissue aging, what's going on? Uh, the. Over and over again what pops up our immune system related issues, particularly with immune cell populations, particularly macrophage populations. So when you look in the gut, the largest population of macrophages in the body and entire body is in what's called the laminate pro Pia, just under the gut lining.

[00:45:42] That's the largest population, entire body, and that's the first place that the immune system gets compromised. So when the gut perfuses. Uh, things get into that lining the inflammatory or macrophages attack. Right. And spread and act like, in [00:46:00] essence, those people listening to this, don't get me wrong, I'm saying they act like a virus.

[00:46:05] They are not a virus, but the way they populate and spread, right. You would call it viral. It's like a viral process, but not a virus. Yes. Right. Then, then you just go tissue by tissue. So you look at the blood like, well with age, what happens to the blood. What's very interesting with age, the way blood gets produced shifts.

[00:46:25] So normally if you've mapped leases, you know, you get this balance of red blood cells and immune cells when you're gone, but as you get older, what happens is. There are very distinct shift in immune cell populations in the blood. So, uh, T cells start to, certain types of T cells start to spin down. We see more of other types of immune cells, less red blood cells, and all of these are immune reactions that make the blood itself a pro declamatory media and, and, and the all the only, I, I'm listening to this and I'm a lowest common denominator thinker, you know, just like, you know, [00:47:00] the gut.

[00:47:01] Inflammation leads to the the, I'm looking at the gut. I sincerely believe at this point in time, given the science that I've looked at, that aging is a result. These changes that you're pointing out are the result of accumulation of metabolic waste in cells. The immune system is always on because it's got all of these.

[00:47:30] Uh, unlikely, uh, uh, boarders living inside the walls now. And I, I really, you know, and I, and again, iron, it could be B six. We, we, um, are exposed to so many things. Now, we know, we just talked about this the other day with a Israel Passwater from a clearly filtered these new, uh. Forever chemicals. They're basically a PFO , uh, like a, like a, um, a Teflon and stuff like that.

[00:47:58] Once they're in your body, they stay. There's no, there's [00:48:00] no mechanism. There's no way. And, and it's not practical to go into each cell and pull it out. So then we have a lot of this stuff. I really believe that the bioaccumulation of metabolic debris, because when you think about aging, what is it that we do?

[00:48:15] We accumulate stuff. We just keep on. And you know, when a house gets messy, and by the way. Do not go out and do a cleanse diet because that's not going to do anything. Nothing at all. Don't let them, Oh, well, yeah, I agree with Carl. You just need to do the, the, the, the tea cleanse with it. No, no, no, no. That, that may, that may make you poop a little bit better, but that's not getting stuff out of your cells that had been, that's been there for the past 1520 years.

[00:48:40] Yeah. It's funny. I didn't know you had this position, which is the very same one that I'm in, and so it's actually a. Very good. I mean, you know, you know, you know what it is, Joel, how can you not, when you look at what happens as we age, the only thing that does happen is that we accumulate [00:49:00] stuff. We eat.

[00:49:00] You know, everything you eat goes into your cells, and the cells have ways of getting some of it out. But some of that stuff, like glyphosate is a synthetic form of glycine. And the body can't get it out, and it leads to, it leads to a phenomenon, uh, called, uh, now I'm going to forget, uh, amyloidosis, and we've all heard of amyloidosis, like in the brain.

[00:49:28] Well, what that glycine just gathers up, the body goes, I don't know what to do with it. We'll just keep stacking it over here. And all of a sudden you have tissue that's not functioning anymore. And what did we call that? We call that senescent cells. Oh, wow. A lot of things are causing senescent cells and it's not mTOR.

[00:49:44] It's not mTOR. I just talked about that last week. Yes. Uh, geez. Boy, we need to, um, well, first of all, eight. I've been so busy lately. I, I didn't catch your show on the forever chemicals. I gotta go back and check that out. [00:50:00] That's really interesting. It's often the consumer bucket is, you were saying that just going, Oh, really?

[00:50:04] What do I do? I know. How do I get rid of that? Uh, yeah, very rich. The senescent cells. Um, again, coming back to the idea of your body fat, it turns out now that, uh, body fat is one of, if not, we might be able to make a really good case. It's the key regulator of, uh, immunosenescence, and I think I mentioned this last time it was on, but there's a.

[00:50:32] There's a distinct state that body fat takes on called secretory associated senescent phenotype. And when you bought it, that takes on that state, it essentially becomes like an immune dysfunction, megaphone. And so your, your body fat acts like a crux variable inputting into the cellular Amelia and into the body.

[00:50:57] Uh. Host of [00:51:00] senescent related accelerates. And it's interesting, the, the, the study that we're talking about right around age 60, uh, starts to point to things that support this idea indirectly. One of them was, is the, um, the fall off of the sex hormones. And what gets really interesting on this is the commonality between studies points to a very few simple things.

