Are your cells dying at the proper rate? Maybe not a question you've asked yourself before, but you should! Today the guys discuss one of Eric's favorite topics: the cell! And specifically, when a cell should die and when it shouldn't.
The good and bad of cellular death.
What is controlled vs uncontrolled cell death?
Love that mitochondria! (It's really the key to everything)
How do you keep those cells healthy?
And, what does cellular health effect? (Hint: A LOT).
You know what keeps those cells performing at peak rate? bioStak! (Eric made it so). Check it out for yourself at bioStak.com
And as always, if you have any questions on this episode (or any questions in general) don’t hesitate to reach out to us at firstname.lastname@example.org, or submit a question on www.lifeinketosispodcast.com.
And if you’re interested in starting your own journey, you can find out more information at biofitcoaching.com or on Instagram @biofit_coaching
Eric: 00:00 So we have a lot of things that can attack the cell and initiate apoptosis cellular death because you don't want a cell that's um, damaged or injured and not functioning properly to start functioning improperly. And when that happens, then you can have, uh, obviously mutations and the cells not functioning properly for the tissue or for that organ.
Chad: 00:29 They say a journey begins in a single step or in my case, one less piece of bread. My name is Chad and I'm a seeker. I have sought out an expert in the field of nutrition and fitness who I hoped would help me feel better. They call him the biohacker, but I call him Eric. I hope you'll join me in a path that leads you and I to optimal fitness, the body and the mind as we live our life in ketosis. This is the life in Ketosis podcast biohackers guide to optimal body performance
Chad: 01:13 Hello everyone My name is Chad and this is my quest to achieving the healthy state of being with a man that can get me there. My mentor and cohost, he has the science to my regular guy. The extreme testing to my, I'll take your word for it, the biohacker himself, Mr Eric Bischof, somewhere along this journey of ours, I realize that feeling better is really one part physical and one part mental and both are needed to achieve the optimal state of being what I call keto, happiness or ketosiness. And today we're talking about self destruction, cellular self distraction. That's true. And maybe, maybe self distraction isn't the best term for it, but I really wanted to be dramatic. Um, it's uh, yeah. And uh, and, and it's fascinating because this is something, Eric, I think this is something I don't hear many people talk about it at all.
Chad: 02:08 Um, you know, we probably talk about it most out of anybody that I've heard because we talk a lot about fasting, recreating the cells, right? Or regeneration. Yeah. Regeneration. And so, uh, but it's going to be interesting to will, I'm fascinated to hear like why our cells die and why is that important to us and how do we prevent it if we need to and all of that kind of stuff. So that's what we're going to dive in today. And I think it's, I think it's a really important topic, but before we get in, how are you,
Eric: 02:40 uh, doing pretty good. Not too bad. How about you? You were out of town, he went in Los Angeles, weren't you?
Chad: 02:46 Yeah, I've been in La. Oh Wow. They're shooting, uh, a conference kind of workshop thing. And so it's been quite a weekend now. You are, you home for a little while? Uh, back for a little while. Yeah. It's really nice to be home and get back into some sort of schedule,
Eric: 03:04 I wish he'd come back to nice sunshine weather, et Cetera. But man, we just haven't had a good week of good weather or leave in three days of good weather. It's amazing.
Chad: 03:16 Yeah. Well it's all right because my vegetable garden is looking really good.
Eric: 03:21 Yeah. I just planted my, uh, my cucumbers actually, and they're, they're the round lemon cucumbers. I don't know if you've ever had a lot of them. Oh, I've never had him to last year. I grew, um, and I, I think probably 30, 40% of what I grew up, cause I eat the heck out of them and they're so good. And I mean, I just, I, I've never seen him in the store. Have you? No, no, no. I've never been able to find them in a store like this, round cucumbers that are yellow and they are the, if anybody out there, you know, they're just the best tasting cucumbers ever. So yeah, I'm excited about that. We'll see. Yep. Me Too. And this rain's only helping them stay healthy and I know I have to look at the positive aspects of branding. I lived in Oregon 13 years and couldn't wait to get out of there because I loved it, but I didn't, I couldn't take the rain. Yeah. It's difficult. Yeah. I don't mind running in the rain. That's the only thing. It's strange. I don't mind running in the rain. Um, but other than that, I just don't have, I like sunshine. Yeah.
Chad: 04:25 Yeah. We'll, we'll, um, shout out to our Pacific Northwestern. Some of them love the rain.
