12/19/18 E68 Keto and Cancer

Eric wants to tackle a difficult and sensitive topic today: cancer. This is one that hits close to home for him, as it does for many of our listeners. So what exactly does the research say about the relationship between ketogenic nutrition and cancer? 

What causes cancer has undergone an evolution.

Why talk about cancer on a keto podcast?

How Eric starts conversations in the locker room...

The interesting origin of carcinogens.

The science behind cancer and how it spreads.

Using that science to combat the attack in the mitochondria.

And how ketosis can increase the odds in your favor.

Eric also discusses how cancer was one of the driving forces behind him creating bioStak. As he says, it's all about that mitochondria. Go to biostak.com and use the promo code bioChristmas to save 30%!

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Eric: 00:00 When you knock out the Mitochondria, you knock out that oxidative phosphorylation and that cancer cell has to be really aggressive on getting glucose and glutamine to survive.

Chad: 00:10 It's 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 owed would help me feel better. They call them 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 and ketosis. This is the life and Ketosis podcast, a biohackers guide to optimal body performance.

Chad: 00:54 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. Here's 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 realized that feeling better is really one part physical and another part mental and both are needed to achieve the optimal state of being what I call keto, happiness or ketosiness. And today the subject, uh, people need to probably just sit down and buckle their seatbelts a little bit. Um, this is, this is a big one and it's a touchy one and we've been wrestling with this one for quite a while, Eric, right? Um, and, uh, and this has been a longtime coming and, and Eric has finally kinda given me the green light of, of go. He, he feels like he's a crammed his brain enough. He has not enough, I won't say enough, but a sufficient to have this conversation. Um, but today we're talking about cancer and um, we're just on the forefront, both Eric and I wanted to make sure that we expressed, um, how we realize that this is an incredibly sensitive topic. Um, lots of people. I don't think there's, I mean there's nobody today, right? That hasn't had their life touched in some way by cancer. Whether you personally have experienced cancer or somebody very, very close to you has experienced or is experiencing it and we're just in that day and age, it's, it's kind of crazy. And um, it is something that unfortunately is knocking on all of our doors. And um, and so we just wanted to start this conversation very, very genuinely, very, very upfront and let, you know, we understand the sensitivities.

Chad: 02:59 We understand that if you can't listen to this, if it's just too close to home, don't, don't feel any shame and pushing stop. Um, but there's also some really valuable, I think, some really valuable things that we're going to discuss and some, some incredibly important findings. Studies, um, preventive care, uh, all of that kind of stuff that we're going to talk about that can really help people. Um, so I, I know you, Eric were very, very concerned about this and so as I, that we just don't, we don't want it to feel like a flippant conversation of like, oh, it's so easy. You just do one, two, and three and cancer's not a problem. Um, there's no, there's none of that pretending at all, um, but it is as touchy it is as it is because it is knocking on each of our doors. It's an important topic for us to address and lucky that we now have medicine and science on our side, um, to help us understand cancer better and, and even though we don't have it cured yet, there are some things that we can do to manage it in our lives. So deep breath after that, after that intro, how are you, Eric?

Eric: 04:17 Doing good. Doing good. You know, this subject I've avoided because I've actually learned my lessons in the last three years of voicing my opinion sometimes a little too strong to those that are touched by cancer and I didn't mean it in, in, in a way that, hey, you know, what you're doing is wrong and what I'm telling you know my voice and my opinion that I'm right and you're wrong basically. So I learned that, you know, there's, there's a way to approach it and talk about it and, and sure, I have my, my belief, this is my opinion. This is what I've learned in research and I feel really good good about and I basically, you know, connected to it and so what we're talking about is in everything, we have a lot of different hypotheses. Okay. And so it in even in cancer, but if we go back to the hypotheses, remember the Diet heart hypothesis we talked about and so keys the saturated fat. Okay. Everybody jumped on that hypothesis and then it became, oh, it's not the fat, it's the cholesterol. And then all of a sudden it's not the total cholesterol. That's the LDL cholesterol is causing atherosclerotic disease. This is the hypotheses. And then it becomes, oh, it's not bad, it's the Ldl particle total count than another hypothesis that's been there for a few years is it's now to cause heart disease. It's the platelet aggregation that causes it not anything to do with cholesterol. So these things change. Even, you know, a sodium hypertension was salt and different things change. And so as myself, as someone who does research and, and I and I have a lot of passionate about different things, I also have to say, hey, here's the hypothesis, incorporate that, look at it, research it, and then obviously like you chad and others out there when it comes to certain hypotheses, you, you connect with one or you believe in one.

