[00:00:11] Welcome back, Episode 4. And today, Jason, we are going to talk about a really cool, I would say from my perspective, learning this for the first time with you. You are obviously, you are aware of, you're the subject matter expert. A Cell Danger Response Model by Dr. Naviox. So, first of all, how are you doing?

[00:00:39] Dr. I'm doing good. How are you doing?

[00:00:41] Dr. Doing well, too. Looking forward to picking your brain on this topic.

[00:00:47] Dr. Yeah, this one I find somewhat exciting as well because nothing made sense until I started looking at Dr. Naviox's model, for sure.

[00:00:59] Dr. Yeah. All right, let's jump into the topic then. So, the Cell Danger Response, or CDR, we're going to use this term a lot, CDR, throughout this episode, has been called a key to understanding how body heals. Can you break it down for us? What is it and why is it such a big deal in modern medicine?

[00:01:25] Dr. Yes. So, the Cell Danger Response, or the CDR, is a pretty groundbreaking concept developed by Dr. Robert Navio. And to explain how our cells react to stress, injury, or threats, think of it like the body's kind of a built-in alarm system, but operating at a microscopic cellular level.

[00:01:52] So, when the cells detect danger, whether it's from an infection or a toxin or injury, it temporarily shifts its priorities. Instead of continuing with normal functions like growth and energy efficient or efficient energy production, the cell goes into survival mode.

[00:02:14] And that shift not only protects the cell, but it also then sends signals to the body and then to the neighboring cells to begin the healing process.

[00:02:28] And really, in that way, the CDR is both a defense mechanism and a driver of recovery, right?

[00:02:37] And it's so revolutionary because it really connects the doctors between many of the biological processes like inflammation and immune response and energy metabolism, showing how they all kind of revolve around these cellular signals.

[00:02:54] And more importantly, it really reframes health and disease kind of at a fundamental level, how well our cells adapt to and recover from stress, right?

[00:03:08] And so, the perspective or this perspective shift is truly a game changer, offering us new ways to understand conditions like chronic disease and autoimmune disorders and even aging.

[00:03:21] And it challenges us to support the body's natural healing process rather than just suppress symptoms.

[00:03:29] And then that opens the door to more effective prevention and treatment strategies.

[00:03:36] And when did you discover this first?

[00:03:40] And you obviously, you mentioned how influential the CDR model has been in your work.

[00:03:48] Can you share how you first came across this research and why it resonated so much with you?

[00:03:56] Sure. So, again, it kind of all started with my family getting cancer, right?

[00:04:01] So, that really didn't make sense to me.

[00:04:04] So, you know, we ate well, mostly organic whole foods.

[00:04:09] We were active.

[00:04:10] We didn't have a lot of mental stress.

[00:04:12] We spent time together and played as a family.

[00:04:15] Yet somehow, everyone got cancer.

[00:04:18] I guess everyone but me.

[00:04:20] And it really left me wondering why it didn't make any sense.

[00:04:25] So, that's the question that really kind of launched my journey into understanding health at its most fundamental level.

[00:04:33] And early on, I became somewhat fascinated with mitochondria and their potential role in driving health and healing.

[00:04:42] And I wanted to understand.

[00:04:45] Remember, I explained this before.

[00:04:46] I wanted to understand why some therapies were working or could work.

[00:04:50] And then when they would work and when they wouldn't work.

[00:04:54] And what was different between those times?

[00:04:57] Why things would work sometimes and not others?

[00:05:00] And so, early in this research, I came across Dr. Otto Warburg.

[00:05:05] It's pretty well known.

[00:05:06] Got a Nobel in medicine back in the 30s.

[00:05:13] And so, he's the one who discovered that cancer cells rely on anaerobic energy production, even when oxygen is available.

[00:05:23] It's actually called the Warburg effect.

[00:05:26] And it's a metabolic hallmark of cancer.

[00:05:30] But here's what doesn't really add up.

[00:05:35] It's fairly well known that cells with severely dysfunctional mitochondria don't become cancerous.

[00:05:41] And yet, once cells become cancerous, their mitochondria becomes dysfunctional.

[00:05:50] That didn't make sense.

[00:05:52] So, it's Dr. Naviot's research in his cell danger response model made everything click.

[00:05:59] So, he states fairly simply that cancer is a CDR2 disease.

[00:06:05] He named the different phases.

[00:06:07] I'll get into those in a little bit.

[00:06:10] And in that case, he didn't come up with real fancy names.

[00:06:15] He named them CDR1, CDR2.

[00:06:17] But in CDR2, the cell is prioritizing proliferation.

[00:06:23] So, the mitochondria aren't actually broken.

[00:06:26] They're doing exactly what they're supposed to do, protecting the cell and shifting into a different metabolic state.

[00:06:33] So, it's not a malfunction.

[00:06:35] It's a survival strategy.

[00:06:37] And that realization kind of reframes the problem.

[00:06:42] It definitely did for me.

[00:06:44] So, now the issue isn't that mitochondria are inherently dysfunctional.

[00:06:50] It's that the cells are getting stuck in the healing process somewhere.

[00:06:55] And they can't complete the healing cycle and return to normal.

[00:07:00] And, you know, so then I also realized, and I say I realized, obviously, Dr. Naviot was presenting this to us.

[00:07:08] So, I realized this by reading his work, that this isn't just about cancer.

[00:07:13] The same framework applies to any disease.

[00:07:17] And Dr. Naviot's CDR model, so it really gives us a new way of seeing cellular health.

[00:07:24] It connected everything for me that I've been trying to understand and provided a roadmap for helping so that you can see how cells move through the healing process.

[00:07:36] And the CDR model focuses on how the body responds to stress, right?

[00:07:45] And how does that align with the idea of salutogenesis and creating health instead of just addressing the disease?

[00:07:58] So, it's interesting.

[00:08:00] Dr. Naviot actually wrote a paper that addresses almost that very question titled,

[00:08:06] Mitochondrial and Metabolic Features of Salutogenesis in the Healing Cycle.