Eric: 04:30 I, sorry, I shouldn't say that. I lived there for 15 years. It's beautiful. The smell is fantastic. The, the, the environment's fantastic. It just beautiful. Everything's beautiful about the noise of other people. People are no more of that yellow stuff that shines in it, in the sky. That's all you need. A little more of. That's it. Yup. Yup. Well, um, before we dive in,
Chad: 04:53 I want to talk about, um, because it's so poignant. I want to talk about bioStak. This, this conversation is so, uh, so related to bioStak you designed Biostak to be cellular health, right? To yes, you support cellular health and regeneration and all of that kind of stuff. So just talk really quickly if those of you who don't know and, and um, go to biostak.com check it out. This is a stack the Eric created over three years of research in self testing. It's five organic ingredients and its main, would you say its main purpose is cellular health?
Eric: 05:34 Oh yeah, absolutely. Yeah. I mean that's everything we're trying to do in our life. I mean everything and our body is trying to do, even though we, we, we don't know it unless you study it. And I figured it all out and that's my passion that I'm trying to do is everything comes down to the cell obviously. And everything comes down to keeping the cell functioning and operating at its optimal level. And the biggest thing in that or component or, or Organelle that does that is my favorite, just cell Mitochondria. The Mitochondria is the key to everything. Life, I mean in every organism. I don't care bacteria, I don't care. It's a, we've got to produce ATP energy and we have to lower what we call the uh, electron leakage, which in results and free radicals and free radicals have a good purpose. But we overdo them just in the environment we live in.
Eric: 06:36 And you just look around it. Our health status, obesity and diabetes and cardio disease and everything else. Obviously we are leaking a little too many electrons going down that electric transport change which converts to free radicals. So I'm free radicals give good signaling, uh, uh, for the cell to maintain its homeostasis and stay alive. So, bottom line is we're just trying to get cellular health at its best and keep the cells alive and avoid what we're talking about today, which is cellular death.
Chad: 07:08 So talk about, um, well yeah, that's great. I mean bioStak is addressing all of that. So go to biostak.com again, check it out, get a bottle for yourself, see how good you can feel. It's incredible stuff. We're getting really good feedback. It's been out almost a year now. And, um, we have a fresh new label on it too, which is fun.
Eric: 07:31 That's great. It looks very, very sexy. Does, but they're getting very, very strict about and what she can put on the label number. I was trying to put, you know, a free radical scavenger and antioxidant, this and this. And they're now a FDA is really cracking down on what you can put on the label, but basically cellular regeneration, there's the bottom line. So, so let's start with, um, why do cells die? What I mean? What is happening inside of our bodies? What is this death of this cellular death happening? Well, all cells have a lifespan, okay? And we know that, but all cells want to do what they want to divide. They want to become, you know, a parent cell into two daughter cells that reproduce. You got it. And just like us actually. And so we're continuously trying to regenerate and have new cells.
Eric: 08:30 Obviously, you know the cells through death, obviously, and a tissue. You want to keep a great community of cells working together and each individually working at its optimal level to maintain that tissue or organ at its highest capacity and so in, in actuality, when you think about it, what do we have about 50 trillion cells, I think for the human body. And, and so there's a lot of cellular activity going on. Everything comes from this out. We all know that. But in this cell, we also have very important components. We have the nucleus, the DNA obviously, but we also have what we call my favorite that Mitochondria. And there's what, what did I say before? In a 10 million billion a mitochondria. If I was a take the fat by my body weight, I would have about 10% would be mitochondria. So I have about 14 and a half pounds. Since I've been losing some weight, I have 14 and a half pounds of Mitochondria. That's a lot. I mean, if you really think about it, that's, that's, that's a lot of mitochondria in the body. And so obviously there's a purpose for this mitochondria. And remember the heart and brain probably is very active, used as has the highest content of Mitochondria and the brain uses 20% of our energy of ATP needs. So between the two, I think the heart and the brain, we're probably looking about to produce ATP to keep that cell alive, keep that organ alive, keep everything pumping and brainwork and functioning. The heart pumping is, I think the last I remember is about 13 1213 pounds of ATP a day to produce that. And so when you think of ATP, you just, you really don't think of it as something just as something that a phosphate added to an ADP to make ATP. And ATP, ATP synthase. And I'm an electrical arching, you really don't think about it, but if you want to wait it out, it's 13 pounds a day just for the brain and the heart. So those sickle, everything's going to come down to the south. So what we're talking about is why do cells, I mean cellular death. Okay. And we'd call that apoptosis. And, and you've heard me say that word and, and, um, some of a podcast, you know, I'm sure you're always for more familiar with autophagy So autophagy is actually getting in there and regenerating the Organelles, cleaning up the cell, uh, before it gets a signal or a, uh, uh, uh, pathway given to say, hey, this isn't going to cut it this, so, so let's do apoptosis and let's do a cellular death. Okay? So we do have a couple of different types of, of cellular death, and I think, um, everybody's familiar with apoptosis.