Eric: 06:18 And that's why I'm trying to say this is what, what I've studied and what I've researched and I think a lot of you out there. No, no, no. This hypothesis that we're going to talk about the difference of the cancer causing hypotheses. But you know, I just want to, you know, come across it. I'm not an expert at this and I've read the books and I think most of you know, I think I first got in touch with the book a three, three years ago. The first one I read was tripping over the truth and I've talked about this in podcast by Travis Christofferson and that was like three years ago. I read that. And then I went deeper and went into everybody knows Thomas Siegfried. Most of you do, somebody would do out there and his and his follow up all the way back from Otto Warburg and his books like cancer as a metabolic disease and that's a little tougher book. Then there's a new book, I just read them maybe eight months ago or it's Keto for cancer. So, um, by uh, I think her name was calomine or something, but anyway, it's a guide with keto with cancer. So we do know that through, through research that keto is connected, you know, Ketosis is connected to cancer. But, you know, I've learned, I've talked to people and I remember being in, in the, in the locker room at, at, at the gym, and I heard a gentleman my age talking about his cancer. He had colon cancer and he was talking to another gentleman, you know, next year everybody's just dressing up to go out. And I just interjected myself in the conversation because I couldn't, I just couldn't help myself. And he was suffering. He went through chemo obviously, and he, you know, he's still struggling with it and talking about, you know, and I just asked him, I said, well, what do you eat? And he said, what? And I said, well, what foods do you eat? And he just looked back at me. He said, uh, my doctor just told me to eat whatever I want basically. And I said, what kind of foods you're eating, but the foods he was eating was, you know, processed food, whatever, you know, a lot of glucose, a lot of sugar, different things he was eating. And then I started to interject myself into, into telling him about, you know, the cancer and the hypothesis. And then I just, I learned from that conversation that then I just couldn't, should have just kept my mouth shut and know you're trying to help somebody. But then again, you're coming across telling him that his doctor, his oncologist is wrong. And, and I really have to. And that's why I've avoided this conversation because I have, I've talked to an oncologist and I, I, I have friend that's an oncologist, I, I'm always sharing this, but in, in my defensive oncologists and learning from them, is it just, they don't understand, most of them do not know this, you know, or have taken a look at this hypothesis mainly because time, I mean they have hundreds of patients. They're continuously in their own education. They're there, you know, keeping up on the pharmaceutical medications that they have to stay up. They just don't have time. I mean they get locked into this one hypothesis, the somatic mutation theory and they just, that's where everybody's going. So anyway, I'm just going to talk about it, you know, and we'll talk about cancer and in fact I don't mean to come across as an expert at all.

Chad: 09:38 Okay. So why are we talking? I think this is a good place to start in. A lot of people might be wondering this, but why are we talking about cancer on a Keto podcast?

Eric: 09:49 Because there's, there's what is the cause of cancer. Okay. Obviously if, if we could cure it, there is no cure. Okay. We wouldn't know the costs because we found the cure for. All right, so just think about it, the last 40 years when they declared a war on cancer, Nixon all, alright, there's been over I think $90, billion dollars plus spent on the research and the treatment of cancer. Um, and you know, we got into the genome, the DNA, um, projects and everything along the way, but there's really, they made some advancements and I'm not going to tear, you know, I'm going to talk about those, those different, a hypotheses, but it's been going for so long and, and we have made it some improvement on some of the cancers. But overall it's really, in my opinion, it's, you know, through research, it's basically failed pretty much into, you know, to have that much money and that much time.

Eric: 10:54 We all expected it to go faster because once they got into the DNA, say no, that's the mutation issue coming from the genome, your nucleus causing cancer. They took off and ran with it. That systematic loop mutation theory and that train's been going so strong and so much money and research and oncologists and, and meds. It just teaching this and every hospital. Uh, I, I just, you know, how do we, how do we change that, you know, obviously through success. Okay. Something that's going that is, is working, okay. And that's what we're going to talk about. But, and that's in keto and ketosis plays a role in the hypothesis that's been carried on from Otto Warburg. Um, and, and obviously ketosis plays a role in that. Then we'll talk about. But.