[00:08:11] And in the title, he's using the CDR.

[00:08:16] He's referring to the CDR as the healing cycle.

[00:08:18] So, he compares salutogenesis and pathogenesis in the same way that we discussed before, right?

[00:08:25] Pathogenesis focuses on disease initiation and progression caused by harmful triggers like infections or injuries.

[00:08:35] And salutogenesis emphasizes the body's natural, he puts this, evolutionarily conserved mechanisms for recovery, adaptation, and health creation.

[00:08:46] And that's what I refer to as, and we talked about the kind of resilience adaptation.

[00:08:54] So, salutogenic therapies aim to help cells move through the CDR phases correctly, completing the healing cycle,

[00:09:01] instead of just forcing the body into actions it's not ready for.

[00:09:06] That's a pratogenic approach.

[00:09:08] And so, salutogenic therapies create conditions that the body needs to heal.

[00:09:14] And so, this shift in perspective, it basically, pathogenesis tells us how diseases develop.

[00:09:23] But salutogenesis shows us how to reboot the healing cycle.

[00:09:27] And it's about what the cells need to get unstuck and progress.

[00:09:34] And that's why the CDR model is so revolutionary.

[00:09:38] It provides kind of the correct advantage for understanding illness and really designing therapies that then support the body's innate capacity to heal.

[00:09:54] And a little bit about, like, I guess the distinction here, right?

[00:10:01] Like, what is, like, pathogenesis?

[00:10:05] And we talked about that in previous episode, too, a little bit, that those feel force to the body, those kind of treatments.

[00:10:11] And here, even though...

[00:10:14] Well, that would be cratogenesis.

[00:10:16] Cratogenesis, yes.

[00:10:17] Sorry.

[00:10:17] So, wouldn't you...

[00:10:20] I guess the response is...

[00:10:22] Isn't the response a forced response in this situation?

[00:10:25] Why would this be considered salutogenesis in that fundamental regal?

[00:10:30] Well, so, the CDR really lays out exactly what the cells are trying to do.

[00:10:37] And so, it really gives us a good...

[00:10:40] I mean, it is a model.

[00:10:42] It gives us a really good model to understand where disease is occurring and what the cell is doing at that point.

[00:10:51] So, we can help it finish doing what it's trying to do and then move on.

[00:10:56] And then it's healing correctly, right?

[00:10:59] So, it's kind of a different viewpoint of, well, why do cratogenic drugs cause so many side effects and adverse things to happen?

[00:11:06] Well, it's because it's trying to force the cells to do something.

[00:11:12] But the cell might be perfectly capable of doing that.

[00:11:16] It's just in a healing phase where it's not prioritizing doing that.

[00:11:20] Now, you know, some doctor or scientist looks at this and says,

[00:11:24] Oh, well, that's what's wrong with this disease is the cell isn't doing this.

[00:11:27] And so, we make up a drug that forces the cell to do this.

[00:11:31] But if the cell is not ready to do that yet, it might go ahead and do it because it's forced to.

[00:11:37] But then that doesn't really stick.

[00:11:40] And the cell can basically fall right back to where it was as soon as the effects of that drug wear off.

[00:11:47] And then on top of that, because of the cell being forced to do things that it wouldn't want to do until a different stage of this, the CDR or the different stage in the healing,

[00:12:01] it can kind of mess up what it's doing elsewhere as well.

[00:12:05] And then everything gets all confused.

[00:12:08] Now, obviously, sometimes cryogenic drugs work.

[00:12:12] And in those cases, we're probably forcing the action that is pretty close to when the body is trying to do that action anyways.

[00:12:27] So, again, I don't want to say that they will never work and that, you know, cryogenic drugs are evil.

[00:12:34] It's just the ludogenesis and or salutogenic drugs are going to work better in that they're helping the cell do what it's trying to do right now.

[00:12:49] Not sometime in the future, not sometime in the past, but right now, get done with that, move on to the next stage, finish that, get done with that, move on the next stage and so on and so forth all the way through healing.

[00:13:02] Did that make more sense?

[00:13:03] Yeah, understood.

[00:13:05] So, I'm just going to go next part of my thought process here, which is the, so the best way to look at it is pathogenesis is more of how to explain the disease itself.

[00:13:20] And salutogenesis shows us how healing is working in this regard or the healing cycle is working.

[00:13:30] Yes, yes.

[00:13:32] Yeah, so exactly.

[00:13:33] So, pathogenesis is explaining the problem that is occurring and the problems occurring from significant, I mean, things that have occurred.

[00:13:41] And then salutogenesis really shows you how the best way the body wants to heal that whatever occurred.

[00:13:49] Got it.

[00:13:50] And I didn't really mean to, right, I didn't, and I apologize if that came across as I was contrasting salutogenesis to pathogenesis in where I was contrasting salutogenesis to tratogenesis.

[00:14:06] We've done both.

[00:14:07] Yeah, I wanted to clarify that.

[00:14:09] So, that's good.

[00:14:10] Good.

[00:14:12] Okay.

[00:14:12] So, now, obviously, you know, the CDR is often described as body's way of responding to danger, right?

[00:14:25] So, can you walk us through how it gets triggered and what it is trying to accomplish in terms of repair and recovery?

[00:14:34] And this is a detail, like we need details here.

[00:14:38] Okay.

[00:14:39] Okay.

[00:14:39] So, I'll try to stay somewhat high level so that we don't get super bogged down here.

[00:14:44] But basically, the CDR is triggered whenever a cell experiences stress, whether that's from an infection, a toxin, physical injury, or even psychological stress.

[00:14:54] So, again, the CDR acts like an alarm system at the cellular level, and it sends out signals to warn neighboring cells in the rest of the body that there's a problem.

[00:15:05] So, the first priority of the CDR is survival, right?

[00:15:08] Contain the threat and prevent it from spreading.

[00:15:11] And so, Dr. Naviot actually maps this out in three distinct phases, each playing a key role in the healing process.

