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
Hello and welcome to the Yes to Life show. I’m Robin Daly, host for the weekly show and founder of the UK’s integrative cancer care charity, Yes to Life, helping people with cancer gain an awareness of the choices they have for their care and for helping themselves back towards health. For the last few weeks, I’ve been dedicating a series of shows to an important new voice in the world of integrative cancer care, Mark Lintern. Mark has spent more than eight years researching the mechanisms and origin of cancer and has a new perspective to share that has the potential to affect the way that cancer is looked at and tackled. I’m talking to Mark over the internet.

Robin Daly
Hi Mark. Welcome to part four of our talk about cancer through another lens.

Mark Lintern
Thank you for having me back.

Robin Daly
Okay, so listeners, if you stumbled across this show at part four, I do recommend you start at the beginning with part one as the material in this episode won’t really have the same impact without the foundation that’s been built up in the first three episodes. They’re all available on Listen On Demand or as podcasts or on YouTube. So I’m going to start off with a little previously recap as per your favourite American series. We introduced the Hannahann and Weinberg Hallmarks of Cancer, which are the 10 key behaviours of cancer that can identify the disease and how you use them to evaluate the accuracy of any theoretical model. The better the model, the better it can explain the hallmark behaviours. You looked at current cancer theories and concluded the metabolic theory is the most accurate currently, as it can explain at least seven out of 10 of the hallmarks. And in your own researches, you’re looking for some consistent factor or factors that could produce such a predictable outcome as cancer. So much current thinking attributes it to random factors, which didn’t really make sense to you. But then we looked in more detail at one of the hallmarks, number seven, the Wahlberg effect, which arguably no one can explain currently, but which seems to be pivotal in cancer as the other behaviours result from it. In your researches, you stumbled across a possible cause for the Wahlberg effect that seems to have evaded research, at least in terms of cancer, a process that’s called the cell danger response, where the Wahlberg effect or the switch to glycolysis, the inefficient backup energy system, even when there’s plenty of oxygen to use, is used as a cell strategy to combat a potential infection. This led you to identify a mechanism that contrasts with other theories of cancer that all cite damaged cells as the central driver of cancer. You maintain that through becoming locked in battle with infection, the cells abilities become suppressed as opposed to damaged, and it effectively becomes co opted by infected pathogens as a vehicle to survive and spread.

Robin Daly
So that’s where we got to and I want to start out this week by looking more closely at the way that your thinking diverges from others in a crucial way. Cancer is described as a multifactorial. This is the natural result of decades of finding more and more factors that appear to cause or to drive cancer. On the surface, it certainly seems to be the way it is. However, your drive to look for consistency in the mechanism of carcinogenesis has led you to a different conclusion, i.e. that it’s not multifactorial, but the direct result of a consistent affection that cells are unable to deal with. So if we take this as a starving point, then how do you explain the way things appear, i.e. that anything from asbestos to radiation or poor sleep could result in cancer. Okay.

Mark Lintern
Okay, so. Yeah, this was a main underlying part of my research was trying to explain this consistency, as you say. The key point for me was that so many different carcinogens appear to be able to cause the disease and they all produce varying degrees of damage to a cell, depending also on the exposure to these types of carcinogens and they are so different, it just didn’t resonate with me that the randomness of damage that they could cause could cause the consistency of the disease. With the consistency of the Wahlberg effect and Hallmark 7 in mind, I was also looking at consistency from different angles and one of the main issues or main sticking point was carcinogenesis, the ability of so many different carcinogens to cause the same disease. So I tried looking at that and I focused on this consistency aspect and I found that there were four particular consistencies that arise from all carcinogens, which obviously aligned with the research I was doing. Now these four consistencies are inflammation, immune weakness, iron overload and lactate overproduction.

Robin Daly
Well, at least some of those are within the Hannah-Hannah-Whiteburg hallmarks, correct?

Mark Lintern
Yeah, so inflammation is a key all mark, all mark 10 because it seems a precursor to the disease and to many other diseases. So that’s one particular factor. And I suppose the Warburg effect elicits an overproduction of lactate because you have a sustained use of glycolysis which produces lactic acid or lactate as a byproduct. So there’s two. However, I did come across in my research this correlation with iron and iron overload that I felt I needed to explain. So as I was explaining all these 10 hallmarks, I felt that all these other aspects of the disease I was coming across that scientists seem to be struggling to explain as well. I also needed to explain them because it would be no good if I couldn’t. He asked that particular question. And so whilst I was doing that research and learning about iron’s involvement, that then aligned with this desire in the back of my mind to try and understand the consistency. And of course then you’ve got the Warburg effect in infection and immune suppression. And they all came to the fore and made me realize that all carcinogens, when you actually look at the damage they cause, not only cause the random DA damage and other various damage to the cell that is de-factorial view, but they cause a consistency. And this consistency of these four conditions that arise, I think is what’s been overlooked and is a large premise of what drove me forward to identify a singular or group of particular causes in the infectious space.