Chad: 11:43 So let me make sure I understand what's happening here. So you're saying, I mean in the grand scheme of things, we are still infants in understanding cancer and, and how it's, what, it's, what it's caused by, what, how, you know, how we treat it, how we obviously, how we cure it. We're not even, I mean, I don't know how close we are there, but um, but, but we're just, right now we're, we're kind of just throwing darts.

Eric: 12:12 I mean the research is, I mean, it's, the path that they've taken is it starts back, you know, you know, a story that I remember reading in one of the books a long time ago. It starts back when that first discovered carcinogens. Okay. And we have all heard of carcinogens, those are something that's going to cause a mutation of the DNA of the gene. All right? It could be different, you know, toxins and we all know there's like benzene and, and different, um, uh, carcinogens, PCB and, you know, different, um, uh, uh, carcinogens that could cause cancer. Well, when we get back to the carcinogens get back to carcinogens when the first one basically was discovered was by a gentleman named pot and it was 1775 and he was a surgeon in London and that was during the industrial revolution. So it was pretty, pretty rough times. And he was in, in the slum areas and he used to, you know, as he tells the story, he'd walk the streets and there's people living in shacks. And it was really a terrible situation. And obviously one of the first things he came across, I was reading the, uh, girls that worked in the, they call it a match plant. They had this Fauci jaw, they called it. So anyway, it was chemical poisoning. And so it literally, they put them in the dark and they'd open their mouth and if it glowed green, a greenish color, they, they'd have to remove that bone, otherwise it would just get really infected and become upset and just organ failure and they would die. And so as he continued, he, he noticed that there was an issue with the chimney boys and those were the ones that cleaning the smokestacks and as the chimney boys were used to the orphans are misfits or whatever, and they basically were coming up with these warts on their scrotums and basically people wanted to just pass it off as warts because they're up and down. The chimneys completely covered with soot oil and everything else. So they kind of pass it off as syphilis, but he wouldn't give up on it. So he started visiting and we went to their, you know, where they're living, they're just stacked on top of each other. They were kind of the really the poor kids and they weren't able to clean up. And he realized then that it was the soot that actually was causing a growth which would lead to cancer. So that's kinda the first carcinogen out there. So I thought it was kind of a cool story when I read it a while back. And so, so that's what we're coming from is we have to go where everybody is today is the somatic mutation theory saying that cancer is coming from your nucleus. Okay, that's in the cell. That's your DNA though.

Eric: 14:52 That did DNA suffers some kind of mutations aided by carcinogens or acquired mutations or you know, uh, or inherited mutation, something that comes from your, your, your, your parents. And so that is what starts the mutation. And then that starts into the sale. And all cancer is uncontrolled cellular growth. That's what a tumor is from. Okay. And so it, and there's a couple, you know, what we call cancer, a couple genes that really play in the role of cancer. And I think you've probably heard these and others, they're onco genes and their tumor suppressor genes. And so what an oncogene is, it starts out as a prototype oncogene, which basically is, remember ourselves, have to grow, they have to multiply, they, they, they, they have to duplicate themselves, obviously continuously for growth. But when that protocol Onco gene becomes a change or mutation alright, it becomes what they call and badging or it's becomes turned on, it's activated and it's not supposed to be. So when this sale starts to grow uncontrolled and out of control, basically it could lead to cancer. And this bad gene is called Onco genes. So that's why you always hear the word Onco genes in cancer because this is something that's causing uncontrolled growth. That's why a tumor metastasizes, okay, it just cells, just dividing and dividing. And sooner or later becomes a tumor. Then obviously you know it metastasizes and then it, it goes invades tissues and everything else and causes death to organs and everything else. So that's part of the, they believe comes from the nucleus, the DNA down. Okay. And then real quick, we have those tumor suppressor genes. That's another gene that plays a big role. And I think people understand a little bit about it with that a tumor suppressor gene does, just to kind of set a little base here, it slows down that cell division.