[00:15:22] I'll explain it briefly.

[00:15:23] So, CDR1, again, it's not the fanciest of names.

[00:15:30] So, the first phase is CDR1.

[00:15:32] You can call that defense and inflammation or the acute phase.

[00:15:37] And that's where the cells – so, that's the cell's immediate response to danger, right?

[00:15:44] So, mitochondria, the tiny powerhouses of our cells, shift into what's called M1 phenotype.

[00:15:54] So, they actually change their phenotype.

[00:15:56] They physically change.

[00:15:58] And instead of now generating energy efficiently and aerobically, they prioritize producing reactive oxygen species, which are molecules designed to fight off invaders.

[00:16:10] That's what causes oxidative stress.

[00:16:13] And they, along with other things, signal the immune system to respond.

[00:16:18] Really simply, this is like calling the fire department when a fire breaks out.

[00:16:24] The goal is to contain the threat, even if it temporarily disrupts normal life.

[00:16:31] Then the next phase, CDR2, that's repair and regeneration, right?

[00:16:37] So, once the immediate threat's under control, the cells shift into repair mode.

[00:16:41] The mitochondria actually transition into a more neutral M0 phenotype.

[00:16:50] And that supports processes like tissue repair, stem cell recruitment, and rebuilding of lost or damaged cells.

[00:16:57] So, you can think of this like the cleanup crew that comes in after the fire's been put out to repair all the damage.

[00:17:08] Then CDR3 is restoration and return to homeostasis.

[00:17:13] So, in this final stage, the cells return to their normal state.

[00:17:19] Mitochondria resume their – they actually switch to the regular or healthy M2 phenotype.

[00:17:28] And they resume their normal, efficient or aerobic energy production mode.

[00:17:35] Inflammation resolves and normal cellular communication and functions are restored.

[00:17:40] So, you can think of this as putting the finishing touches on the rebuild after the fire.

[00:17:46] And it leaves the structure as good as new or even better than it was before the fire.

[00:17:56] And the response is only triggered specifically when there is a stress event, right?

[00:18:06] In that case, it's not like – are there anything – is there anything else when it is triggered for other functioning at all?

[00:18:15] Or it's just – that's how it works.

[00:18:17] Like whenever there is a stress or infection or whatever caused by it, that leads to the trigger of this.

[00:18:22] Or is it something that's always running in the back end for our bodies?

[00:18:25] No.

[00:18:26] No.

[00:18:27] Yeah.

[00:18:27] So, the cells only enter the CDR with triggers.

[00:18:32] Now, those triggers can be lots of different things.

[00:18:36] Basically, anything that is a cellular threat or danger signal, right?

[00:18:39] This is the cell danger response.

[00:18:43] Now, so like in CDR2, we said that that's when it's rebuilding.

[00:18:49] So, that's a proliferative stage of the cell.

[00:18:52] But to be clear, the cell can do – it's growing.

[00:18:57] It's healthy growing, I suppose.

[00:19:01] Normally, it doesn't have to go into the cell danger response cycle to get to that proliferative stage.

[00:19:08] They're two separate things.

[00:19:09] And actually, in the danger cycle in CDR2, it's actually repairing or rebuilding, proliferating faster than it would be under a healthy state because things are much more critical.

[00:19:24] Now, we're in a survival mode as opposed to just regular growth.

[00:19:30] Can you point out again the difference between CDR2 and CDR3?

[00:19:35] Justin, fundamentally, repair and regeneration is happening at CDR2 stage itself.

[00:19:42] So, the 3 – what happens in 3 after the repair and regeneration is done?

[00:19:48] What's the step that happens really in 3, CDR3 response?

[00:19:53] So, what happens after 3?

[00:19:55] Yeah.

[00:19:55] Or –

[00:19:56] No, starting at 3 and then afterwards.

[00:19:58] Okay.

[00:19:59] So, go through them again.

[00:20:01] CDR1 is the acute phase.

[00:20:03] That's the immediate reaction to contain the threat.

[00:20:08] Then CDR2 is rebuild and repair, and that's basically replacing lost biomass.

[00:20:15] And then CDR3 is everything starts to go back to normal and return.

[00:20:23] So, homeostasis returns to normal.

[00:20:25] So, at the end of CDR3, you are back to being a completely healthy cell, assuming that you had complete healing through that process.

[00:20:37] Got it.

[00:20:38] And if there is not complete healing, you are still in CDR2 kind of phase.

[00:20:42] That's right to assume?

[00:20:44] No, not necessarily.

[00:20:45] Actually, that is one of the theories on what aging is, and it's just not – something less than 100% healing through the CDR.

[00:20:56] So, every time we go through the CDR cycle, if our cells don't heal 100%, there's a little bit of damage that's left over.

[00:21:05] And we're getting off topic, but as that gets to a certain point, the cell can basically shoot off a different direction, and it becomes a senescent cell.

[00:21:18] And that's basically a cell that is otherwise healthy in that it's not malignant, it's not doing the wrong things, but it's not actively adding to the rest of the organism.

[00:21:35] And in small amounts, that's almost imperceivable.

[00:21:39] But over a lifetime, those build up to the point where we start to see wrinkles in skin, muscles not quite as strong, because you've got some random little cells around that aren't really tied to and associated with all the other cells around it, not doing the right thing.

[00:21:57] It's just kind of off doing its own thing.

[00:22:01] I guess they could be producing a little bit of inflammation, but not really a lot.

[00:22:07] And again, and that's why for a long time as you're aging, we don't notice any of this stuff, because what's a couple little cells that aren't coordinated with all the others?

[00:22:20] It's almost meaningless.

[00:22:22] So kind of like, it's not damaging in any way, but it's also not the optimal state it was earlier, but it's like what we call like, you know, it's there, but not in the optimal state, but not damaging.

[00:22:39] And that's, yeah.

[00:22:41] Well, I mean, eventually it is damaging, right?