Eric: 11:32 I think most people are. And then, uh, that is what we call a programmed cell death. Okay. So you might just call it a controlled, uh, your bodies, you know, uh, in charge basically. Um, and it's going to give signals, uh, to provide that out of the cell to become, uh, uh, no longer, they're no longer participating because there's a reason. All right. But there is some natural developmental reasons that apoptosis takes, you know, care of besides the immune system, which I won't get into that. But you know, when, when a fetus or an embryo is developing on everybody uses this and, and you're familiar, um, to get your, your, your fingers and your toes, uh, you have to have apoptosis. So you have that tissue in between your fingers and your toes. Um, and so during the embryonic stage, when it's developing a pop tosa for take care of that tissue between the fingers and the toes and eliminate that tissue.
Eric: 12:42 So you have five fingers and you have five toes. So it, it's the separation. Um, in fact, uh, I don't know if you, I have a friend that his son was born without that being done on his toes. So he actually had webbed toes. So it apoptosis didn't take effect there. And so those, when he was born, the tissue was there. Uh, did he remove it? No, I don't know to this day I last I knew him. He was six, seven years old and he still had his web toes and his dad actually told me he thought that would be unique for him.
Eric: 13:25 He can go and have it cut and removed. But that does happen. So that's a natural development, developmental type of apoptosis. The other that isn't a program type, uh, of apoptosis is necrosis. And not sure if you're familiar with necrosis. I think you've heard of the word, but necrosis is the other way of cellular death and that's it. That's it. Uncontrolled unprogrammed type. So let's say that you have a big a trauma or a super big infection or a and big injury to something, some tissue or something. Then obviously that's a very quick death. It's not programmed. It's uncontrolled, a heart attack, um, hypoxia, stroke, things like that. So the cell just quickly, quickly dies because it's, it's, it's almost very traumatic to the cell. And so, yeah, so basically we're dealing with a couple, but we're talking about apoptosis today as far as programmed cellular death.
Eric: 14:24 Okay. And so, um, obviously we have to ask, why are you can ask me why or why do we have this? Okay. Um, well there is a purpose for it and you know, we do have things start out these, you know, Mike, one of my topics is, is reactive oxygen species. When we have those free radicals being produced in the Mitochondria, okay, we're back. You know where the electron leakage, when I say that word electron leakage, that's uh, an electron that's unstable, that is leaking from complex one and we'll get too sciencey. But it's coming from the elect transport chain and it's not making its way down to eventually get too complex for which you have an oxygen being the acceptor of these electrons and that will make water and carbon dioxide. But so what happens? You do have leakage. You know, it just producing energy and breathing and just day to day living, you're always going to produce and leak a little bit of electrons.
Eric: 15:28 All right? So when that happens, you get those free radicals. And so that's super oxide, hydroxyl radicals, which are the worst hydrogen peroxide and peroxides and uh, approaching nitrates and all these different free radicals. So what happens if they get too many and they start damaging the cell itself, not just the Mitochondria, which happens, which we'll talk about my Topher g, um, also, but basically that could be a signal to, you know, start to DNA damage. It starts to Lipid peroxidation of the cellular membrane. These free radicals, if they just get uncontrolled and not out of balance completely, then that can initiate, say, Hey, let's initiate cell death here. All right? Then the other's DNA damage. Anytime you get a mutation going in, you know, until the nucleus, which we know what can happen, uh, mutations. If they, if they're allowed to mutate and proliferate, then obviously it gets to a cancer type of developments. So you can have apoptosis initiated then to go ahead and kill that cell, which is what you want because you don't want a mutated DNA to become a proliferating into cancer. Then there's other things like infections and viruses that are attacking the cell. We have stress, you know, environmental stresses, toxins, um, things like that that are attacking the sound. So we have a lot of things that can attack the cell and initiate apoptosis, cellular death because you don't want a cell that's, um, damaged or injured and not functioning properly to start functioning improperly. And when that happens, then you can have, uh, obviously mutations and, and the cells not functioning properly for the tissue or for that organ. So you, you, you need to have cellular death.
Chad: 17:29 Okay. So there's the natural life cycle of the cell. So what, what kinds of other things kill it? It's like in cells be killed by things that we do or take into our body or in what other causes of cellular down
Eric: 17:45 environmental toxins, pesticides, poisons, things that are going to attack the cell. All right? Uh, and injury, trauma, all those things, infections, all those things. You know, diseases basically when people are dying, obviously the tissue cancer and whatever, um, degenerative diseases, it's harming the tissue. Uh, the cell, the joint, whatever. It's basically going to the cell and causing damage to the cell. And what happens with age like myself is obviously, you know, when, when, uh, to many of the cells start dying off and they're not producing new cells. My ptosis, which is, you know, the generation of new cells, um, the tissue obviously is going to shrink and it's going to become not working very, very viable, you know, to keep the other organs in the body alive.