Eric: 17:01 Okay, so it actually gets called in and say, Hey, we've got a kind of a rogue cell that is damaged and okay, so let's send that back up the chain to the DNA and find out let's make a repair of the DNA gene or it's a mistake or or whatever. And so it goes in and says, Hey, let's repair this lets you know because we want to stop it from growing out of control. That's a tumor suppressor gene. And so it'll actually try to do the repair, if not, it can actually go in and basically a pop ptosis and kill that, that sale. So that's what you have to really rely on is that tumor suppressor gene. And we call that the p 53. And I've talked about that before. The Guardian of the genome, the P53, that's one of your strongest tumor suppressor genes. And when I do gene a consultation, that's one of the first things I look at Chad when I go into people's genes when we're talking about cancer, is I look at that p 53 gene and see if there's a mutation there. And it's very rare but it, it can be inherited. So I'm looking for genetic inherited a gene mutation on that, but it also can be damaged from carcinogens and environment and everything else. Okay? So in fact, all cancer, I mean, 50 percent and above cancers all have a mute, mute, mutated p 53 gene. So what it's doing is saying, Hey, I'm, I, I'm not there to protect you and you got to cell that starting to is damaged and it can go rogue. Um, and I'm, I'm not working efficiently to, to either repair that a gene or two to basically a turn it off and fill it. Okay,

Chad: 18:53 great. So just to, just to recap, kind of what you've talked about in just a couple of sentences, we need to understand that cancer is cells that multiply uncontrolled. That's what a tumor is. That's where cancer originates. We have genes that are called gene or mutation or sorry, suppressor genes basically that once that starts to happen in the body, if there's not a mutation in that gene, if it's working properly, that thing goes in and says, nope, you're not multiplying anymore. And uh, and it doesn't grow, is that correct?

Eric: 19:27 Yes, yes. And simplified it will kill it. And then, and what happened, I mean, it, it, it when, when the pay 53 gets involved, you know, obviously it, it has to, uh, in, in, uh, damage. Now let's say you've got to damage DNA, obviously the p 53, once it's phosphorylated and it actually will prevent what they call an MDM two gene complex that'll actually increase the levels of P53 and get rid of that cell. Either get arrested or, or, or kill it or fix it. So yeah, the P53 is a big player and I think a lot of people might know it because the Li-Fraumeni syndrome comes from it. Those who have just don't have, they haven't completely inactive p 53 gene that's not working and they get multiple cancers and Li-Fraumeni, talked about a lot because the P53 gene and they can have even as a kid you'll end up with adrenal cancer all the way up to a leukemias and everything else, multiple five six types of cancer, but I think there's only like four or 500 cases. I mean families that are involved with that genetic mutation, but it's also done from, you know, carcinogens and environment and unhealthy mitochondria cells. Okay, great.

Chad: 20:48 Great. Let's push pause there for a second if that's okay. Um, this has been super heavy. It's really good. It's really good. No, no, don't be sorry at all. This is a good baseline understanding of cancer, how it grows, where it comes from, what is built into our bodies to supposed to prevent it, and that those are, could possibly have mutations are damaged, that allows the camp and then that allows the cancer to grow. So let's, let's pause there. I want to talk about bioStak for just one second if that's okay. We'll let, we'll let our audience have a little bit of a breather. Um, and uh, and then we'll jump back in and talk about the role of Ketosis and ketones and why were, you know, why those are related as we talk about cancers. Does that work? Yeah. Great. So I'll make this. I'll make this really, really quick about BioStak, especially if you've been listening for awhile. You've heard some of the stories, you've heard some of the experiences that people are having with bioStak and it's been, it's been an incredible ride and it's been so fun to get this feedback and hear people's stories and experiences, how it's changing their lives. It's changing their workouts, it's changing their diets, it's changing their, uh, you know, their appetite and all of those sorts of things. And it's really, really cool. Here's what I want to tell you right now. BioStak is a great gift for Christmas right now. We're running a, you guys are running a promotion, but, uh, with the Promo Code Bio Christmas, that's bio Christmas. You can give the gift of bioStak, uh, for 30 percent off and whether that gift is for yourself or somebody you love, I assume a lot of it's going to be for yourself and you deserve it. Um, especially this time of year. But go to bio, go to biostak.com. Put in the Promo Code Bio Christmas, get 30 percent off. That's all I'm gonna. Say about BioStak. Is that okay, Eric? Yes, that's perfect.