[00:22:44] At some point you get so many of them that will now you've got a much higher percentage of cells that aren't doing the right thing all within a little area.

[00:22:53] And that's, so that's a whole different topic as to, well, why don't those cells just go through apoptosis and self-terminate?

[00:23:02] Because they're not shifting back to be a healthy cell.

[00:23:05] They're not still in the self-danger response.

[00:23:09] They're kind of just kind of kicked out the other direction.

[00:23:15] And that wouldn't make sense.

[00:23:17] Why not just have them turn themselves off?

[00:23:19] And then there actually are all sorts of, it's anti-aging therapies that are trying to look at that and how to reduce or eliminate senescent cells and or get senescent cells to fix whatever caused them to become senescent in the first place and revert back to healthy or revert back to healthy, or at least, how do I describe that?

[00:23:44] But heading towards that direction long enough to where then they can say, yeah, I'm no longer viable.

[00:23:50] I should just self-terminate.

[00:23:51] And then the body can get rid of those cells entirely.

[00:23:54] Otherwise, they're stuck there because they're not dead, in which case the body won't get rid of them.

[00:24:00] Yeah, I guess that is what in science, especially in anti-aging world, we try to find that fountain of youth to pull those things.

[00:24:12] And that's what it is.

[00:24:14] Very interesting.

[00:24:15] A little side topic from this, but maybe a different discussion.

[00:24:20] All right.

[00:24:21] So let's go talk about a little bit on chronic illnesses because the thought I had with this question, the previous one was like, well, you get inflammation in your body and then it still exists for years.

[00:24:34] It might not be damaging at the moment, but it's a slow damage because it's not at optimal level at that point.

[00:24:40] It's not malignant.

[00:24:41] It's not malignant, but because if it is too much together, then it's a chronic problem.

[00:24:46] It becomes the chronic problem.

[00:24:48] It becomes a chronic illness.

[00:24:50] So chronic illnesses like autoimmune diseases and metabolic syndromes are complex.

[00:24:57] It's like many different ways.

[00:24:59] So how does the CDR model shed light on why these conditions can be so hard to treat?

[00:25:09] So this is one of the things that really makes the CDR model revolutionary.

[00:25:13] So instead of just looking at symptoms or isolated systems, it explains how the cellular dysfunction, especially when healing is incomplete or interrupted, can ripple outward and lead to chronic conditions.

[00:25:27] It gives a framework to understand not just the acute recovery, but also what happens when body gets stuck in a cycle of incomplete healing.

[00:25:36] And that's really the key to understanding chronic conditions.

[00:25:40] So specifically, chronic illnesses are or occur when the CDR states persist and the cells fail to fully complete that particular healing phase and the healing cycle in general.

[00:25:55] So they're literally stuck in one of the phases of the cell danger response.

[00:26:00] Let's run through them again, right?

[00:26:02] So remember, you've got CDR1 and that's the survival mode.

[00:26:09] So in persistent CDR1, mitochondria stay in that M1 state.

[00:26:16] Remember that.

[00:26:16] So inflammation persists and immune activation dominates.

[00:26:22] And that's linked to innate immune disorders, conditions like allergies or asthma or chronic infections.

[00:26:32] Where the innate immune system remains on high alert because cells haven't moved forward to the repair state.

[00:26:41] Then CDR2, that's the repair and proliferation phase.

[00:26:46] So in persistent CDR2, cells are focused on rebuilding and they don't progress to full resolution.

[00:26:56] So remember, that's M0.

[00:26:59] That's the mitochondria.

[00:27:01] Those that are elevated is M0 mitochondria.

[00:27:03] And while also M1 mitochondria aren't fully resolved.

[00:27:10] And so what that does is it leaves lingering inflammation and incomplete repair.

[00:27:17] And so the phases or so I guess the diseases associated with CDR2 are or persistent CDR2 are proliferative disorders like cancer, diabetes and liver cirrhosis or vascular diseases.

[00:27:37] And that makes sense, right?

[00:27:41] Then CDR3, that's where the body should resolve inflammation and restore homeostasis.

[00:27:48] And the other thing that's happening in there is differentiation.

[00:27:52] So the cells, any of these stem cells that had been produced in CDR2 are now differentiating and coming into homeostasis with all of the cells around them doing what they're supposed to do.

[00:28:06] So in persistent CDR3, you still have that M0 mitochondria remain slightly elevated.

[00:28:15] And M2 mitochondria, the one that we think of as normal mitochondria or healthy mitochondria, are never fully dominant.

[00:28:23] And let me back up and just address that.

[00:28:26] I actually don't like calling M2 healthy mitochondria because they're all healthy.

[00:28:33] And that's one of the differences in this viewpoint here is just because the mitochondria isn't producing energy aerobically doesn't mean it's not healthy.

[00:28:46] In this model, it clearly shows that in the different stages, specifically CDR1 and CDR2,

[00:28:57] the mitochondria aren't supposed to be producing energy efficiently.

[00:29:05] So that's why I stopped there for a second because even I am saying the healthy mitochondria.

[00:29:13] But in the healthy state of the cell, the dominant mitochondria is M2.

[00:29:21] So when I say healthy mitochondria, that's what I'm talking about.

[00:29:24] Healthy?

[00:29:25] You're saying the healthy mitochondria.

[00:29:28] Yes.

[00:29:29] So again, so right.

[00:29:31] So the M0 kind of the in-between mitochondria is still elevated or at least slightly elevated.

[00:29:40] It's dropping.

[00:29:40] And the M2 mitochondria aren't aren't completely dominant.

[00:29:45] So what that does is it creates kind of a low-grade inflammation.

[00:29:51] You've got inefficient energy production.

[00:29:54] And that leads to cellular dysfunction.

[00:29:57] And so Navio tied that to differentiation disorders, such as chronic fatigue syndrome and fibromyalgia and neurodevelopmental disorders like autism spectrum disorder.