Eric: 18:40 And so our, our whole, you know, our Ho ideas to just keep, you know, we want cells to die off and regenerate, you know that we want proliferation of good cells. My ptosis. Okay, we want that, but we don't want healthy cells getting attacked for no reason. Okay. And so the bottom line is trying to keep our, our, our cells function at, at its optimal level. And we do that of course through Mitochondria and everything else. But how we have different cellular desk real quick. So on some of them, you know, we have the cell and then this is where mitochondria comes back in because Mitochondria plays a role in initiating. So you learnt death. And so we have what we call intracellular, um, programmed death. And we have extra cellular, and we call it x, external, extrinsic, and intrinsic, but it's outside of the cell, inside the cell. Uh, then we have actually inside the matrix of the Mitochondria. So we have different ways of getting signaling pathways to initiate cellular death. So how does it do it? Um, it's basically what we call a caspace, a mediated, and I'll keep this really, really show. And so, so what happens to say, let's say intra cellular. Okay. Intrinsic. Okay, we're going to have a controlled death is coming from within the cell. All right? So we have to have something initiating, a signal to tell the cell. Let's, hey, we're, we're, we're, we're going to do apoptosis. We're going to have cellular death. So what happens in the Mitochondria, you have the outer membrane and you have that inner membrane. And inside that inner membrane, we have those electric transport chains. And I'll make this really quick. We have what we call cytochrome C it complex for remember cytochrome c is that it takes the electrons from complex three and just moves it to complex for this is called the reduction.
Eric: 20:41 All right? But so complex for the cytochrome c actually takes those last electrons and now oxygen excepts it shoves protons up into the Proton Matrix, a gradient, and that comes back down with all the proton gradient being forced down to produce ATP. So that's very life giving. I mean we have to have cytochrome c but also [inaudible] c is what initiated the death of the cell. So here we have it producing life, okay? Through the ATP complex four and now it's this molecule's being used to promote death. And so how does that happen on the outer membrane of the Mitochondria? Don't do this real quick. There's what we call the BCL two that is what you call an anti eight a pop toxic. Okay? So it's actually protecting anything from coming through the Adam Membrane and it's actually keeping anything puncturing or it's keeping it more, less, uh, uh, where things can't get through it to cause, you know, uh, damaging to the Mitochondria itself.
Eric: 21:53 Okay. So what happens when when something's initiated, we usually get a something from the nucleus, like the pee, he heard me talk about the TP 53, that p 53, that's a tumor suppressor gene and that usually goes out and tries to fix any mutations or anything that's going on, uh, as far as repair. But it also can say, Hey, I'm going to initiate a cellular death apoptosis. So what happens real quick? That P P 53 initiates p p 21, as I remember correctly, and that initiate a protein called backs. All right? Be a acts and backs. We'll go to that outer membrane of the Mitochondria. And you have the BCL two there. That's actually we tie a pop Todrick versus pro a pop tonic, which is back. So that's saying, Hey, I'm going there in the backs, adheres to the membrane. And it actually, they say it, it creates a channel.
Eric: 22:53 It pump, it punctures the membrane at different spots. So it is now stopping inhibitor, which is BCL two and backs is, hey, I'm here to promote cell death. It punctures it and then all sudden that cytochrome c I talked about, we'll just come right through that outer membrane. It crosses through the inner membrane and that's where it's leaving from. Then it goes out of the outer membrane and when that goes through, it initiate what we call a casp pace, uh, uh, pathway and the caspace nine, then that initiator caspase three, and it goes through all these a path. One, I won't go into all the, uh, chemical pathways, but eventually says, hey, the caspase three takes off and starts, it goes to the nucleus, goes into the DNA, starts destroying chromosomes and everything else. Other components start getting degraded. And then you have macrophages, the auto, uh, uh, phagosomes come in and do a cleanup and recycled through the lysosomes.
Eric: 23:52 So that's one way of cellular death, intracellular death. Does that make sense? I hope I'm wrong. I'm sorry, but that's fine. That's Mitochondria. Now the Mitochondria, it initiates that cytochrome c to initiate cellular death. Okay. Then the extra cellular, same thing, we call them death receptors and I'd just make it really brief. Death receptors and death activators on the cellular membrane. This is extracellular extrinsic and that will initiate the same thing. Once it death activator is on the death receptor at the cell. It actually initially, uh, initiate cap paced eight, which is different than nine and caspase and it goes to three negotiates his same kind of death caspase. Caspase mediated goes after the DNA, the Mitochondria, everything organelles and starts to kill it. Okay? So that's, those are a couple of death ways. Then there's one that works in the neurons and they called it a pop tonic inducing factor and that just straight from the Mitochondria Matrix and that'll go out to the nucleus and kill it. Okay. So anyway, those are a couple ways that we have pathways for cellular death.