Eric: 22:40 Bringing up bioStak. The biggest one, the biggest motivators of bioStak is we're going to have to get back to the Mitochondria here real quick because in talking about Ketosis and cancer and why the bioStak, what we're back to the Mitochondria and naked and everybody knows I talk about the Mitochondria over and over again and the biggest reason is because of cancer and I just never, you know, discuss cancer before because I just really didn't want to get in the subject of it. But in the Mitochondria, the Otto Warburg is 1930's. It's a lot of years ago and he was a noble prize winner. I think he was nominated two or three times. Brilliant. Otto Warburg, brilliant guy. He, he actually, um, uh, I mean, he, he started, I think he graduated from med school in 1918. He actually was in the war, a world war one, and just a brilliant person basically. And reason being is way so interesting. And I, I follow him. I've read about him. This is where the Otto Warburg's theory comes from. The cancer begins in the Mitochondria. He wasn't quite sure the Mitochondria then, but he knew that without cellular respiration, without that, you know, oxidative phosphorylation. We've talked about that when the Mitochondria becomes damage, okay. Obviously that the cell becomes damaged and it starts to ferment a different way to obtain energy. And so what Warburg, when he, you know, and what makes him unique and interesting because it, when, when he was in the service and I found it interesting, he's, he, he got a letter saying, hey, you shouldn't. He actually volunteered for the world war one after he graduated from med school. And I just found it kind of interesting that he got a letter saying, hey, from a gentleman that said, hey, your experience and your knowledge and your talent should not be in the war, you should we need you to stay alive. We need to figure a way, know that they can bring him out of the war and get him back to the lab, get them back to, you know, what he knows best, and because he basically, you know, his parents, his dad was a well known physicists and very educated, very smart. But this letter that was written to them to say, Hey, we need your knowledge was from Albert Einstein. So I thought I was. I mean this, this guy has a fantastic history of knowledge. And he's the one that said, hey, cancer begins in basically we'll call it the mitochondria in which it, it's back to energy production. Okay. So you have a normal cell and you have a cancer cell. All right? So when the Mitochondria becomes damage, okay. So we're saying from a mitochondria being damaged, it actually starts to signal to the nucleus, to the DNA, to the mutations of that, to help the cancer, the mitochondria that cells survive.

Eric: 25:44 So basically do the damage. I'm a mitochondria. It's telling the nucleus, that's where the mutations are coming from to say, hey, a gear up, I, I need more fermentation. So when cells have to stay alive, of course we need atp and that's what Mitochondria does. It produces ATP. But when it becomes dysfunctional, obviously it can't produce the ATP and the electron transport chain. So it has to rely on a fuel so that cancer cell has to stay alive. So it goes into fermentation and we call that like an ancient way of producing energy. Alright? So fermentation, we'd go back into those energy pathways and um, you know, I, I, you know, you heard me talk about over and over lactate, lactate, lactate. So basically the cancer cell to survive says, Hey, I need two things to survive. I need glucose because I'm going to have to ferment okay in the Cytosol, I'm going to take glucose, pyruvate to lactate. And that's going to be the energy source to keep my cell alive and to grow, proliferate, and become a tumor. So it actually signals the DNA, the nucleus, a, hey, you know, I'm going to give you the signal of what a DNA I need to survive. And so it's going to upregulate transporters to get more glucose, more glutamine, which is another, uh, energy substrate for, for the cancer cell. So there's two fuels it's going to bank on through fermentation is glucose and glutamine. So there we go. We have a normal cell and a cancer cell. And obviously without energy, without ATP, the cell will die. So the cancer cell becomes very, very, uh, you know, it's a survival as the cell will. It'll do whatever it has to do to survive. And that's the mitochondrial metabolic theory that Otto Warburg all the way down to the books that I've talked about, Thomas Siegfried and, and these guys have kept it alive because it got squashed when the somatic mutation theory came in saying, oh no, it all comes from DNA genetic damage. That's what produces cancer cells. But they all know that all cancer cells live on two things, glucose, and glutamine and, and everyone knows that. So basically the Mitochondria becomes defective. So I'm all about protecting the Mitochondria and that's everything I talk about is we've got to keep our mitochondria functional. When it becomes dysfunctional, it becomes that uncontrolled growth progressing to be a cancer cell. So I hope I,

Chad: 28:26 I've never heard you talk about this mitochondria thing,

Eric: 28:32 but see, that's why I go back to the Mitochondria and that's like the bioStak, the whole thing. Every, every root cause of illnesses. We come back to the Mitochondria and this is really a simple theory of cancer. When you think about it. Wait a minute, we're spending all these billions of dollars chasing the DNA from one end. The nucleus, okay? That ends up damaging cells and, and proliferating and creating tumors. It's, well, let's start. It doesn't start there. It starts in the Mitochondria, but if we basically cut off its fuels, which is glucose, glutamine, alright, then guess what? The cancer cell will not survive. And when they tested this over and over, and I have the papers here just piled up everywhere, all the tumors of every cancer reduced when they went on in Ketosis. And they also did some glutamine. Okay. Reduction, which is another process. They did hyperbaric oxygen. Uh, they did some other things I won't go into, but the tumors all decreased. They shrunk. And, and that's what ketosis does. What is Ketosis do? It drops calorie restriction to, to a certain point. Okay. But its main thing is it brings down your glucose and it offers Beta. Remember that reactive oxygen species we've talked about. When a mitochondria becomes dysfunctional in that electron transport chain, it's what results in reactive oxygen species, species kicking off free radicals.