[00:30:15] So again, so the CDR reframes what's often called mitochondrial dysfunction as mitochondria doing exactly what it's supposed to do in response to stress, depending on which phase it's in.

[00:30:32] With chronic disease, the problem is not mitochondria is not doing what it's supposed to do.

[00:30:37] It's that the progression isn't occurring for some reason.

[00:30:40] So why might that happen?

[00:30:42] And really, it's just that the cellular signaling is not allowing that progression.

[00:30:48] So one example is actually oxidative stress.

[00:30:51] Oxidative stress is not only that part of the CDR's signaling system.

[00:30:58] Remember, reactive oxygen species are produced in CDR1.

[00:31:04] Not only do they help destroy pathogens and trigger immune activation, but if it persists for too long, it can.

[00:31:18] So under that case or under the normal case, it's an output of the CDR, right?

[00:31:24] CDR goes into CDR1, starts producing oxidative stress, inflammation.

[00:31:30] And that's a good thing because that tells the other cells that something's going on and the reactive oxygen species that are being created are killing pathogens.

[00:31:42] The problem is if that persists too long, that can now become a trigger in and of itself.

[00:31:48] And so you can get into this vicious cycle.

[00:31:55] And so that's one possible way that the cell gets stuck in one of the healing phases.

[00:32:10] Now, this makes the most sense or it seems most obvious in CDR1.

[00:32:15] Well, that's where it's supposed to be producing the oxidative stress.

[00:32:19] And so it makes sense that if you stayed there for too long, well, then it can become a trigger for CDR1, keeping you from ever removing or ever transitioning out of it.

[00:32:32] That one's kind of straightforward.

[00:32:34] But the same type of thing can happen in CDR2 and CDR3 as well.

[00:32:39] Remember, even though we've got M1 in CDR1, M0 in CDR2, and M2 in CDR3, it's not complete.

[00:32:53] Actually, the only one that's fast is M2 dies off really fast in CDR1.

[00:32:59] It drops down to zero almost immediately.

[00:33:00] But honestly, then it slowly creeps up in the concentration of M2 mitochondria all the way until you get to exiting CDR3.

[00:33:14] And I know I'm starting to get a little bit technical here.

[00:33:16] But my point is that it's not completely black and white in any of these, in which case oxidative stress is still being produced in the other two,

[00:33:29] especially if something occurs that keeps the cells from moving on.

[00:33:36] And then the oxidative stress can be a trigger to keep it at that point and doesn't let it continue.

[00:33:44] So the short answer was, why would that happen?

[00:33:52] What could mess up the cellular signaling?

[00:33:54] Well, oxidative stress could.

[00:33:57] Got it.

[00:33:58] So would it be okay to say that because the cells are stuck in different stages, that is the reason for chronic illnesses typically.

[00:34:16] And but then how do we get them out on the healing side, especially in terms of treating the chronic illnesses?

[00:34:23] It seems like it seems like a circular or cyclic loop kind of situation here.

[00:34:30] So.

[00:34:31] Yes.

[00:34:32] Well, honestly, any vicious cycle.

[00:34:34] Right.

[00:34:34] If you can break the vicious cycle and start making things better, they normally come into or become a virtuous cycle.

[00:34:41] Right.

[00:34:42] If you can change the signals that are pushing you in the wrong direction and reset them,

[00:34:48] it normally starts pushing you in the right direction.

[00:34:51] Yeah.

[00:34:52] That's a.

[00:34:54] I feel like that's a topic in itself.

[00:34:57] It should talk.

[00:34:59] But yeah.

[00:35:00] So to just kind of recap there.

[00:35:04] So remember, chronic disease really is just the cell has been doing what it's supposed to do in this healing phase for too long.

[00:35:15] And so it's not it's not a failure of the mitochondria or the failure of the cells themselves.

[00:35:24] It's a failure of the signaling to have that cell move on.

[00:35:30] Now, that signaling failure could be because we're continually getting triggers and those triggers could be environmental factors,

[00:35:40] could be all sorts of things, in which case the body.

[00:35:46] I don't want to say shouldn't move on, but isn't moving on because you keep on re-triggering.

[00:35:51] And that again, that this makes a little bit more sense when you consider CDR1.

[00:35:56] But the same type of thing can happen in CDR2.

[00:36:00] Honestly, it's more likely to happen in CDR2 and CDR3 if CDR1 had been being triggered too often or for too long before.

[00:36:11] You know, it had been there for too long before it came out.

[00:36:14] Well, now things you do get what's called or what I like to call immune fatigue.

[00:36:20] Now, that might actually refer to something systemically.

[00:36:22] I use it to refer to local immune fatigue, where locally the immune system in the cells kind of get exhausted.

[00:36:32] And that can cause some of these problems or exacerbate some of these problems.

[00:36:38] Okay. Now, you mentioned how CDR model has influenced your understanding of therapies like eyeball.

[00:36:48] Can you explain how the model might help us understand why certain approaches like the eyeball-based therapies are effective for some conditions?

[00:37:01] Sure. Okay. So let's readdress eyeball.

[00:37:06] So remember that ion biotechnology, aqueous ligands, I-B-A-L, and pronounced eyeball, so I don't sound quite so pretentious.

[00:37:15] So really, it just works by addressing some of the key factors that keeps cells stuck in the CDR.

[00:37:21] And there's a reason why I focused on oxidative stress before.

[00:37:26] Not only is it one of the biggest ones and has ramifications to all sorts of other signaling, but that's also the one that eyeball does really well with.

[00:37:38] Remember, so we addressed and touched on how oxidative stress can be both an output of and a trigger for the CDR.

[00:37:47] And especially, well, in the early phase, right, CDR1, the reactive oxygen species are produced to help eliminate pathogens and signal danger, right?

[00:37:58] But if it's not resolved, it becomes a bottleneck keeping the cell stuck in CDR1.

[00:38:06] And then, as we addressed, it also then disrupts progression through CDR2 and 3.

[00:38:14] And remember, so basically, and again, this is where eyeball shines, right?