Chad: 25:06 Okay, so let's bring it to the ground, bring it to the, to the sidewalk. Like why do we care about cellular death? Obviously there's natural cellular death, but then there's things that we can do to induce cellular death. Why do we care? Like what's, what are we, what, what are we going to feel or notice in our everyday life? Um, whether it's overtime or immediately if we are prematurely killing off cells.
Eric: 25:37 Okay. And, okay. And that's a very good question. Do we feel it all the time? No. No. Okay. So cellular death happens because it's pro, you know, the cells are going to die. Okay. All right. So there was that turnover of cells. All right. Um, but overall the issue is when, when you have unhealthy cells functioning and usually that's a derivative of a dysfunctional mitochondria. Okay. Because the Mitochondria without ATP energy and with those extra electrons leaking that are producing those free radicals that are beyond the bounce that you should have. Okay. Then obviously that's going to start the degenerative diseases, that fatigue, you know, basically everything is a derivative of coming to the Mitochondria again. And that's why I have such a passion for the Mitochondria because the Mitochondria is the key to keeping the cell alive and functioning. Okay. And so bottom line is we don't need extra cellular and, and death is good because if it's a mutated type of mutation hitting the DNA, we don't want those cells to duplicate. Okay. We don't want that proliferation. So we want good apoptosis taking place. So apoptosis is a good thing, but when it gets out of balance and it's not a good thing because if it has to go in and kill off good cells that cause the mitochondria sticks function or the reactive oxygen species free radicals are attacking everything in the cellular membrane and everything else and wreaking havoc, then we don't want that.
Eric: 27:20 Okay. Uh, eventually if you lose too many cells, the organ will will shut down and you eventually get a disease and you're on a path to, to death basically.
Chad: 27:32 Gotcha. Okay, great. So, um, obviously there's ways we can regenerate cells. Um, one of my questions about cell regeneration or I guess cell, cell health is actually, it's more about reproduction. Does the cellular reproduction, does it start to diminish as we get older?
Eric: 27:55 Yes. Uh, and that's, that's what we call my tosas. Okay. And when, when we had the cells cycle. All right? And creating new new cells as we age, that diminishes on and what causes that diminishment is basically we back. I, you know, I sound like a broken record, but we're back to the Mitochondria. Okay. And when we get to the Mitochondria, what's so key to keep that cell going? Obviously first of all, his energy.
Eric: 28:26 Okay? We have to have ATP to make a new cell. The cell cycle requires a lot of ATP. And so when these parents house break off to have daughter cells, all right? It requires a lot of ATP, but when they break off, they have, they obviously have to take, Mitochondria will each daughter cell. So they want to make that pretty even because you don't have dysfunctional Mitochondria. I say they're all dysfunctional in that style and the cell hasn't died. Then all of a sudden this cell splits and now you've got two dysfunctional daughter cells with dysfunctional Mitochondria. So what the, what takes a lot of energies that might, when that cell divides, it's got to take an even amount of, of good mitochondria otherwise weren't daughter cells. Going to be at a deficit and that cell isn't going to produce and it's not, it's, it's basically going to die and you don't want to reproduce with bad mitochondria.
Eric: 29:26 Okay? So everything comes back to what you know, and we talk about autophagy a ton, but we will never concentrated on my Tawfiq g. Okay, so you, you could guess what my topic g is. I said autophagy. It's the Mitochondria self digestion. So Ron Mitochondria to be self digestive, because remember your Mitochondria only lasts in, I think in the liver. It's a couple of dailies. Okay. Uh, the heart's a week I think. And then the brain's like four weeks or five weeks. So the Mitochondria is always being turned over. So you want my top witchy because you want to the cell to be allowed to dispose of any underperforming Mitochondria. So the quality of the Mitochondria is maintained at the highest level you can have. So in chronic health, my topic g is not taking place like it's supposed to. And so many of the Mitochondria become dysfunctional and they struggle.
Eric: 30:28 And so they really become beyond their use. And so when we struggle, what happens? That's a low energy output, that electron transport chain and it starts to increase more reactive oxygen species, more free radicals, which will increase the damage, dysfunctional Mitochondria. So it's really a, a vicious cycle. And, and I don't think I've ever talked about it, but what's cool in the Mitochondria, you when, when I say Mitochondria too, what do you think of the Mitochondria in the show? Do you think it's just sitting there doing its job or is it moving around?
