Transcript Disclaimer – Please note that the following transcript has been machine generated by an AI software and therefore may include errors or omissions.

Robin Daly
Hi and welcome to the Yes to Life show. My name is Robin Daly, hosting the show as usual today and also founder of the UK’s integrative cancer care charity, Yes to Life, supporting people with cancer in taking a broad holistic approach to their cancer care. Today’s show is part 3 of a series of episodes showcasing the findings of Mark Lintern, resulting from over 8 years of intensive research into the mechanisms and origin of cancer. If you missed parts 1 and 2, then I strongly suggest you make a point of listening to those first. Both are available on Listen on Demand, as podcast and on YouTube, in order that you get the most from today’s conversation. I’m speaking to Mark over the internet. Hi Mark and welcome back again for part 3 of Cancer Through Another Lens.

Mark Lintern
Hi Robin, thank you for having me.

Robin Daly
So for anyone who’s just joining us now at part three of the journey, I strongly recommend listening to the first two parts before continuing to listen to this episode, as it’s highly valuable information that builds as it goes, so it’s very well worth hearing from the beginning. As a reminder, I’d like to do a very top level recap of the science that we’ve covered so far. So we introduced Hannah-Hannah Weinberg Hallmarks of Cancer, which are 10 key behaviors of cancer that help with identifying the disease, and explained how you Mark have used the ability to be able to explain these behaviors as a benchmark to evaluate the accuracy of any theoretical model. You told us how the kind of mainstream theory, the somatic mutation theory that states it’s all a matter of damaged mutated genes driving the disease, not only has some major holes in it, but it can explain very few of these Hallmark behaviors. We went on to mention a raft of other theories that all have their strengths and weaknesses, but then we looked at the metabolic theory in some more detail, as this measures up much better against the Hallmarks, and it can explain at least seven out of the ten. A central focus of your attention was that in two respects, the mainstream narrative has sought to explain cancer in a way that requires the orderly process of cancer, sufficiently orderly in fact to be characterized by at least 10 predictable Hallmark behaviors, to be the result of random occurrences. Firstly, the lists of things that can cause cancer are wildly different from ionizing radiation to burnt food, viruses, asbestos, the list is endless, and the way of trying to tie these all together is to say that they cause damage to genes which then go on to drive cancer, but we now know that any damage that’s found is actually completely random. There’s no pattern to it that could predict an outcome like cancer, and the final nail in the coffin of this way of thinking is that in some instances there isn’t any damage found at all. You then honed in on one of the Hallmarks in particular that seems to be more important than the others, Hallmark 7, known as the Warburg Effect, which describes the distinctive metabolism or energy system of cancer cells. You identify that this can’t really be satisfactorily explained by anyone, and yet most of the other Hallmark behaviors occur as a result of it, so it’s a key Hallmark to investigate. So that’s where we left it, and now I want to pick up directly from there and ask you where your investigations into Hallmark 7 took you.

Mark Lintern
Okay. Thank you, Robin. Yes, it was interesting identifying Hallmark 7 as one of the key hallmarks. So from that conclusion, I began to look at the different possible aspects of biology that could explain the switch to glycolysis that occurs that Hallmark 7 refers to. So we’re talking about aerobic fermentation here or aerobic glycolysis. And in doing so, I was trying to identify the underlying mechanism that was driving Hallmark 7 that could possibly explain all the other hallmarks of cancer as well. And this led me through a process of looking at, say, exercise, for instance, because that stimulates glycolysis. If you overly exercise to a certain degree, you’re using both systems. Insulin resistance would be another one because insulin stimulates the use of glycolysis. Hypoxia, inflammation, iron overload, and glucose abundance, all these different aspects as well as faulty mitochondria and DNA mutation. Now, at this point, I’d gone through the process of looking at faulty mitochondria, understanding the process of defective oxfoss put forward by the metabolic theory and DNA mutation. And I’ve discounted them. So this is why I’m looking at these other aspects to try to determine what else stimulates glycolysis. So in the sense of insulin resistance, what I found to be against this aspect was that not all patients appear to harbor insulin resistance. So I always think that when I’m looking at this process as well, I’m trying to see the process as being caused by one particular predominant factor. So I’m assuming looking at the consistency of the disease that I’ve already concluded that there will be potentially an underlying mechanism that’s driving the disease. So we’ll touch on to factorial aspect of cancer shortly, I’m sure. So as I’m looking through insulin resistance, I’m finding that approximately 60% in several studies show that people have insulin resistance, but it’s not present in all of them. So from that perspective, insulin resistance cannot be the underlying driving mechanism of cancer in general.