[00:38:19] So it helps reset the cellular signaling pathways tied to oxidative stress by delivering that highly bioavailable zinc and copper ion.

[00:38:32] We talked about this maybe a couple times already.

[00:38:36] Remember, zinc and copper are the critical cofactors for superoxididismutase or SOD.

[00:38:43] And that's the enzyme that the cells use to reduce oxidative stress, the first line of defense.

[00:38:49] And it's often the zinc that is the limiting factor for SOD functionality.

[00:38:56] And by eliminating that bottleneck, cells can then reduce oxidative stress naturally, essentially as fast as they want to.

[00:39:05] And again, that process is entirely conditional.

[00:39:10] Because if the immune system still needs to produce oxidative stress, like for fighting pathogens,

[00:39:18] then eyeball is also supplying copper ions.

[00:39:23] And then the immune cells will essentially pick up the copper ions and use the copper ions to help produce the reactive oxygen species that it needs.

[00:39:38] But so that kind of is all focusing on CDR1.

[00:39:42] So I need to point out that eyeball supports progression through all of the CDR phases, right?

[00:39:50] So, for example, it's that the antimicrobial properties that we addressed before help eliminate pathogens in the first place.

[00:39:58] And not only is that critical for transitioning from CDR1 to CDR2, because in many cases that is the critical threat,

[00:40:07] but those pathogens were also the main reason for the higher levels of oxidative stress in the first place.

[00:40:16] So here's a good example.

[00:40:18] I'm going to step back for a second.

[00:40:19] If we had just an anti-inflammatory, you could take an anti-inflammatory.

[00:40:25] It forces the body to reduce inflammation.

[00:40:28] And, oh, well, everything's fine, right?

[00:40:30] Well, no.

[00:40:31] If you haven't addressed the microbial threat, the cells are immediately going to,

[00:40:36] as soon as the acetaminophen or whatever that drug was wears off,

[00:40:40] the cells are just going to immediately ramp right back up into inflammation because it hasn't done its job yet.

[00:40:46] The cell is still in CDR1.

[00:40:48] It shouldn't come out.

[00:40:49] So that's a really good example of a cratogenic drug there versus what we're trying to get to here is salutogenic drugs,

[00:41:02] that if we can get rid of the pathogens and reduce oxidative stress, well, now the cell will accept that.

[00:41:12] And once you reduce the oxidative stress, that can allow you or allow the cell,

[00:41:17] that's the reset button and allows the cell to go on because there's not this trigger that's still there that's going to pull it back.

[00:41:28] And then, you know, essentially you can kind of have the same type of thing occur in CDR3 that then lets the cell go into homeostasis, right?

[00:41:40] And so we've seen this in the kind of real-world cases.

[00:41:44] I'll come back to our rapid healing of the untreatable diabetic wound, right?

[00:41:54] So I guess I want to point out here for the wound, for that diabetic wound to heal, first thing that had to happen,

[00:42:02] we had to get rid of the pathogen, right?

[00:42:05] Whatever the infection was, we had to get rid of that.

[00:42:08] Then that allows the cell to transition to CDR2.

[00:42:15] Now, with continued eyeball product use, in this case, that was the ion gel, it's not forcing the cell to move into CDR3

[00:42:25] because now we've got this big, huge wound that we need to heal.

[00:42:30] And remember how I mentioned that it healed really, really fast?

[00:42:34] Well, that means that the cell must have stayed in CDR2 and stayed there really well because it healed very rapidly.

[00:42:45] And then not until that stage is done does it transition to CDR3.

[00:42:53] And, you know, the eyeball products have been used on other proliferative diseases and have helped those cells transition from CDR2 into CDR3 very rapidly

[00:43:04] and then self-terminate when they needed to.

[00:43:08] But my point is we didn't force that to happen.

[00:43:12] And the healing of diabetic wounds is a really good example because if we forced the cells out of CDR2, they wouldn't heal.

[00:43:20] They wouldn't rebuild.

[00:43:22] You'd still have, you know, a big, huge hole in your foot there.

[00:43:28] So I guess this really the CDR is an ideal model that allows us to explain how and why eyeball is working.

[00:43:46] Right?

[00:43:47] It doesn't really help eyeball do it.

[00:43:49] It's going to do what it's going to do.

[00:43:50] The cells are going to do what they're going to do.

[00:43:53] The fact that eyeball works really well under various conditions could be very confusing.

[00:44:02] The CDR explains why it works as well as it does.

[00:44:06] Yeah.

[00:44:07] That's kind of like eyeball therapies keep the cells on course and then make sure they progress in the right way.

[00:44:19] Yeah.

[00:44:20] And again, but really it's more resetting.

[00:44:23] Right?

[00:44:24] So and that's what our cells are really good at healing normally.

[00:44:29] And that's fine.

[00:44:31] It's only under repeated exposure to the stresses that we get this local immune fatigue and or local cellular fatigue.

[00:44:41] I don't mean that when I say local immune fatigue, I'm not only talking about the immune system.

[00:44:46] I'm also talking about the cells themselves.

[00:44:48] They become fatigued as well.

[00:44:50] In which case, they're not responding as quickly and as efficiently as they should.

[00:44:58] And all we have to do is get rid of those triggers.

[00:45:01] Now, in many cases, those triggers are pathogen.

[00:45:06] Eyeball's really good at that as well.

[00:45:08] So we can get rid of those triggers.

[00:45:10] Once the triggers are gone, then you can still have that oxidative stress, vicious loop,

[00:45:19] and everything else, all of the other signaling confusion that occurs with that.

[00:45:27] Now you can reset that.

[00:45:30] And if you can reset that well enough and efficiently enough, then the cell without the triggers

[00:45:39] can finish that stage of healing that it's in.

[00:45:42] Now, if it was in there too long, then we might have had chronic illness.

[00:45:46] And then that's what we're fixing.

[00:45:48] If it wasn't staying in there too long, and that's just the normal time that it was in there,

[00:45:53] well, then it is just transitioning to the next stage when it needs to.