Chad: 31:04 I mean, I guess I've always just, I know that this is a logical, I've just always imagined it as like the nucleus, like,
Eric: 31:15 but remember Mitochondria are constantly moving. They're actually on tracks and they have these protein motors that move them through, uh, Moreau basically. So you want the Mitochondria, if you, if you've actually seen him, a film of it, it's really cool. They're just moving. Then I'll send you see some that are in really dysfunctional cells that are just stagnant. Okay. So what makes it move? You want this? A Mitochondria always moving. And we have that, that fusion and vision that I really haven't talked about before. I don't think, I just probably just never got into the, at that point. But Mitochondria constantly undergoing fusion and vision to help maintain the quality of the Mitochondria. Okay. Just keep everything function properly. All right. So few Gen, you know, real quick, what fusion, obviously you're fusing more than one mitochondria together. So now they're discovering that your mitochondria, instead of these just floating around these little Organelles, you know, that are weirdly shaped, okay? They're actually fusing together for a purpose and it becomes elongated and it's actually becomes more productive. So let's say when it fuses with another one, let's say that it, we want fusion, okay?
Eric: 32:31 And we also want fusion, but we, we want a certain amount. Okay? So basically it went, it went, when you see all these, um, fusion, they're the merging of the Mitochondria. Okay? It makes one big single mitochondria. Okay. Which becomes better at, at operating, uh, then Wapa sit. Is that Finjan I said that's the splitting off the Mitochondria into smaller Mitochondrias. Okay. Uh, so they, they, they're constantly dividing and combining. Okay. And so when we do this, the, obviously you've got to divide with healthy mitochondria so it can choose, offer a fuse off, you know, and say, Hey, are, you know this, this part of the DNA is an operating cause every mitochondria has its own DNA. It can actually fuse off or it could pinch off and vision and pinch that off. Okay. Then my Tawfiq, she can come in and clean it up. Okay. Or it could say, hey, let's make this one stronger infused with another and another and another. Then all of a sudden you, you just kind of dilute that bad, uh, portion of the Mitochondria. It taken over by all the good DNA and, and, and components in, in the new Mitochondria. So they're constantly fusion and fission is happening all the time. But the only thing, we don't want to be careful that you don't want too much vision because then if it breaks off and all you got is these singular mitochondria and not moving around, then they're not going to be functional. They're not going to be functional. And so you're always trying to, uh, fusion was what it, you know, it, it has a balance of homeostasis. I mean, too much fusion. You can get what we call contagion Mitochondria, which basically contagion is, it has when you fuse, uh, I might have bad mitochondria with another bad mitochondria, then all of a sudden they started to spread their dysfunctional components to healthy ones. And so that's like a contagious disease. They call it contagion. Okay. Mitochondria. So you want to avoid that. I don't wanna go too deep and efficient infusion, but bottom line, we've got to have our mitochondria continually moving. Okay. And divide and Fijian and feuding fusion fusing together to make a stronger mitochondria. Basically wish I could stop for a long time on it because it's such a fascinating, uh, by a chemical process.
Chad: 34:57 Yeah. Yeah. And I think people like the biochemical I, how do we, um, what are ways that we can promote mitochondrial health and s and cellular health so that premature death or dysfunction or dysfunctional fusion, all of that guys, can we present that day to day?
Eric: 35:20 That's a really good question. In fact, because you do you one thing, you have to understand everybody. I mean, and I'm on the Mitochondria hypothesis all the way, okay? Um, we don't buy our years, okay? We really, really, really, it's engaged by our free radical leakage. Okay? Those are the electrons that are leaking at will. Cause remember all the oxygen's the acceptor and you lose 4% member. Every free radical has to be, you know, most that's attached to an oxygen. Okay? So we'll lose up to 4% of our oxygen, uh, to, to free radicals. Okay? So everything you, you're aging by free radical leakage. And how do we produce more mitochondria are, and as a great question, because when I do genetics at first, you know, I do the first evaluation. One of the first things I look at is the PGC one alpha.
Eric: 36:22 And this is required for mitochondrial biogenesis. All right? So that's the process of producing new Mitochondria. All right? And what are the two best, I mean, what helps you produce more PGC one alpha. And you'd be amazed, Chad, how many of those have a mutation in this? So they're already at a, a, a, a deficit and they don't even know that they're not producing new mitochondria. You've got to produce new mitochondria just to, to stay alive. I mean, to stay longevity. I mean, life, life expansion has been proven. So two things, exercise and calorie restriction will express more PJ's PGC, one alpha. And you know, keto, I mean it's, you, I know you've heard me say calorie restriction and promotes a lifespan in every mammal. They've tested it. Monkeys Fried Evanston, right? And so we're back to fasting again and uh, it promotes calorie restriction and why we remember on that electric transport chain, the only thing it's getting electrons from to pass to produce that Proton gradient is from your food.