[00:51:27] And I have some conjecture on this. I kind of want to hear your take on, uh, but I'll just net it out for you here. So we see the next drop off at age 60. And what's interesting at this drop off is it is the sex hormones seem to play a big deal in it, particularly you're gonna laugh HCG. Um, we see HTG and then we see, um, a couple of other sex hormones that seem to play a role at age 60, which kind of just.

[00:51:56] Loosely points to your theory, Carl, your, your, your notion [00:52:00] of your, your viability sexually has gone, so things go downhill. Yeah. Evacuated, evacuating evacuated. The other thing that I, I started it again. I'm speculating. So, um, I have, uh. I have, I'm going to give my testimony. A testimony is not the same thing as a theory.

[00:52:23] So this is not a theory. It's just an eye witness as to what I've seen over about 40 years. What I have seen. Is that people who take anabolic steroids early and young, uh, you know, teens, 20s and on in that you look mind boggling in your early twenties but what I've seen later on as you get 50s, 60s is the body just can't even put muscle on anymore.

[00:52:47] And my, what I have seen or witnessed is there seems to be about a 25 30 year window where they really work well and they don't work that great. That's just my eyewitness to what I've seen. Um, and I've never been against those [00:53:00] things. Uh, I will use them. Um, but I've always said that I'll, I'll wait till about 65.

[00:53:06] I'll see if I can get that far. It's a year by your proposition right now. You know, you don't know until, you know, so I'm 55 and I'm, I'm probing in 65 is when I'll probably start using those things. Um, which by the way, as an aside, what I love about guys like you and Mark Bell, you guys tell the truth, right?

[00:53:25] You guys. Uh, w the, the scorch of our industry are people that are on stuff and saying, look at this, and I've got these, this, and you'll get the result. And they're not telling you what they're really doing. And there's a very few guys in our industry. You guys like you guys like Mark Bell that just lay it all out.

[00:53:52] Well, look what happened to it. Poor Christian Tippett is a Christian Thibodaux, uh, you know, uh, Christian. Uh, he was, he's [00:54:00] like the most photographed model and he was in a, he was in Mark, Mark, uh, Chris Bell's a bigger, stronger, faster, and I admitted on camera. That he used gear and they fired him from BSN or one of these companies that he was like, he was the spot he's sponsored by.

[00:54:18] Right? Like, you can't tell that. You can't say that. Well, why? It's the truth. No. We want them to think it's all supplements that make you so big and strong that that whole little con game, uh, it's always been there. Probably always be there. And, uh. Uh, me as a consumer spending year is just getting like swindled because I thought, Oh, all I gotta do is take this.

[00:54:39] You're little, you're, you're approaching powder, and I'm going to look like that. But you know, so I, luckily we're in an era where there really are people who will tell you what's really going on, you know? And so that's, that's refreshing. But that aside, um, what, what this latest wave of aging suggests to, to my line of thinking is that the time [00:55:00] to begin to augment.

[00:55:01] With the, uh, with the things like HCG or ebox. Steroids really, really should be the 60s. That's really, you're getting a late fifties, early sixties. That's about the time you want to start. Um, because if I'm correct and there is sort of a window here, then you want to not take it too soon because then you run out a window.

[00:55:22] That's it. Exactly. Yeah. Again, this gets us back to what's the goal? The goal is to put off the third, the second wave of aging. Okay. What's the, what, when, and how. The what the, what are things like, you know, whatever, testosterone, growth hormone, HCG, all these different sort of, you know, things we can, we can look at.

[00:55:38] And the, when is late fifties early sixties seems to be a, there's a, there's a wave of aging. It seems to be sexual, non-related. We seem to have a window of utility with these things. And so maybe that's the place that we save them for. Um, again, I don't claim to know the answer to that. I'm speculating, but, um, I'm very, very peaked by, well, this whole area of research and it's something I [00:56:00] think that, um, Maritsa lotta further talks.

[00:56:02] So, so, um, I, I want to just mention this real quick because this is really important. There's a whole group of people out there that think  is bad. There's that baby talk again. Empty bed a and P. K. good. Yeah. Um, there's a study that was just published. I talked about it on the show last week. That's been completely ignored by that community.

[00:56:25] Now granted, they were young men. They were young men, so they, this doesn't translate to us older guys. However, there's studies. The summary of the study is a single bout of resistance training, reduced senescent cell load in muscles by 48% right? I sent this to Ron and you know, we both read it and was like, and here's the beauty of this study.

[00:56:54] Yeah. They had a low protein and a high protein group. The high protein group was eating four [00:57:00] 84% of their daily calories was from protein, which you and I both know am Tor was turned on baby. It was turned on, but yet these senescent cells, they didn't turn into  and cells. They somehow were removed from the muscles.