Mark Lintern
Arguably, people who will look from the multifactorial angle will say, well, that’s just part of it, that I’m looking at it from this different perspective of trying to identify an underlying mechanism. So then we come to hypoxia and the obvious issue there with hypoxia is that glycolysis occurs in the presence of oxygen. So, I don’t know.

Robin Daly
Just to be clear, hypoxia means a shortage of oxygen.

Mark Lintern
Yes, a lack of oxygen. So hypoxia, when there’s a lack of oxygen, obviously mitochondria are unable to produce energy via oxvose, so glycolysis will be instigated to adapt to those situations to provide the ATP energy needed until the oxygen supply is resupplied. But in cancer, even though there’s sufficient oxygen present, glycolysis is stimulated.

Robin Daly
And just to refer that back to what we were talking about last week, so this is the Wahlberg effect effect. It’s not just that it switches from using oxygen to glycolysis, it’s that it does what it doesn’t need to, because there’s plenty of oxygen around. That’s the kind of defining factor of a cancer cell.

Mark Lintern
Yes. And it’s referred to quite correctly as aerobic fermentation. So fermentation happening or glycolysis happening even in the presence of oxygen. And obviously this is what Otto Warburg identified as being the Warburg effect. And because there’s oxygen present and mitochondria should technically be used for creating energy when there’s oxygen present, this led to the conclusion that mitochondria are faulty, which obviously led to the metabolic theory. So we have inflammation as well. Now inflammation is a precursor to cancer and quite a number of other diseases. But it appears more so that inflammation is an effect of other factors rather than the actual underlying cause. It plays an intrinsic role, which will be defined later. But it’s an effect, not necessarily a cause. That iron overload is another one. Now this can stimulate glycolysis through the mechanism of damaging mitochondria. We’ve already established through this that faulty mitochondria are potentially not the underlying mechanism involved. And then you have glucose abundance. Now this in particular studies in the lab when you’re growing cells on a glucose substrate, this can stimulate glycolysis even in the presence of oxygen, which suggests that mitochondria are faulty. This is known as the Crabtree effect and doesn’t actually signify that mitochondria are faulty. It’s just a case of where there is an abundance of glucose, the body will tend to utilize glycolysis because it consumes far more glucose in order to reduce the level of glucose in the surrounding tissue. And of course either one I mentioned was right at the beginning was exercise. Exercise stimulates glycolysis depending on how intensive that exercise is, but that can’t be the underlying mechanism driving cancer because exercise has been found to be a massive preventative measure, up to 60% preventative in cancer. Same.

Robin Daly
So there are six things there that you looked into, all things which are known to be able to play some part in the Waldberg Effect, but for one reason or another you dismissed each of those as being fundamentally to do with driving cancer.

Mark Lintern
And there’s bound to be more that I haven’t covered, but these are the main ones that I’ve identified.

Robin Daly
Okay. So, uh, okay, you’re empty and at that point, where did you go next?

Mark Lintern
Well, that was the moment at which through all the other research I was doing, remember that this time I’m literally looking into everything, every possibility. So this wasn’t such a linear process all the time. It wasn’t like I took this and went, oh, here’s the six. I was building this model constantly, adding to, oh, right. So later on, our glucose abundance can cause glycolysis. So I had this in mind as I was going through all this other area of study. And I’ve later developed them into an easy, easy format to understand. So as I continued my research, I was looking at infection bacteria, viral and fungal infections and parasitic infections as well. And I came across a couple of studies that suggested within the body of the results that a Warburg-like effect had been initiated. And that caused me to sit back and pause because I wasn’t looking specifically at that point for an explanation for the Warburg effect. I was just trying to understand how microorganisms interact with the body. And that just jumped out at me. It was almost like a light bulb moment. I was like, well, okay. But at the moment, I’m looking for an explanation for the Warburg effect. And here we have an infectious agent potentially stimulating a Warburg-like effect, so let’s look more into this. And that’s what I did. I then found some current evidence confirming in many situations, not only in immune cells, but in epithelial cells when they are challenged with an infectious agent of some kind, a pathogen. They actually resort to instigating the Warburg effect. So glycolysis is instigated in spite of abundant oxygen present.