Eric: 37:37 So if you're restricting your calories, what are you slowing down? You're slowing down the electron transport chain. Those electrons being passed from complex one because you're not allowing the food to come in all day long, okay? To have that electron leakage, it, they're always going to be some, but you want to keep the flow of electrons. That's the whole key to life right there in a nutshell. It's the flow of the electrons guys. And you don't want them leaking. You want them going from one to complex, two to three to four to oxygen, pushing those protons up, making that ATP coming back through. You don't want them to leak. That's the big thing. And so that's producing one alpha. Then [inaudible] is another promoter that's kind of your, your nutrient sensor that I've talked about and that actually through low energy, you two working out, you're calling that amp k to say, hey, give me more sub straights but I'm low on producing ATP so guess what?
Eric: 38:39 I'm going to make more Mitochondria, so more Mitochondria biogenesis. So through forcing amp k through exercise and working out of course, that's why I'm on a high intensity guy cause I am pushing all the Mitochondria biogenesis I can because I want more mitochondria. And you know, they've done it as a centenarians. They know they've tested them and they found that there's actually, there's, they have a mutation actually dealing with, with um, the complex one. And so context one that is, we're on most of the free radicals are leaked out of and they have less leakage but just a little bit, but over years and years and years of living it, it makes a big difference. And that's why they live to a hundred years old. They're just discovering these things. So, you know, we're, we're, we're really onto a lot of new things about the electrons guys. Yes.
Chad: 39:32 So, so, so your health is doing obviously everything for us. It's creating vitality of life really. I mean, it's, it's, it's longevity. Um, it's how we feel through that longevity, right? I mean, we're, because obviously there's Mitochondria in every organ of our body, including the brain and the heart. Um, and um, it's, it's energy, it's clarity. It's, um, you know, all of these sort of Muscle building, right? Um, being able to utilize and burn fat if we're fat adapted. Um, and so, so I just want to be very clear, like, why, why we need to understand this science and this process of cellular self destruction, but also cellular health and regeneration and rejuvenation through autophagy. Right? That is one of the biggest benefits we get from fasting and the acceleration of autophagy
Eric: 40:35 and my topic g the Mitochondria. You want those. If there are any dysfunctional mitochondria, you want my Topher gt come along and say, Hey, I'm getting rid of you. I will break you down. I will use those components and I want to keep healthy mitochondria constantly. So my top a g autophagy and pop ptosis, fusion, Asian all have to work together. They all have to work together and in. And the key is it got to get to the Mitochondria. You really do. You really do.
Chad: 41:05 Yeah, I think about, I think about like, um, the forest. We spend a lot of time outdoors and um, you know, I've been learning a bit recently about the health of a forest and the lifecycle of a forest. And this just, our conversation kind of reminds me of it. So I'll give this kind of analogy is like us, how a healthy forest has a lifecycle and fire plays a really big role in that lifecycle. If you prevent fire in a forest for too long, the forest becomes very unhealthy. You have issues with beetles and you have, uh, you know, issues with trees that become too old and then they become a danger to the other trees around them through falling and I'm rotting and all of that kind of stuff. And so you have to have a healthy amount of chilling off the forest basically, um, to, you know, a healthy amount of that to regenerate it and get new growth.
Chad: 42:07 And, you know, and then that obviously plays a huge role in the, the rest of the health of the forest with wildlife and the other plants and, you know, all of that kind of stuff is just, it's destruction or death that has to happen to recreate or, or keep alive the, the entire, um, the entire system. So to me, just as you were talking about this, it feels very similar to that, where there is this process that happens within a swear cells need to die, um, to be able to read juvenate and re come to life and build up. And, um, and so this natural life cycle, however, uh, in the forest, that can happen prematurely right by man or, or lightning or whatever. Right? And it's not always the, it's not the best thing for that to happen premature the, or too late. You've got it in, in a forest, right? Because then you create danger and, um, you know, all of that kind of stuff. So I just think it's interesting to think about that. Like all of this is life and all of it's site. Colon is as much as we can promote the healthiest cycle that the healthiest of timing, he bet. Um, and we're better off than, we're more happy. We're clear, we're have more energy and, and I just think we would live a more fulfilling life.
Eric: 43:31 No, in fact, he made me think of something in just in the Mitochondria by itself, let's say there is, you know, uh, through calorie restriction, you actually decreased the half life of Mitochondria member. I sit on liver one to two days. Mitochondria is always been, you know, uh, through my topic g turned over. But through calorie restriction, like, like, like ketosis. A, you're actually shorting the lifetime of the Mitochondria, meaning that you know, it, it, it's actually going to, yeah. Cause if you, if he got too long a life time and you know, you're just, you're dietary, you're an excess and you're always eating and the Mitochondria light, uh, uh, uh, half life is longer, gives more time for, to become deficient and, and, and not functioning. So you increase that Halflife, that shorter living of the Mitochondria, your Mitochondria actually, it's, it's more healthy and the integrity of it, it's, it's better and everything else.
Eric: 44:28 So it's kind of interesting on some of it. You, you, you kind of want really move that shelf life pretty fast.