[00:57:16] So those people out there who was saying, no, you can't get rid of senescent cells unless you turn off  that that ship has sailed. That's not true. We now, we now know that. And if you don't incorporate that into your knowledge base and you keep telling people, Oh, you've got to suppress mTOR, you've got to suppress mTOR because you made this big case for it, and you're going to dig your heels in and stay in that camp while the while the science marches away from you.

[00:57:43] Then, you know, be warned, you're wrong. You're absolutely wrong. And I, and I, I don't care. People say, Oh, well they were young guys. It doesn't matter. M toy was turned on and a single bout of resistance training eliminated 48%. These weeds were done with muscle biopsies. This is no [00:58:00] guesswork. They took, they did a core sample in muscle, and they looked at the senescent cells beforehand and after hand, and this was unequivocal.

[00:58:08] This was it. Uh. Oh yeah. Quite a lot on it. So I talk about that in, in, in my book, uh, my own experience without around 2011 and I was in a, you know, a tough Fiji as a way of life camp and I just was always sore. And then what really the fix I found was balancing out. It was that work balancing, uh, balancing out cycles of growth and cycles.

[00:58:35] That was , which is mimicking famine and feasting. And one of the. The moments, I think in anyone's journey, they're going to figure out is the growth cycles or where you get the most healing or where you get the most, uh, resolution of inflammation. That's, that's, that's where you get the bang for the buck and getting the healing part, uh, and grow growth and input are essential for healing.

[00:58:58] Uh, the, [00:59:00] the question I would have on that study is that there are. Very key. And this is not to refute the idea, I think ideas. Got it. But there are very key differences in aged muscle versus young muscle senescent cells and the way satellite cells work, uh, no disputing is the effect of exercise on senescent cells.

[00:59:22] Like any agility. The only thing that I would throw out with that is that, um, there are other. Other very specific growth proteins that do not function. The same with age. Uh, I mentioned ERK one half, which is, uh, in the TGF beta family of proteins. Uh, so I think that there's a, there's a few other things to look at.

[00:59:42] Um, one of them, a big one is the connection between body fat and aging muscle. So as muscle ages, uh, w lipid drugs deposit in muscle. And it creates a feedback loop between fat and muscle that suppresses muscle growth. [01:00:00] And so, uh, there's a, there's a mix of factors in there. What I would say is that, uh, the, the state of your body fat as you age, dramatically impacts muscle, uh, in a very, um, either positive or negative way.

[01:00:13] And so that's neither here nor there. I agree on the concept. So, yeah. So, uh, what exactly all the proteins. So, so a couple things. Uh, the new emerging science is, it's all about methylation, right?  methylation is the way to tell if what you're doing is reversing aging or not. What is your opinion of that? Um, methylation?

[01:00:36] Good. Yeah,

[01:00:41] I would say that, uh, it's a point of view. Uh, there's validity to it. Uh, what we're talking about today is. Equally and I would say probably more valid than the methylation point of view. It's not to say that methylation as a marker isn't a ballad. It's just [01:01:00] to say that you can put it down for a second and come and look at serum ly cans or look at serum proteins like we're talking about.

[01:01:07] You can, you can get all the same things you can, you can measure biological age and you'll get a different mix of sort of. Causal relation from that. Just back to agents, not one thing. And that's the point. So there I am going to be using multiple approaches to reverse aging, not one thing. That's, and that's, you know, so if you see a product that has some valid, uh, application, you want to use it, but not just that, that not only that one thing.

[01:01:42] That's the thing. Absolutely. Absolutely. Yeah. And the idea that, that, that we've figured out aging, um, now I'm going to say we handled it, I want to say like, we're, we're, we're figuring out aging, but we haven't figured aging [01:02:00] the one, the one thing that we can all agree on an equivocally is remaining active and continuing to maintain or even build muscle has been shown.

[01:02:13] And large scale longitudinal studies over long periods of time to equate to longevity and health span. And the magic number is if a, if a man can get to the age of 65 and have a decent amount of muscle, he's going to fare better. So if you're still growing muscle at 65 you're really going to do well.

[01:02:37] That one thing has come, it's come back whether they looked at strength. Grip strength, leg strength over at the California VA. a couple of more recent studies have actually just looked at lean body mass and looked at men over the course of 20 and 30 years. A frailty is an indicator of, of, of, uh, [01:03:00] of, uh, not living long.

[01:03:01] The slowness in your gait, how fast you walk is an indicator of not living long. Well, those all have to do with mechanical strength of the body. Yes. Yes. Uh, as you were saying that at 62, you put on muscle, I, it took me back to a convo I had at dinner one night with, uh, you know, you, you get, you get certain types of trolls online and sometimes you meet them in real life.