Robin Daly
amazing so you know this is to me is absolutely major firstly is a well-known mechanism that’s actually called a warburg like effect it’s not like beating around the bush all right uh that could exist in infectious diseases and never be mentioned in cancer circles i mean when you told me this i was awfully shocked that i’d never heard of such thing in almost two decades of years to life i was like what you mean there’s something happening over there in infectious diseases i mean how do you think this could have occurred that that this effect was kind of so off piste if you like from cancer

Mark Lintern
Um, I, I think it’s because at the end of the day, the human body is incredibly, incredibly complex and that’s, that’s why I suppose, uh, medicine is broken down into many different areas. Um, and these areas specialize in the complexity, uh, within each field. Uh, I think it will probably be, I mean, I’m not an expert on this, but I’m assuming it’s probably to do with, uh, maybe so much complexity between each field means that each discipline doesn’t necessarily communicate directly with each, with each other as much as you would need to, to probably solve problems such as this.

Robin Daly
Well, that does make sense, but anyway, considering they actually named it after the Waldorf effect, which is specifically about cancer, it’s just extraordinary. Because you were telling me not just that you came across this thing, which was a surprise, but you then made the assumption, well, of course they must have looked into this and discounted it as being anything to do with cancer, but you found out it wasn’t the case.

Mark Lintern
Yeah. So I think my initial surprise was that it was mentioned as such. And I didn’t pursue it because I was just more interested in understanding mechanisms of invasion and how infection plays out in the body. And it was only when I came back to it, when I realized I tried to search for information to do with infection involved in cancer, because obviously it’s recognized that about 20% of infection is related to causing cancer. When I looked at those infections, those oncogenic viruses and certain bacteria, such as helicobacter pylori that increases the risk of gastric cancer, there was no explanation of this Warburg-like effect in the sense that these infectious agents weren’t causing a switch in energy metabolism. And then I think the reason for this is probably based on the fact that most oncologists are looking purely at this from a somatic mutation viewpoint, a metabolic viewpoint. So at this point, I studied the metabolic theory as well. And I kind of acknowledged and realized that the metabolic theory wasn’t really at the forefront of the minds of a lot of these scientists looking into cancer. So I could rationalize why they maybe hadn’t seen this link. But at the same time, I realized when I looked at this infectious side of things that was recognized within the mainstream as being a potential cause or risk factor of cancer, I realized that these infectious agents weren’t being looked at from this angle of causing this energy switch. They were looking at it from the angle of causing DNA damage to the cell. So that’s when I pushed more research into looking at the Mach 7.

Robin Daly
That does make sense and of course if you presented Otto Wahlberg with this information he’d have got pretty hot on the collar immediately I would say. You’re right, the Wahlberg effect is something that’s acknowledged by everybody. Nobody says it doesn’t exist or it’s not true or anything. Everybody appreciates that it happens but it’s the amount of significance attached to it that varies whereas the metabolic theorists attach huge significance to it. The somatic mutation theorists is just one of the things that happens with cancer, it’s like a symptom.

Mark Lintern
Yeah, and that’s kind of surprised me as well. Because there doesn’t appear to be, like I say, there’s a siloing even within cancer science between the theories. I was quite shocked with the proponents of the somatic mutation theory, kind of not necessarily ignore, but focus all the attention on that theory and don’t tend to stray into the field of other theories as such.

Robin Daly
If it was a well-supported theory that actually there’s plenty of evidence for, that would be fair enough, I think. You’d be backing the front paw, so to speak, but given the fact it’s got evidence to show that it’s actually not true these days, you could say it was disproven by the fact they now know that some cancers don’t have any DNA mutations, that pretty much disproves the somatic mutation theory in my book.

Mark Lintern
Yes. But again, there’s this aspect of cancer that is multifactorial. So I suppose proponents of the somatic mutation theory will say that, well, okay, those particular cancers that don’t harbor any driver DNA mutations are likely caused by something else, another mechanism. And I suppose that’s kind of an explanation, almost an excuse, but a way of explaining away the controversies of the somatic mutation theory, in a sense.