Chad: 30:03 Those free radicals is what's doing the damage and the signaling to the DNA to mutate other genes. So the cancer cell can survive. So what happens when you're in Ketosis, you reduce your reactive oxygen species and free radicals. And so basically we're back to antioxidants to, to, to squelch free radicals. We're back to protecting the electron transport chain and the Mitochondria from more free radical production being released. So that's where ketosis comes in and you lower your glucose. So the cancer cell can't ferment glucose to Piru vate to lactate and it makes a ton. It's so hungry Chad, the cancer cell, because when you lose that electron transport chain, that oxidative phosphorylation, we call it [inaudible]. What do you lose? You lose 32 ATP molecules. Alright? So for the cancer cell to keep that massive growth that it wants to do, it's really got a kick in and ferment a lot of glucose. And also it's got to bring in what they call. It's a substrate level phosphorylation, which I won't go into, but that's what glutamine is used for. It's another energy source for cancer. So it really kicks in and it has to just be. I mean it's just sending out more transporters to the cellular membrane. More glute for say bring all, bring all the glucose you can, and then it converted to lactate, kicks that lactate out, obviously member the Cori cycle in the liver. And so it's back to lactate.

Chad: 31:37 So if I were to put this simply, I know how many really what I'm hearing you say is that obviously the cancer cell is starving and, and what it wants is glucose and when we're in Ketosis. Yep. And, and are in the ketones. It basically starves that cancer cell. It doesn't get the food that it wants. Right? And it can no longer survive. It can't multiply because it doesn't have energy.

Eric: 32:08 And why is it starving? Why is it, why is it the mitochondria. Because you're cutting off its energy. The Mitochondria, the electron transport chain you're cutting off oxidative phosphorylation. That's where 90 percent of our energy comes from that. Okay. But when I, when I kick you in, like I've always taught the phosphocreatine energy pathway and anaerobic glycolysis, I'm kicking you in to the ATP that's there in the cytoplasm and then into lactate. I've always, you know, I'm always trying to build up my lactate threshold and all that stuff. So when you knock out the Mitochondria, you knock out that oxidative phosphorylation and that cancer cell has to be really aggressive on getting glucose and glutamine to survive.

Chad: 32:50 Yeah. Yeah. Let me say this and you can kind of let me know if this is, if I'm on base or off base here, but what we're saying is cancers. I mean if we, if we talk about it realistically, cancer is a game of odds, right? Um, I mean there's so many things that we're finding out more and more what, what affects it, what causes it, what, what helps it grow and it's. And it's quite literally a game of odds and, and so we're not here on this podcast saying keto and ketones are the, the, the cure or the or the or the 100 percent guaranteed preventative. But what it does is it significantly decreases the odds of your chance of getting cancer or, or that cancer taking over to a point to where it's fatal. I'm exactly. Is that fair to say?

Eric: 33:45 You're protecting your Mitochondria and you've heard me over and over might've. I might've remember in our lifetime you 40 percent of us including me are going to get cancer. Forty percent of us. And so I'm aiming. That's obviously something that, that I can't self experiment and I don't want to self experience, but if I, and I can't say that I've never been in those shoes before being diagnosed, I have not been diagnosed with cancer, so I feel really bad to say what I would do, but I, I believe that this is a path I would take, but I can't say because, hey, I'm not in your shoes. Those have cancer. I who am I and tell the doctor I get diagnosed with cancer and then then I, then I'll be able to relate to those that have been diagnosed with cancer. I have friends. My mom died of cancer at friends have died of cancer and in I'm touched that way but, but, but not directly. And so that's why I'm saying this to what I'm saying and what the research is showing that. Is there a way to integrate this. Okay. And I've talked to an oncologist about this. Why not like Turkey? They've integrated member. I've mentioned Turkey, that four stage cancer. They can do any with the patient's permission, they can do any treatment and this is where they're doing this treatment, that this is the mitochondrial metabolic therapy, so, and they're mixing in a little bit of chemo at a very low dose, which, you know, can it integrated work together with reducing glucose and glutamine and, and they have these therapies and they're having success from it with somebody in than the roughest, a Glioblastoma, cancers and leukemias. They're having success with reducing the cancer. And basically people were, our goal is to get people to live longer and, and, and some of the somatic mutation theory and some oncologists, there is some five year life expectancy is what everybody goes by. And so there has been some extension Yeah. But not enough. So I.