[01:03:29] I was telling, I was at a dinner talking to this one guy and. And we were talking about putting on muscle and, and I said, yeah, you know, it's pretty easy if I want to, I can, I can put muscle on readily anytime I want to. And he goes in and he's like, BSD, I'm like my back. And he's like, how old are you? And I'm like, 55 he's like, absolutely no way.

[01:03:48] It can't be done. And I was like, Oh well I know it can be done cause I can do it. And then when what stood out was when you said at 62 that you're doing it. I think that's a, it's a [01:04:00] myth that really needs to be exploded that after a certain age you can't put muscle on. I personally, you're farther down the road than I am, so you would know more.

[01:04:09] I'm just saying where I'm at at this point in life by easy, I quite easy for me to put muscle on. Jude, I'll give you order. You know what it is. Yes. It definitely training. But it's eating. That is the thing. Food is the most anabolic building fat. That's anabolic building muscle. That's anabolic. If you, if you couldn't put muscle on after 60 you probably wouldn't be able to put fat on either.

[01:04:35] Yes. This is such a, we'll have to put a pin in this one and do another shell cause this is so fascinating. In fact, in fact, dr Marl D Pasqual came on my show a few years ago, probably four years ago. And he said that he wants to coin a new word, and this is going to, you'll get to love this, the Annabel loam.

[01:04:56] I love that because he said, he said, if we [01:05:00] start to understand what happens when the body becomes anabolic, we can actually Dodge out of the way of diseases. And he started, he called, he coined the phrase antebellum.

[01:05:13] What's, let's use it. I love it. I think it's a very Bible, a thing. In my book, I make the contention that, um, there are key markers of a young body and that if you can keep those markers active, uh, you are going to, you're going to slow the aging process. And one of those has to do with, um, the, the utility of the muscles and their athletic range.

[01:05:37] And so I've been in a space for a number of years where, um. All right. You know, I still train a little bit for muscle. In fact, I'm, uh, I'm about to go back on a, a phase of adding a lot more just through food, which your point, it's easy if you know how to manipulate food and lots of food, and if you do that anyways, I think muscle, it's easy to put on the thing I've been focusing on for a number [01:06:00] of years.

[01:06:00] Um, it doesn't get talked about too much, but I think it's worth mentioning. Is the athletic range of the muscles and the athletic range of the body. And those are, those are not necessarily the same things that we see in, in bodybuilding or, you know,  the strength training. But I think that they're worth talking about.

[01:06:17] Um, the guy that comes to mind is George Saint Pierre. So when you think of George Saint Pierre and the way he trains, uh, he has a very, very athletic range to his physique, uh, extreme sort of athleticism. And. Those involve very specific types of things and movements and, um, particularly training what I call a star.

[01:06:39] We're called the stopping muscles. That's where you get hurt and you get old. It's the, it's the sudden stops you get your snap a hair spring. Exactly. Kelly's, yeah. Yeah. Yeah. Um, I met a, uh, a professional trainer in the world tennis who, uh, is very, very knowledgeable in the area. In fact, you might want to have him on, he's super knowledgeable and [01:07:00] biomechanics.

[01:07:00] Um. And he was really walking me through some of the training that he takes tennis stars into because the tennis starts on how fast you are, how fast you can stop, because you need to stop on a dime. That's the key. And he walked me through some of the aspects of training, the stopping muscles, and I added those to the things that I've been doing, which all involve, um, keeping my athletic range in.

[01:07:20] It's in, it's late 20  early 30 something range. The ability, you know, just go from zero to a sprint in and go to a handstand. You know. Things that are more about things or young body can do, right? Using this guy's stuff. I noticed an immediate difference in a lot of different parameters and it, it's a bunch of weird little movements, but I don't want to steal this guy's thunder, but we'll definitely have him on.

[01:07:41] There's no doubt about it. That's a great idea. I want to take a last commercial break. When we come back. I want to talk about the 70s cause now we're nearing death. Know if we are, let's be honest, unless we've done everything right, look up, you know, my, my father didn't do anything right. And he lived to be 86 my poor [01:08:00] mother, she lived to be almost 90 but, but she was in a nursing home with Alzheimer's disease.

[01:08:05] She had a really bad stroke and she never recovered from it. So, but, but you know what? I have the longevity on my side, that's for sure. There's no doubt about it. We're going to take our last commercial break. In the meantime, go to V E P nutrition.com and order the book peak human, become a peak human yourself.

[01:08:23] There you go. Stay tuned. This is the superhuman channel where we use oxygen for the power of good. Welcome back.  talking with Joel green, author of the book, peak human. His website is VEP, nutrition.com you can go there and get the bundle, which is the hard cover and the ebook. That way you can take it on a plane with you and read it on your tablet.

[01:08:47] So before we talk about the 70s, I just want to make sure that I'm not doing a dis, a disjustice and unjustice and injustice to my audience, but the proteins we're talking about that seem [01:09:00] to have this linkage, uh, to, uh, aging outcomes. Are these, these glycans correct? Uh, well, not, yes and no. Uh, so just to summarize, we began the show talking about.