Chad: 44:33 So yes. Let's just recap really quickly as we close up. What are the ways that we can promote cellular health? Are a diet obviously, obviously, and um, you're, you can test and I tend to agree because I think you're pretty Dang smart that keto is the best way to promote cellular health. Um, uh, exercise is really important. Movement is really important for cellular health, for that Neuron, cellular health. We want that there. Okay. Okay. Yup, Yup, Yup. Getting, getting, getting nutrients that, that aren't readily prevalent in your current diet. Obviously that's where biostak comes in. Super important. Um, anything else? Just as a list, not stress.
Eric: 45:29 Yes, everything is going to come back to the functioning of your mitochondria and yourself to keep the cell functioning properly. And it's stressors. I mean he, and you know that better than me. You're dealing with people and on that kind of coaching and I'm liking the most nutrient dense foods and everything else, but if I operate under that umbrella of constant stress, that damage is very damaging to the cellular components. Very much so. You know, you're just constantly under stress mode. So, and sleep of course.
Chad: 46:06 That's a great point. And here's the thing too. We know the more you move and exercise, the better your diet you're getting the nutrients you need. Yeah. Plus add in meditation, quiet time, prayer, any of that kind of stuff. We know scientifically that those things without a doubt, lower stress levels. Yeah. So it all works as a beautiful kind of system and package together for cellular health
Eric: 46:37 and bottom line if you can get, and I don't get it, you, I shouldn't get sciencey, but we have to keep our ourselves, our mitochondria and that low reduction state. Okay. And passing on electrons, obviously they call it reduction, but if you can control the flow of electrons by in, in calorie restriction. That's why I'm one meal a day now and I love it. I'm staying longer in a facet state and due to the science and the research and everything that I'm studying about the Mitochondria, it's, it's, you really realize how key that is just to keep that electronic flow really running smoothly and keep them from leakage. That's why I had that antioxidants, the free radical scavenger. But there is a balance between, you know, the pro oxidants and anti auctions. We always have to be concerned. I don't want to be just totally antioxidant antioxidant. There is a balance because there is a purpose for, for these free radicals cause they're signaling molecule. They are signaling molecules to do things like a pub ptosis. Okay. And my end, my Topher g so you just got to get to the bottom line of controlling your mitochondria. That's longevity. Uh, it's becoming improving more and more by all the studies. I look at that. Yeah. Yeah. That's great. That's great. And I appreciate getting to talk about, yeah, I love a topic. Gee, I love my topic. G and apoptosis is key. It really isn't trying to control it because it is programmed, but, but you also can do the right things to keep it under control.
Chad: 48:11 Yeah. Well, I know we got super deep into the functionality of the cell and how its lifecycle, but I also hope that was interesting. I also hope people are coming away knowing how to promote cellular health and why it's so important. Um, especially as we, man, we're in the age of cancer where like in the, in the era of answer and um, and that's a big deal. And um, it doesn't impact you fully until you're experiencing it firsthand with somebody either that you love or yourself. And, um, at that point we're going to wish we did some more to create more cellular health. Right?
Eric: 48:51 It's like Alzheimer's. You know, we do know that it's a glucose related issue that's not getting glucose. And obviously the Mitochondria is not kidding, a fuel source. What happens? No ATP cells start to die, neurons start to die, they don't operate. Everything has to operate with some fuel. And now they know with Alzheimer's. So obviously ketones, I mean we all know like gives you, we could give you 70% of your energy to, to your neurons and your, your brain cells. And so bottom line, it all comes down to we need energy. We got to have ATP to keep ourselves functioning and vibrant and, and, and, uh, proliferating and, and continuing life basically. So yeah, that's a good point. Good point. Cause it all, you know, rheumatoid arthritis, diabetes, I really comes back to you don't produce enough energy to keep things functioning, your Beta cells, things like that. Everything has to have the energy production and energy. Cause the might've, it does a lot more than just energy production. But that's another podcast.
Chad: 50:02 Well. Uh, I I want to thank you for, for biohacking with us today and I, and I hope this has been really helpful for people. It's, I found it fascinating and enlightening. Um, thanks for all your work that you do on it and thanks for biohacking with us Eric. I appreciate it. And I want to thank all of you for joining us on this quest for optimal fitness. If you're ready to begin your own journey and live your life and Ketosis, be sure to check out biofitcoaching.com or biofit coaching on Instagram that handles @keto.biohacker lots of great tips and tricks and a, and you can just connect with Eric there. Also, if this podcast has helped you in any way or entertain you, we encourage you to go to iTunes or wherever you get your podcast, leave us a five star rating and a review so we can reach more people. And finally, the greatest compliment that you can give us is sharing this podcast with your friends or family, those who need it the most. Those are the who are looking for a different way of living, both in their body and in their mind. And until next time, stay keto.