Robin Daly
Okay. So I just want to go over one thing, which I think is very important to the population at large. And that is that what you’ve just described is a very different story to the narrative we’ve been fed forever by the medical world and the media about sort of mutant cells somehow getting a mind of their own, becoming sort of evil and self-interested and attacking us from within. It seems to be something between a 1950s sci-fi and a religious notion to me. And now we find out that the central behavior of cancer cells could be depicted as a normal natural method of defense against infection, a completely different ballgame basically. And just hearing that, my common sense meter is bouncing off the top end is actually a relief to hear something that fits in with everything else we know about our bodies and the way they act to continually keep us safe and well in every circumstance. So I think, you know, that that’s a very important aspect of it. And so you mentioned this multifactorial thing several times. This is a big deal, really, isn’t it? And something we should speak about. So this is the mainstream view of cancer. And the fact goes, I would say, beyond mainstream. It is the view of cancer generally held everywhere by most theorists.

Mark Lintern
Yeah, so I think the idea pretty much springs from the concept that in smashing mutation theory is unable to fully explain the disease, especially given the randomness of the mutations that appear to occur. As well as this, you have the introduction of all these carcinogens and how different and varied they are and the different damage that they cause. So what you have is an amalgamation of a huge abundance of randomness, essentially. So how do you explain that randomness? How do you explain that causes the consistency of the disease? Well, the only way of really rationalizing it, if you are still in support of the somatic mutation theory, is to actually claim that it’s a multifactorial disease that can be called by a multitude of different mutations and different levels of damage to different parts of the cell. That would then make the disease incredibly complex and give more time to try and carry on with this perspective, I suppose, to try and work out exactly what’s going on. But that doesn’t seem to make sense in terms of the disease being consistent. The other notion is, obviously, that just maybe the somatic mutation theory has misinterpreted the underlying mechanism of causing the disease. So the multifactorial aspect is trying to explain away, in effect, the inability of randomness to cause consistency by stating that so many different factors possibly could cause the disease. Now, I think there’s two aspects to the multifactorial side of things that need to be mentioned. One is that, obviously, carcinogens that I mentioned earlier, there’s so many of them and they cause an incredible amount of damage to varying degrees. That side of cancer is multifactorial in the sense that so many different carcinogens appear to drive the disease. So I’m in agreement with that aspect of the multifactorial trigger, if you like, of cancer. What I’m not in agreement with is the multifactorial mechanism that drives the disease, that randomness can cause consistency, which brings us back to Hallmark 7 and the influence of infectious agents or microorganisms. Like you say, it provides a consistency to the mechanism that drives this switch in metabolism.

Robin Daly
Okay, understood. Well, look, we’re going to come back round to how you would explain how all these different carcinogens can seem to lead to the same disease a bit later. But for now, I’d like to come back to the path we were on and go a bit further with finding out a bit more about this Warburg-like effect because there’s been some recent science on cell behavior that plays right into your story in a remarkable way. So do you want to tell us a bit more about that?

Mark Lintern
Yes. So, Dr. Navio is a scientist who has been trying to explain chronic disease through a metabolic perspective. He’s created a model called the Cell Danger Response Model, which has been looking at how the cell reacts to certain threats. Now, when I looked at his model in terms of infection, it goes something like this. Okay, sorry, before I go through that process, I’ll just quickly explain. There are three aspects to Navio’s model. The Cell Danger Response 1, or CDR1, CDR2, and CDR3. CDR1 is about containment and innate immunity, so it deals with a response to, say, an infectious agent and hopefully kills that infectious agent. CDR2 is the second phase, and it moves to this phase once the infectious agent is killed. That’s the phase of aerobic glycolysis and proliferation, so essentially cell repair. And then once cell repair has completed its task, we go to the CDR3 phase, which is differentiation and development, and it’s essentially a return back to homeostasis, back to the original state of the cell. Now, if we were to look at how an infectious agent or a pathogen invades a cell and the response to that, once a pathogen is detected by a cell, and this is an epithelial cell as well as an immune cell,

Robin Daly
Explain what an epithelial cell is, will you?

Mark Lintern
An epithelial cell is a type of cell that essentially lines most of the outer layers of the body, essentially skin is an epithelial cell layer. Mucous layers, the layer that surrounds your lungs and various organs, so these epithelial cells are essentially the cells, the outer barrier if you will, of cells that infectious agents come into contact with. So upon detection of a pathogen of any kind, through the cell danger response CDR1 phase, the cell will, and this is quite interesting, the cell will intentionally, or the mitochondria I should say, will intentionally restrict OXFOS. This is for the purpose of flooding the cytosol, the inner part of the cell, with oxygen. The priority here is to prevent the ability of the invading pathogen to synthesise proteins RNA and DNA. So it’s a response to inhibit the infectious process. Now, that is essentially what kind of happens with the Wahlberg effect. So because the mitochondria are trying to deal with the infection by blocking OXFOS essentially, glycolysis is instigated during this infection process. So what we have here is an infectious agent coming into the cell, mitochondria intentionally restricting OXFOS to use the oxygen to target and restrict the pathogen whilst glycolysis is increased in the presence of sufficient oxygen in the surrounding tissue, which is essentially the Wahlberg effect.