[01:09:17] A very specific study in 2019 out of Stanford, uh, that talked about the serum, the serum protium, uh, very specific proteins in the blood and he sort of junctures in life where there were some commonalities of these proteins. Uh, in the early thirties, it seems to be proteins related to structural integrity and energy production.

[01:09:39] In the 60s, it seems to be proteins related to the sex hormones and. There's a second study that was published in 2014 specifically on Sarah glycans and looking at a whole other suite of things, looking politically at the Sierra black hands. So, so my question to you is this, if you are [01:10:00] someone who's eating a very low protein diet, uh, and, or, uh, you're a staunch vegan, um, is it reasonable to think that.

[01:10:11] Like the analogy I gave about the 17 hundreds and the printer and him not having W's, so he couldn't use, make any words with W's in them. Um, if you don't have the inventory of those individual amino acids because your diet, your intake is actually vacant of those, uh, could that influence the early onset of aging because of disruption of the.

[01:10:37] Uh, ability to produce these messages, these, these, these big folded proteins. Um, not so much. It's actually really the opposite. But, um, there's two issues. One is length of life. One is quality of life in terms of length of life. Uh, you'll get a little more out of the vegan based diet [01:11:00] purely because they restrict the thianine and the diet by virtue of all them assigning rich foods or animal protein.

[01:11:05] Right. Oh. So they can dies accidentally restrict the . And so in the stock, in the fining, you need with thianine for growth, it's the stock code on when you're making proteins, right? So, so it's kind of the reverse argument in that sense. The less Matthias and you have, the less substance, the less raw materials you have to make growth related things.

[01:11:27] But then the other issue with that gets to sort of a quality of life issue. And, um, particularly B vitamin production and B vitamin production in the brain and all sorts of issues related to that. So, um, what you'll, what you'll see longterm on vegan diets, uh, you know, I'm not trying to offend people, I'm just trying to give you what, what, what seems to be supported is that, um, you're not going to have quite the mental punch that, uh, someone who.

[01:11:55] Either mixes it in more of a balance in their diet or, or maybe leans a little bit more on [01:12:00] animal proteins. Just you, there's no getting away from the need for animal proteins, uh, for, for high brain function, I don't think. And in fact, uh, according to the winter grant foundation, that is when our brain started to grow and our guts started to shrink when we started to eat, uh, animal protein, uh, the Astra Australia  robust, this was our last vegan ancestor.

[01:12:22] It had a very short lifespan. Um, a grass seal Australia pedagogy, grass seal or Africanas started to eat meat. Uh, Dr. Daniel Lieberman came on and told the story on my show once, and they over, you know, thousands of years, their jaws got narrower. Those big chomping teeth got smaller. Their guts got smaller because they weren't trying to extract nutrition out of it.

[01:12:52] Bark and tree limbs, you know, they were, they were eating high quality protein and their guts got smaller and smaller and smaller. [01:13:00] And they are our direct ancestors that, that w that we came from. So that's, that's, uh, that makes perfect sense. Um, and then for those of you who are eating a lot of animal protein, like me getting an adequate amount of glycine can actually, uh, blunt the, uh.

[01:13:20] Aging effects of a high protein diet, because that is what keeps  from being damaging to your body. And some say about 15 grams of glycine a day that can be achieved by eating more of the . You know, the, the, the, the, the, the tripe and the stuff that no one wants to eat anymore. Sweetbreads uh, you know, chewing like me, if you ever eat chicken with me.

[01:13:46] Yeah. You think you're eating with the dog because literally there's this much left to the chicken bone when I'm done, cause I eat all the, I'd suck the marrow out and every one of them. So, but, but, but it, paying attention to glycine can really [01:14:00] pay off in the long run for a lot of high protein animal protein eaters.

[01:14:04] I think we're going to have one thing to that, which is. Mechanistic, I always like to kind of get into the mechanisms because, um, it's gives us reasons to believe certain things. So, um, mechanistically, one of the issues you get into with, um, fats from plants versus fats from animals. And you know, I, I'm not in either camp.

[01:14:27] To me that's all baby talk. I, I'll use both laterally, but there are mechanistic differences that are just simply how things work in. If we want to get where we want to go, we have to deal with how things work. So, uh, there are certain types of carnitine transporters specifically indulgent, specifically in the brain that are found in an animal fascinator they're really not present in plant fats.

[01:14:56] And so it means that the way that fats can move into my [01:15:00] cadre and the brain. And the way energy can be utilized in the brain. There are some key structural differences between animal fats and plant fast. And so that's one of the reasons that we sort of see animal proteins, which have animal fat. Um, work a little bit better for brain function.