[00:45:58] Yeah.

[00:45:59] Okay.

[00:46:00] Now, could the CDR model change how we approach healthcare overall?

[00:46:07] What impact could it have on treating even mental health for that matter?

[00:46:13] Um, so you might suspect that my answer is absolutely.

[00:46:19] So the CDR model really fundamentally can shift our focus in healthcare by or from merely treating

[00:46:27] symptoms to addressing the, I don't want to say the root cause, but the root causes of cellular

[00:46:33] stress.

[00:46:34] And that really can transform how we think about chronic disease management, preventative care,

[00:46:41] and yeah, even mental health.

[00:46:43] Uh, so, okay.

[00:46:45] For, for example, um, instead of trying to, you know, suppress the symptoms of inflammation,

[00:46:51] we can focus on identifying what's triggering the inflammation in the first place, address

[00:46:57] that.

[00:46:58] And then once you, uh, then once you address the, the inflammation, if it got out of control

[00:47:04] again, now it'll stick this time.

[00:47:06] Right?

[00:47:06] So that approach can lead to a more personalized medicine where treatments are targeted, uh,

[00:47:12] targeted more to the specific stressors of each, that each patient, um, is facing.

[00:47:17] And by understanding, uh, CDR, we can gain, you know, gain or, or develop new tools, uh, to,

[00:47:25] for the cells, um, to complete the healing cycle rather than just making the sign or, or, or,

[00:47:34] I guess, uh, making things that mask the signs of an incomplete process.

[00:47:41] Right?

[00:47:41] So you, you asked about mental health.

[00:47:43] So, um, uh, the CDR model could, uh, reframe conditions like, uh, PTSD or depression as prolonged

[00:47:54] cellular stress responses.

[00:47:57] And this opens up entirely new, uh, avenues for treatment, um, focusing not on just on the

[00:48:03] brain, but on cellular recovery throughout the body.

[00:48:06] Um, for, for example, uh, therapies that support mitochondrial function.

[00:48:13] Uh, reduce systemic inflammation, resolve autonomic dysfunction could become a key components

[00:48:19] of mental health care.

[00:48:20] And, and I guess this is a little bit of a cheeky example, but have you ever gotten a

[00:48:25] massage and felt better mentally as well as physically afterwards?

[00:48:30] Yeah.

[00:48:31] And that's because it's kind of all tied together.

[00:48:35] Um, so really, I guess the, the big picture here, uh, or the big picture perspective challenges

[00:48:41] us to move away from ratogenic approaches.

[00:48:44] I hope that's coming across, um, that are forcing body into certain actions and instead

[00:48:50] focus on, uh, salutogenic treatments that support the natural healing processes.

[00:48:56] Um, and it's a shift toward, you know, working with the body's innate systems, ensuring, uh,

[00:49:02] cells have all the resources and signals.

[00:49:05] That's actually really important and the signals that they need to restore health.

[00:49:09] Um, and so I, I guess, you know, imagine the input that this could have on chronic disease

[00:49:18] like, uh, diabetes or autoimmune conditions, uh, but on complex multifactorial diseases, uh,

[00:49:27] like, uh, long COVID or neurodegenerative diseases or aging cancer.

[00:49:33] Um, so by addressing these root causes, the CDR model can make healthcare more effective, um,

[00:49:44] and, uh, preventative and, and truly patient centered.

[00:49:50] So I guess, uh, specifically for mental health, uh, I think because a lot of things in mental

[00:49:59] health is a response to stress, which is a response to cells changing in stress.

[00:50:06] And yeah, absolutely.

[00:50:08] But remember stress is systemic on the body as well as local, right?

[00:50:13] And so the, the brain doesn't necessarily look at mental stress versus physical stress, any

[00:50:20] different, it's all stress.

[00:50:22] And the, the brain, depending on what's in everyone's brain is different, depending on

[00:50:28] where we're at and what's happening, um, uh, you know, what our resilience is.

[00:50:33] We've talked a little bit about that.

[00:50:35] A lot of different factors.

[00:50:36] You basically can kind of think of it like a threat bucket, right?

[00:50:39] And your body can be, you know, your brain essentially is I'm fine with anything below

[00:50:44] this level.

[00:50:45] And, you know, you can roll your ankle.

[00:50:47] Ah, that kind of hurt a little bit.

[00:50:48] It doesn't really matter.

[00:50:48] Not a big deal.

[00:50:49] Um, you know, my wife's yelling at me, I've got to get my kids, you know, all of that can

[00:50:55] just be, you know, water off your back until you get to a certain point.

[00:51:00] And then the brain says, yep, this is enough.

[00:51:02] And then any little thing can basically start triggering you.

[00:51:09] And I, I know that that word is, uh, um, charged, but truly that then can start triggering the

[00:51:18] CDR and where is it triggering you?

[00:51:21] Well, we don't necessarily know.

[00:51:23] It kind of could be all over the place, whatever your brain is most concerned with.

[00:51:27] And it's not that, oh, well, you know, everything was fine until I whacked my arm here and now

[00:51:33] everything is problematic.

[00:51:34] Well, the brain doesn't think that your arm is more important.

[00:51:37] It's just, that was the straw that broke the camel's back.

[00:51:41] And, and actually, now that I say that we often then look at this as, oh, this is where all

[00:51:47] of my problem was because everything was fine until I hurt my arm.

[00:51:50] And now all of this other stuff is that, well, again, it was just the straw that broke the camel's

[00:51:55] back.

[00:51:56] And by reducing all of the other stressors, you can make your arm feel better.

[00:52:04] Yeah.

[00:52:04] This is, this is getting into kind of the whole, uh, somatic, uh, or the neurosomatic integration

[00:52:11] that, uh, that eudaimonia focuses on a lot.

[00:52:14] Interesting.

[00:52:15] Yeah.

[00:52:15] We should probably talk about this in probably one of the episodes later, but, uh, that would

[00:52:20] be great.