Robin Daly
Right, so just to be clear then, by switching over to the backup energy system, all the oxygen is then available to be used as a weapon basically against the invading pathogens.

Mark Lintern
Yeah, to inhibit the pathogens’ ability to take control of cell pathways. And what we find as well is in other studies of infectious agents, if the infection persists within the cell, if the CDR phase, the containment and elimination of the pathogen isn’t complete and ineffective, then this energy switch to glycolysis is sustained until the pathogen is eliminated. So it appears, if you look at Dr. Navier’s model, that the cell with an intracellular infectious agent present is stuck between the process of CDR1 and CDR2, which is where the cell is attempting to obviously continue to kill the pathogen, but also is stuck in the process of aerobic glycolysis, which is a proliferative state, which perfectly explains the Wahlberg effect or Hallmark effect.

Robin Daly
Okay, so there, you’ve stepped across into cancer there, Slaveen, as much as you’re saying that the Warburg effect is obviously not just a one-off of cleaning up of some of the finishes, it’s actually protracted, it keeps going, and the reason for this being stuck between these two phases of Navio’s cell danger response is because it hasn’t succeeded in killing the infection. So it’s actually busy all the time trying to kill the infection, which looks like a consistent switch to glycolysis.

Mark Lintern
Absolutely, and until that infection is eliminated then the process won’t be able to move to CDR3 and back to homeostasis. Right, right.

Robin Daly
Oh yeah, very interesting. So, looked at in terms of where we’ve placed Hallmark 7 in the overall scope of things, and now you’ve come up with a known mechanism that actually does actually kick off the Wahlberg effect and maintain it. With all the other Hallmarks being downstream of Hallmark 7, all kind of results of Hallmark 7, you’ve actually come up with a mechanism which could be the driver of cancer.

Mark Lintern
Well, yes.

Robin Daly
Yeah, amazing. Okay, so a little bit of compare and contrast. I mean, I’ve already alluded to the mainstream narrative which puts the blame, if that’s the right word, squarely on the rogue cell for causing all the trouble. There’s a crucial way in which your explanation of cancer differs from all the other attempts at explanation. Do you want to tell us a bit about that?

Mark Lintern
Yes. So when I was looking at all the other theories and analyzing them, it became apparent that they all tend to view the disease from pretty much the same paradigm, which is that carcinogens and infection causes inflammation and cell damage, which results in cell malfunction, which is the cell gone rogue aspect you’re talking about. So with the cell malfunctioning or becoming faulty in a particular way, it almost gains autonomy. It’s broken free from its restraints of growth signaling and cell death, and it’s developed to the mind of its own, essentially. So the cell malfunction concept of the cell being blamed or the cell going wrong kind of underpins most of the mainstream theories. And then that also moves into the realm of randomness. Again, the damage to the cell is the problem. And then it’s the randomness of the damage that then causes the consistency of the disease, which again, doesn’t sit well with me, because we can’t find or uncover the specific randomness or the specific damage or replicate the specific damage that we think is responsible. So from this concept of looking at this infectious agent coming into the cell, triggering Dr. Navio’s CDR response and the Warburg effect and sustaining it, I realized that there’s potentially a completely different mechanism driving the disease, which is that of cell suppression. So in this instance, carcinogens would cause the inflammation and cell damage, and that would enable infection to occur. And once the infection takes hold, that infectious agent, that pathogen, suppresses specific cell mechanisms, which then leads to the rest of the conditions of the disease.