[01:15:18] And so there's, there's some, there's some valid mechanisms at work there. Um, they've got another show we can dive into that. I don't want to get too far into it here, but I want to throw that out and we're going to talk about the 70s now, but you just reminded me of something. So for all of those, excuse me, auntie M Tor people, uh, M Tor also.

[01:15:36] Is what helps the brain repair itself. Shrinking brains are part of aging and probably can be avoided by doing certain things that up-regulate BDNF. But  is what builds the brain. So if you're shutting down MTR to live longer, you may also be shutting down your brain's ability to repair itself. So just a thought, just a thought.

[01:16:00] [01:16:00] So talk about the 70s what do we have to, what do we see in the 70s and what can we do. The, so the, the one commonality or key markers seems to be, seems to send around inflammatory related proteins. Uh, one that really stands out is a GDF 15, a growth density factor of 15, and that's very, very interesting.

[01:16:22] So GDF 15 is a signal signal protein. Um, it mediates inflammatory signals between macrophages and immune cells. That's what we see is this uptick of this inflammatory potentiator right at about the late stages of life. And this, this gets to such a fascinating host of topics that all interconnect across different studies.

[01:16:50] So what this essentially is saying is that right around 80 there's this inflammatory wave. It hits the body and it [01:17:00] essentially pushes most people over the cliff and creates the rapid decline. Now, where that's interesting is in studies with sanitarians and very long lived individuals. So what's interesting is if they have inflammation and it's beneficial.

[01:17:18] Really? Yeah. So, so cemetarians seem to be able to hermetically adapt. To inflammation and senescence in a way that allows them to upregulate key defense mechanisms so that the thing that's allowing them to live so long is they have inflammation in a chronic low grade state that they have adapted to.

[01:17:44] And other people don't do that. They don't make those adaptions and therefore they fall off the cliff. So this, this is a whole series of shows. I mean, this is. Really interesting. Really, really. So is it, is that, are [01:18:00] they actually able to resolve inflammation still at that advanced age? And that's where the magic is.

[01:18:06] Uh, got it. I won't say that it's, it's not so much that they're resolving it. It's that, um, think of like the mitochondria and keto diet. So what makes cure diets effective? One of the mechanisms is in the mitochondria. There is a low grade oxidative stress that the mitochondria are able to automatically adapt.

[01:18:27] Yeah. And upregulate  fat. And in fact, if you take very powerful antioxidants, you want that adaptive, right? Yes. For all those people out there taking C6 the and go, man, it's going to make me live forever. Okay. Yeah, we are. We are selling the same page with that. Yeah. So, so take away is that the body. Has hormetic adaptive reactions to low grade oxidative stress, low grade inflammation, and there's a, there's a lot of tissues where the body seems to be able to [01:19:00] upregulate its defense mechanisms, particularly in two and when anti pathway and create an adaptive response that is being fueled by the low grade inflammatory response.

[01:19:12] So what sanitarians seemed to be able to do is take this senescence and take this inflammation inflammation, and make it into a positive by four medically up-regulating key adaptive mechanisms. So where that takes us to. Is well, what, what, what can we do? How is this switchable? I mean, can we all do this?

[01:19:32] And, and I'm going to dance that the case that actually it's very, very, very switchable. So the key, which is kind of the gist of a lot of what I talk about my book, is a concept I introduced called steering macrophages. And what I mean by steering macrophages is you have to understand that if. Um, aging and immunity are related and even body fat and immunity are related.

[01:19:57] Then understanding what [01:20:00] macrophages are and how to steer populations one direction or another becomes an essential life skill. So broadly speaking, there's two classes of, of macrophages, two classes of these kind of frontline immune cells. There are the inflammatory macrophages, which are , and then there are the two which are the anti-inflammatory macro anti-inflammatory macrophages.

[01:20:26] The thing to know is it's not black and white. Sometimes in some tissues, in some cases, the anti-inflammatory can be from flammatory and vice versa. But for the sake of simplicity, in most cases, this kind of holds the M one or the inflammatory, the M two or the anti-inflammatory. Well, the key is learning how to steer populations of those.

[01:20:47] That's what you can do. And the key to learning how to steer macrophage population is to go tissue by tissue cause each tissue has different requirements. So my book, I lay out the case, we start with the gut lining. You have to learn how to steer [01:21:00] macrophages in the laminate for Pia next is your fat mass.

[01:21:03] You have to learn how to steer macrophages in the adipose tissue. And then we just go down the list. We all need to muscle. We're going to the brain. We go into the cellular mill, you. And so it's not any one thing, but there's a cluster of techniques per tissue that you can learn to steer macrophages. So if I'm 80 years old.

[01:21:22] The first thing I'm doing is I am restoring the macrophage polarity or ratio of inflammatory to anti-porn. I'm going through the gut lining first. Okay? I'm going to rebalance that and get that into something resembling a 12 year old dog. What I'm going to do, right? That will have massive implications across the entire body.