[00:52:21] Yeah.

[00:52:22] So obviously, you know, maybe this is the last question for today, but, uh, learning about

[00:52:29] the CDR totally fascinating concept and everything, how it's coming together, how it explains why

[00:52:35] eyeball works, uh, to, to that level.

[00:52:38] But for someone listening right now, what's one thing they can do today to support their

[00:52:45] body's healing and health creation?

[00:52:48] Um, talk about that.

[00:52:50] Um, so it feels like a cop out to just say, uh, start living that salutogenic lifestyle

[00:52:57] that we discussed.

[00:52:58] Um, so I'll, I'll try and tie it more directly to the CDR, right?

[00:53:04] Um, but really this is the salutogenic lifestyle, right?

[00:53:07] So one of the things that we haven't discussed much, um, about is, uh, I mean, I touched on

[00:53:13] it a little bit is that the CDR gets triggered, um, or what happens when the CDR gets triggered

[00:53:19] too often, right?

[00:53:20] And that does cause that immune fatigue or local immune fatigue.

[00:53:25] And, um, I, I, I pointed out that that can make it hard for yourselves to continue progressing

[00:53:30] through the CDR.

[00:53:31] Um, and now remember that's their levels to this, right?

[00:53:36] So that doesn't mean that, you know, you're going to develop cancer.

[00:53:40] Um, although it increases the chances for sure, but it also increases the chances that your

[00:53:46] cells then don't finish healing correctly and get spit out as senescent cells.

[00:53:52] Have you ever wondered why, you know, you can look at somebody who lives, you know, a healthy

[00:53:57] lifestyle and they look 10 years younger than somebody who doesn't.

[00:54:01] Well, that's why it's there.

[00:54:05] They're, uh, you know, well, everything that they're doing, actually, a lot of it does come

[00:54:09] back to mitochondrial function, right?

[00:54:10] So almost everything that we do to be healthy increases mitochondrial function.

[00:54:14] Um, but that also then means that the CDR is functioning better.

[00:54:23] And cells that shouldn't exit or as they come out, they're not viable.

[00:54:30] They should, uh, self-terminate and that should happen in CDR3.

[00:54:34] Um, that then happens more rather than whatever's going on where they don't, uh, exit to health,

[00:54:43] but they don't get stuck in the CDR and the exit is as senescent cells.

[00:54:49] Remember we explained those as aging.

[00:54:51] Well, if your body is producing them at a faster rate, that means you're aging faster.

[00:54:57] That's exactly how that works.

[00:55:00] Um, so, uh, what is one of the most, uh, relevant things, relevant to the CDR, uh, that you can

[00:55:07] do to support your body's, uh, healing and I guess health creation is to start reducing

[00:55:13] CDR triggers or just start reducing cellular triggers.

[00:55:16] That means reducing your exposure to chemical, using organic foods, filtering your water, uh,

[00:55:24] avoiding unnecessary toxins in your environment.

[00:55:28] Um, you can manage stress, get better sleep, spend more time in nature.

[00:55:33] Um, anything that lowers your body's overall stress load.

[00:55:36] Many of these things are the same things that I listed off as to what's a ludogenic lifestyle.

[00:55:41] They're all the same.

[00:55:42] Um, uh, oh, I guess another one is, uh, getting proper nutrition for sure.

[00:55:49] Um, you need to get enough vitamins and minerals, uh, regular movement, um, supports circulation

[00:55:55] and optimizes mitochondrial function.

[00:55:59] Um, and I guess any lifestyle that, uh, um, encourages and promotes balance mindfulness practices,

[00:56:09] uh, or, you know, something as simple as, you know, trying to stay hydrated.

[00:56:15] Yeah.

[00:56:17] Um, and again, the key is consistency, um, supporting the body, uh, doesn't have to be complicated.

[00:56:24] It's about small, regular actions, uh, to help the cells do what they're naturally designed to do.

[00:56:32] Um, and over time, the, the, your small choices add up, allowing the body to stay resilient.

[00:56:37] Um, and, you know, with our little scale, um, every day improve the resilience adaptations

[00:56:46] as opposed to the dysfunction adaptations.

[00:56:48] And then that helps cells progress through the natural healing cycle.

[00:56:54] Great.

[00:56:55] Um, uh, if people want to listen or go more detail on Salutogenesis, we already have an episode,

[00:57:03] uh, people who have not heard it go back.

[00:57:06] I think it's episode two or one or two, check them out and you'll get a good idea of, uh,

[00:57:12] more on this direction.

[00:57:14] Um, so again, this has been great.

[00:57:18] Um, uh, uh, I appreciate you, you kept it slightly high level than people like me can understand.

[00:57:24] So that was great.

[00:57:25] Thank you so much for that.

[00:57:26] And, uh, and, uh, and I think, uh, it's, uh, we have a, we have a foundational blueprint

[00:57:33] of understanding CDR and more so why therapies are working with eyeball.

[00:57:38] That, that was a great insight to just wrap it up in this episode.

[00:57:42] So thank you so much for your time again.

[00:57:44] All right.

[00:57:45] Thank you.

[00:57:45] And yeah, I, I apologize if I, uh, uh, I, I do get a little bit more excited with this

[00:57:50] one because again, this, this is what started to really tie things together for me.

[00:57:55] Um, I think in, in, in, uh, a few more episodes, we're going to, uh, touch on the next thing,

[00:58:02] um, that was, uh, uh, really big for me to buy everything else together, but this is a

[00:58:07] big one for sure.

[00:58:09] All right.

[00:58:10] Well, stay tuned, uh, everyone, or you can go to our website, power of salutogenesis.com

[00:58:16] and you can catch wherever you catch your, uh, uh, uh, uh, your podcast video, how say

[00:58:22] what, which format you prefer.

[00:58:23] You can catch it there.

[00:58:25] Thank you so much.

[00:58:26] Wonderful.

[00:58:27] Thank you very much.