Robin Daly
very interesting. So this is the very heart of your new proposal for the mechanism and indeed then the origin of cancer. So you’ve talked about this now as cell suppression, and you’ve contrasted that with cell malfunction, which everybody else is talking about basically. Regardless of theory, everybody says some bit of the cancer cells gone wrong. They argue about which bit, but it’s the same idea. Essentially, you’ve got this cell which is autonomous and is not in line with the rest of the body all of a sudden. So you’re describing the cell as kind of a victim of circumstances here. And as I’ve already said, the effect for me of understanding this was a sort of ah moment in which the relentless march of cancer began to fit in with everything else that I know about the human body, nature, and health. The weird behavior of cancer cells is no longer attributed to some dare I say woo woo idea. They’ve developed a mind of their own and like zombies who’ve been irrevocably turned to the dark side, they’ve simply been overcome by a parasitic pathogen and despite their most valiant efforts to keep as well, are being exploited for the benefit of the pathogen. So in other words, they’re acting like aliens that want to take over our bodies because they really are being driven by aliens whose success is at our expense. This is like any infection scenario. It’s us versus invading bugs. So the whole thing begins to make some sort of sense and as I say, to line up with what we know about the human body and nature. So do you want to just go over this most important part of what you described about cell suppression versus cell malfunction? I just want to make quite sure everybody understands the difference between the two models.

Mark Lintern
Yeah. Okay. Well, the cell suppression model, as you just described, as I’ve put it forward, would be that evolutionary programming, or millions of years of evolutionary programming, has our cells working together eventually. And what’s happening here is that because of our poor diets and overexposure to certain toxins that we now have in the environment, the control mechanisms within the cell are becoming damaged and the surrounding tissue. And that allows these pathogens to take hold. So all the while this pathogen is invading the cell and trying to do its thing of sequestering nutrients and suppressing the cell’s response in defense, the cell is trying desperately to commit apoptosis. It’s trying desperately to commit cell death. Which is what it should do. Which is what it should do. So the cell is trying to do what it should do. But the outcome of the failure to eliminate the pathogen results in a cascade of the conditions we call cancer, essentially. And so when you go through this whole process and you look at cancer through the lens of a pathogen and the cell suppression paradigm, all the different aspects of the disease, angiogenesis, metastasis, random DNA damage, immune evasion, all these aspects begin to make sense. And the different ways cells or tumors tend to use different fuels at different periods can all be related to this battle between the cell trying to protect you against this infectious agent. It nicely explains all these abnormal behavior that simply occurs. And if we’re to switch it and look at the cell malfunction side, it’s very difficult to quantify the personality of a cell and analyze a cell gone rogue. We’re saying here that a cell’s developed a mind of its own. It’s developed a personality. That’s great theoretically and hypothetically, but we can’t measure that. Or do anything about that in terms of treatment. It doesn’t help to explain the reasons why something happens, why certain damage occurs, or why the cell operates in the way that it does. It’s just a way of trying to rationalize the randomness that we think causes the disease. But it’s not an end point to itself. You can’t measure the personality of the cell or change it, the personality of the cell, if that’s what you believe is driving the mecca as a concept. And that way, if you’re looking at it from that perspective, you’re going to try and kill the cell because you think it’s turned evil. But that has negative connotations for patients because you’ll attack yourself mentally because you’re thinking, why is my body attacking itself? When, in effect, it’s probably not attacking itself. It’s doing its best to defend you. It just is overwhelmed by this process of invasion by this particular pathogen.

Robin Daly
Well, it’s interesting. I mean, obviously, the biochemistry of this is enormously important and you’re saying something quite different. But that other aspect, which is the psychological and emotional relationship we have to the disease called cancer, is also hugely important, both in the terms of our relationship to life generally and our trust in life, but also in relation to how we try and treat the disease. If we think it’s something evil is trying to kill us, then we’ll use any measure, however, vile to try and kill it. But if we think that it’s actually ourselves doing their damnedest to keep us well, then what will we do? We’ll try and help them. We’ll actually support them in doing that job. That is a much more obvious route to take. So I think it’s enormously important, this kind of rewriting of the story. And I think it’s very important to point to the aspects of the general myth that are just so utterly unrealistic and unscientific, this mind of its own self thing. It just doesn’t mean anything to me at all. I mean, cells don’t have minds, you know, they basically are part of us and they’re always acting to keep us whole and well.