[01:21:44] Um. The book is peak human. You want to stay with me for this next segment? It's just going to be about 15 minutes long or do you have to go? So you're welcome to stay if you want. Oh yeah, no problem. I, I'm, I am taking out new life [01:22:00] insurance and I just had a big workup, done a couple of tests, shocked me. I was, Oh my God.

[01:22:06] But then after I dug in. I realized that, uh, athletes have to be treated very, very differently. And I refer to myself as an athlete. It's kinda gratuitous, but I'm more of an athlete than the average 61 year old. And so, or what's that? Or? Sure. Yeah. So I want to just talk about this because, um, people get all freaked out about blood work and sometimes it's not what you think it is.

[01:22:31] So we're going to take one quick commercial break and we'll be right back with more supremer radio.  this is the superhuman channel evolution. Just got kicked up a notch.

[01:22:45] Welcome back. We're here with Joel green, kind up to stay with her. You've tried to the pastry, right? Well, first of all, dude, I'm super butthurt super butthurt. You haven't tried it yet. Oh, [01:23:00] I have, but I saw the box you got from it wasn't that.

[01:23:06] They are amazing. The strawberry is, has added this frigging world, man. And when you, when you put it in a toaster oven, do you know the, the icing on top is like real icing. I have a feeling they used Al yellows to make the icing because it, it melts and it starts to move around and it gets clear and it's, Oh my God, it's so freaking good.

[01:23:27] It's unbelievable. Well, not in my mind right now. I'm going to text Ron. They're too, they're too good. They're actually too good to unprovable. Anyway, so I'm getting a new life insurance policy because, um, I want to have more money in the event that I die. I want to make sure that Elisa first and foremost is, is cared for.

[01:23:48] And then if there's a little something extra for me, I told her she's going to be the executor of all this, and so, you know, give my kids. A nice little parcel of money to help them through their lives too. [01:24:00] So I shopped around. I found a really good life insurance company, easy to work with, very upfront.

[01:24:07] In fact, the guys listened to the podcast now that the, the guy that I was working with to get my life insurance, he's like, he's listening to the podcast now kind of minute. I don't know right now, but he's, he's been listening to the episodes. Can you, can you send me after we're done that guy's info? Oh yeah.

[01:24:24] And so, you know, they send somebody out to the house, they do the EKG, uh, they draw blood, they do all this information. And so I got my blood work back today and everything is, looks great except two things. One of them is a pro BNP or BNP, which is a, is a, an enzyme, I guess the or protein at the heart makes when it's like under a strain.

[01:24:52] Well. So let, let, let me say this first. There are pathological changes in your body and there are physiological [01:25:00] changes in your body that look the same, but for different reasons. So if you're a sloth and you sit on your 300 pounds and all you do is sit around, you don't exercise, you don't, you don't even get a thousand steps a day.

[01:25:12] You will start to develop problems with your heart. If you have plaque buildup and your heart is starving for oxygen, it'll produce more of this BNP. But also if you're  what's that like your workout if you, Oh my God, my, my BMP was like shocking. It was like 700 and something. I was like, what the hell is that?

[01:25:35] And then my micro albumin was high, like th it's supposed to be zero to four and mine was 14 but my creatinine is perfect. There's no blood in my urine. I don't have any of the classic cofactors. Of kidney failure. So I thought, you know, I get on NIH and I started reading and I start looking for these two [01:26:00] markers in hard training athletes and weight lifters resistance training.

[01:26:04] And then I F I found out what's going on. I had just come off a three day, so I'm training three days on, three days off, and I trained for three days, and the next morning she showed up at the house and drew my blood. And all the research shows that. A, B and P goes up if your, if your heart has to work hard, all right, but see, doctors think pathology.

[01:26:26] Your heart is working, your heart's working hard. You're sitting on us on a sofa. If they still have that, how fast I moved from thing to thing and how much weight I handle and how, you know, they would go, Oh dude, I can't eat that. That's where that's coming from. And the same thing with the micro albumin.

[01:26:41] And so. Um, I just think it's interesting because many of us we go when we have blood work done for a job and they'll say, Oh, your creatinine levels really high. You've got to watch out that your, but meanwhile, you've, you've, you've been training every day for the past week. Or if they tell you your [01:27:00] BNP is high, Oh man.

[01:27:02] That's a sign of, um, because BNP is a hallmark sign of congestive heart failure. But I don't have any of the other symptoms. I don't have any fluid retention. I don't, I don't get out of breath if I run up the stairs, you know, I don't have those. But it's amazing. I, I'm waiting for, uh, the medical orthodoxy to start including hard training individuals because there's a lot of us out here today.