Chad: 35:58 Yup. And I would add to that, I would add to that I'm living longer quality of life, right? I mean that's really, we're really trying to increase our quality of life for the maximum time that we can. Um, so that we can be together with our loved ones and experience more and all of that kind of stuff. And so this is, this conversation is incredibly difficult to fit into a 40 to 45 minute.

Eric: 36:28 Passion is there's, there's 1600 deaths a day from cancer. Okay. And you think about it, there's, you know, there's, there's going to be over what 1.7 million and next year of cancers that are new cases of cancer. 1.7 million in the United States. I mean it's just amazing how it just scary. It's really scary and I have a passion for it and I, I, I'm gonna continue to just keep digging in and learning more and I could talk about it for hours and it just.

Chad: 37:06 Well I don't, I don't think this is the last time we're going to talk about it on this podcast, especially as new discoveries are made and, and you learn more and all that kind of stuff. Is that fair to say?

Eric: 37:17 We had to boil it down. Just remember there's, there's basically two theories of cancer, somatic mutation theory. That is what's been around since they declared war on cancer, 40, 50 years. That's working with the nucleus. The DNA mutations either inherited or acquired carcinogens promoted. It's all about DNA and mutations that are causing these cellular, uncontrolled growth, proliferation. And then we have the mitochondria metabolic theory say, Hey, it starts in the Mitochondria. That's where the mutations actually get signaled to the DNA. That's what causes the uncontrolled proliferation of cells. And it's all about energy. We've got to, we've got to address the energy issue that feeds cancer and that's what's coming from this theory is. And it started with Otto Warburg. There's from Darlington to Peterson to Thomas Siegfried and these guys have done a brilliant job of, of research and there's, there's funding available places you can go to fund this research. Uh, you know, our government, the given what, five point $5, billion dollars for this year, but none of that's going to go for this type of research. It's all going to go where it's, you know, for research and into treatment and etc. So there is money being given, but uh, it's gonna take a lot of funding. But again, Success when success comes through and it, it, it's getting more and more people talking about it. Like this podcast is sharing this, this view. I think people will share it with their doctors and maybe people take a better look at it.

Chad: 38:56 Little wins. Yes. That's great. Thanks so much for biohacking with us today. I appreciate it. I just hope it was like, I have so much stuff, eight of that too. And it's so hard to, to tap into it. And even my wife said, you're talking about cancer like, yeah. And she's like, please keep it simple. I've heard you talk to because I, you know, I do clients and I look at, I look at their cancer genes, Chad and, and I've got pages and I know where my, my inherited risk are is as far as gene mutations and like mine we've talked about is. And I, I get the churn of five, then that's a gene that really promotes um, uh, your nicotinic receptors, which I would be definitely really pre predisposed to lung cancer. So I have to look at their p 53 and all their brcca and where the brcca 1 brcca 2 all these different genes. And it just, you know, it's your blueprint. But again, again, it just gives you an idea that, you know, through lifestyle, through epigenetics, you can make changes in and none of these will come to pass. So, you know, it's just part of the picture.

Chad: 40:11 Well, I think, I think you did a fabulous job. I think it's a great baseline for future conversation about more of this stuff and how we can nurture the, the genes in all of the, uh, you know, the mitochondria and everything that's going to affect it. So thanks so much. You bet. And I want to thank 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 @biofit_coaching. There's a lot of great keto tips, recipes, just always good stuff going up on. They're Both on the posts and the stories. So check that out @biofit_coaching. also, if you, if this podcast has helped you at all, if you've enjoyed it, if it's entertained, you, please, uh, please consider going to itunes or wherever you get your podcast to leave us a five star rating and a glowing review so that we can reach more people, grow the podcast, grow the community, help more people out. And finally, the greatest compliment that you can give us is sharing this podcast with your friends or family, those who are looking for a different way of living. And until next time, stay keto.