Mark Lintern
Yeah. They’re working collectively. And can I just interject there and get a quick example? So migrating cancer cells tend to have a protein on their surfaces called GLEP10-3. It’s expressed quite extensively on a number of migrating cancer cells. So if you look at the cell malfunction side of things, the cell’s gone rogue and it’s to blame. When I’ve looked at studies into this, scientists have concluded that, well, you know, the solution is to block the gene that produces GLEP10-3, which is a sticky protein. Okay. Because this enables migrating cancer cells to stick to other areas of the body, which allows it to spread. So the thinking behind it under the cell malfunction paradigm is that the cell is purposely generating the sticky protein in order to advance. But there is, if you look from the cell suppression perspective and the infection perspective, there’s a completely different interpretation of the same data. So GLEP10-3 is an antimicrobial protein that’s issued against particular pathogens. So one could argue that what the body is trying to do at this latter stage, when a cluster of cells are migrating from the initial tumor site through the bloodstream, they’re trying desperately to actually kill whatever microorganism is present within that cluster of migrating cancer cells. And so they’re bombarded with this GLEP10-3 protein. Now, that tells you that the body is working for you under the cell suppression paradigm. But the problem is, whether it’s because the immune system is weak, or whether it’s because the infection is protected within that cluster of migrating cancer cells because there’s stem cells involved maybe, then this overproduction of GLEP10-3 in this desperate attempt to defeat the pathogen actually enables the migrating cancer cells to then stick to a site in another part of the body. So it’s an accidental occurrence from the attempt of the failed attempt of the body to essentially suppress the infection.

Robin Daly
Well, very interesting. Yeah, completely different story. Same observation, but completely different conclusions. Yeah, really interesting. OK, well, look, we’re about coming to the end of today. I want to point towards what we’re going to start off with next week. I want to go in. You’ve already mentioned some of these sort of contributing factors. Where do they fit into the picture? That’s where I want to start off next week. You already mentioned inflammation, for example, as being a contributing factor to all cancers. And it obviously gets in there somewhere, but you’re placing it in a different position in relation to cancer than anybody else’s, I think. And so it’d be very interesting to hear about all those contributing factors and what actual role they place in it. So that’s where we’ll hit the ground next week. So big thank you again for today. Lots of complex stuff we’re going through. Thanks for taking the time and travel to really do the detail.

Mark Lintern
No problem, it’s an absolute pleasure.

Robin Daly
I hope you are able to follow that okay, a little science heavy for many listeners, but it is well worth taking the trouble to understand Mark’s perspective for yourself, at least in broad terms. For any of you listening who have a time imperative hanging over you and who literally aren’t in a position to wait for the coming episodes, Mark has compiled all his findings with their scientific references into a book called the Cancer Resolution. This is not published yet, it’s scheduled for late spring, but he has released a pre-publication extract of all the key chapters titled Cancer Through Another Lens, which is available for download from the Yes To Life online store, which you can find by going to the Yes To Life website, that’s yesterlife.org.uk and clicking the link to the online store right at the very top of any page. Furthermore we’ll shortly be releasing three videos of Mark presenting his findings, which will also be available in the online store. These videos and the pre-publication book extract will also be of interest to practitioners interested to know more. Also if you are someone with cancer who would like professional support in evaluating the impact that Mark’s findings could have on your situation, the Yes To Life helpline can supply details of practitioners ready and willing to help. You can call the helpline on 0870 163 2990 or alternatively use the web form on the website by choosing the time new here menu and selecting our helpline. I want to end today by letting you all know about the Yes To Life conferences for 2023. This year we are pairing a one day online conference with our annual in-person conference under the joint banner of you and your cancer team. Across the two events we have a seriously impressive array of experience and expertise in the form of our speakers and workshop leaders. Part 1, the online element is subtitled Building Your Cancer Team and features many specialists who have appeared here on the Yes To Life show including Kirsten Chick who has been instrumental in devising the programme for both events, Sophie Drew, Dr Catherine Zollman, Scarlett Roberts, Isabelle Galliano, Tracy Story and Hayley North. The subtitle for the annual conference will be held once again in the autumn in the fabulous Friends House Euston London is Working With Your Integrative Team. Speakers include Kirsten Chick again, Dr Sam Watts and Patricia Peat with workshops led by Aga Kehinde, Dr Britt Cordi, Maria Sardina, Claire Winterborn, Catalina De Ana Portela, Dr Shireen Kasam, Sophie Trew, members of the Yes To Life team, the list goes on. A veritable feast of resources combined with exhibitor stands where you can talk to suppliers, therapists etc about what they have on offer. There’s a bundle price for tickets to both and as always the prices are as low as possible, below cost in fact, in order to support those with limited means as best we can.

Robin Daly
There’s a dedicated website at YesToLifeAnnualConference.org or you can navigate from the main Yes To Life website that’s YesToLife.org.uk if you look under events. Thanks very much for listening today, I’ll be back with part 4 of Cancer Through Another Lens next week.