[01:27:28] There's a lot of us doing CrossFit, a lot of us doing triple sets with heavy weight training and heart, and we're in our fifties and sixties too. And I'm just wish the medical orthodoxy will catch up and start including athletic types into epidemiological study so that they can have a doctor ask, did you just lift weights yesterday?

[01:27:50] Yes. Oh, okay. Alright. I get it. Huh. That's interesting. I'm going to do a podcast coming up with, uh, one of the Senate genics [01:28:00] doctors, and I'm going to ask him about that, like what they see and they do it. Yeah. Yeah, let's get it. Those guys are probably a little more switched on. Yeah. They've been taping doing this.

[01:28:10] The whole anti aging thing for a long time in Las Vegas, they used to have a guy, I want to say his name was dr Jeffrey self. Was that the guy? Super Jack? He had the bald head and he had the glasses, but he was like a cot. Yeah. Go ahead. No, I was gonna say, I don't know if he's still around. That dude is, is exactly the picture in my mind of what the body looks like.

[01:28:36] If you haven't done steroids when you were younger and you waited, and then you know you did them like 50 that's what you get. You get that look like that dude Jack. You know the, the, the, you know, I, I'm officially old because this is really nice kid that I know from the gym and we always sit in the sauna.

[01:28:55] And yesterday he said to me. How old are you? I says, all, I'm going to be 62 I [01:29:00] don't even say I'm 61 I'm so proud. Oh, I'm going to be 62 and he said, man, I hope I look as good as you when when I'm your age. And Elisa said, well, that was a compliment. I says, no, that's what you say to old guys. I said, that's, I'm the official old guy now at the gym.

[01:29:14] But the reality is that from the neck down, my body looks really good by abs and now coming back in, but from the neck up, I look like an old shoe. That's the part that I have a hard time getting over. I, I think that you're the like, uh, you're, you're the, you're the target. Now you're like, you know, a standard bearer for what's, what's possible now.

[01:29:34] You know, as you get to a given age and there's a redefinition that's happening, I think right now, like the stuff that you do would break me in half. I don't believe that. I think you could stay right with me. I've seen you train, dude. I've seen you sprint. Yeah, but that's different. I mean, the stuff that does the kind of weight that you're handling and all that stuff, I mean, it's like you're, when you're doing those, a Helvic thrust with 9,000 pounds on your homework.

[01:29:59] I've [01:30:00] watched those and I'm like, what? And then I go right over and I do a super set. I do it with, and I go, I stopped that. I do five to six reps with that. And then I go over and I do five to six reps of heavy squats. Unreal. Unreal, unreal. But it's coming back. But anyway. So if you're getting blood work done for a life insurance policy or for work, be sure to tell them like there may be some markers that are high because I lift weights really heavy weights and tell the person so that they can at least make a note on it.

[01:30:32] Cause I know I'm going to have this discussion now with the underwriter. They're going to buy. Wow, you're, you're, no, you're a BNP. Is is supposed to be under 90 it was 470 I'm like, yeah. I trained three days in a row like an animal. You know, my heart Def, definitely, my heart works hard. It works hard.

[01:30:50] There's no doubt about it. And it usually happens when the left ventricle has to really stretch to get a good job. And you know, Val Salvador, [01:31:00] people don't realize it. Um, if you squat and dead lift heavy, your blood pressure could easily go up to 400, over 300 momentarily. While you're holding your breath and you're pushing out of the hole and you've got heavy weight on your back.

[01:31:14] For sure. For sure. Yeah. And that actually though, it's conditioning the heart and cardiovascular system really strong. So yeah, it's upregulating the plumbing, it's in the pump pumping. That's the difference between physiological and pathological changes. We, we have some of the same markers, but it's because all of our plumbing and our pump have been upregulated that they're like put in heavy duty stuff.

[01:31:41] And that happens over decades of training. That happens over decades of training. I did a life insurance test at 42. Same thing, you know, they come out and they give you the EKG and all that. And uh, I was, I was pretty ripped at the time and I think I was probably 7% body fat. [01:32:00] And had more muscle on and the BMI put me in the obesity risk.

[01:32:07] Oh, isn't that crazy? Yeah. I had to pay more. Yeah, and they have no idea that muscle is not the same thing as fat. They don't, they don't even take that into account. I'm 228 pounds right now, so I know that I'm in that like, Oh, maybe not obese, but. I'm definitely in that. You're, you're overweight. Oh, we lost the link.

[01:32:32] Hold on. I don't know what happened. I don't know if anybody could still hear me.

[01:32:42] That's really all I had to say. I can't open, I'm trying to open up the page and I can't get it to open. So we lost Joel and lost me. So we're going to end the show here and we'll see everybody tomorrow with more. Super human radio. Oh wait, wait. May be coming back. Maybe coming back. [01:33:00] It's trying to. Who knows?

[01:33:03] I see you tomorrow. Thanks for listening. .