Robin Daly
OK, so if you like, you’re placing all four of these things which are the result of some kind of damage from a carcinogen. You’re putting those kind of precancer, they’re kind of preconditions of cancer.

Mark Lintern
Absolutely. So whenever, say for instance, you’ll have toxic damage from a particular carcinogen, you’re going to generate inflammation because it’s going to be the cell’s response to damage that occurs, which will elicit possibly hypoxia in certain situations and a switch to glycolysis because glycolysis is required to generate an inflammatory response and help with the repair process. Now, prolonged chronic inflammation is the issue here because what we see happening is an extensive reliance on glycolysis, which will then overproduce lactic acid within the surrounding environment. Now, lactic acid overproduction suppresses the immune system at this site of damage when the inflammation is chronic. Now, you also have what’s termed as anemia of inflammation, I think it’s called, which is where when you have chronic inflammation, cells recognize the danger that iron release poses because infectious agents use iron in order to proliferate. So it’s almost like rocket fuel, as is lactic acid or lactate. So the body essentially tries to restrict the availability of iron whenever damage to cells occur, because they’re aware that if this iron is released or becomes available to pathogens, then they will use it to their benefit. Not to mention that when iron is released or freely available, it also suppresses immune cells at the site of damage. So you have this anemia of inflammation, which is where information initially occurs, cells attempt to draw in all the iron that’s available in order to suppress its availability to pathogens, which is quite an intelligent thing to do really. Definitely. So we have this chronic information and information itself enables the increases and facilitates the infectious process because it opens the pores of the cell and makes it more vulnerable to opportunistic pathogens. But then over a long period of time of chronic inflammation, you have lactic acid build up and iron overload occurring because the cell can no longer over a long period of time, contain the iron that it’s absorbing. Right. It becomes released within the damaged cells. And both this lactic acid overproduction and iron overload suppresses the immune cells at the site of injury. Now this is the interesting aspect. This lactic acid fuels and the iron fuel opportunistic pathogens or particular opportunistic pathogens. So you now have a an environment where a carcinogen has managed to damage the cell for a prolonged period of time. And that damage instigates these four conditions that not only suppress the immune response at the site of damage, but at the same time stimulates and facilitates infection of opportunistic pathogens if they’re present in and around the area of damage at the time. So you have a beneficial aspect for infection to take place based on these carcinogens. And it doesn’t matter which carcinogen it is. They all tend to produce chronic inflammation if it’s sustained exposure, which results in lactic acid, iron overload and immune suppression.

Robin Daly
Okay, so it’s interesting, so these things that are, I mean, everybody acknowledges they’re part of the process, they’re things that occur in cancer, but they’re not being thought of as having a relationship with infection particularly, that piece is not there, that connection is not there, but you’re making that connection saying actually, somehow before the process of cancer has even begun, you have this setup of prolonged infection, which is actually beneficial eventually to the attacking pathogen. It starts off as a defense against it, but actually after a period, it runs out of juice, so to speak, and the situation turns to the advantage of the pathogen.

Mark Lintern
Yeah, so prolonged, I just want to correct you there, it’s just prolonged chronic inflammation, not prolonged infection. So you’ll have a microbiome that is generally commensal, and you may have opportunistic pathogens in there that aren’t actually operating in a pathogenic sense at that period of time. But the chronic information itself will, over time, and depending on other factors, will benefit the opportunistic pathogens that may be present. So yes, like you say, the mainstream, in a large part, don’t appear to be viewing the disease from this perspective. This is where the multifactorial aspect comes into play. Because you’ve got the notion that cell malfunction is the cause of the disease, so carcinogens will damage various aspects of the mechanisms within the cell, and then the cell goes ory because it’s been damaged, and then that leads to the disease. And because there’s so much randomness to that damage, that’s where this multifactorial view or notion comes from. So because you can’t explain, obviously, the randomness of the DNA damage, and we’ll have you, there’s no consistent pattern there to explain the consistency of the disease, it’s then assumed that it must be multifactorial. So many different combinations of this damage can cause the disease. But again, there’s no evidence to show, to confirm which combination of damage it is. So that’s where the multifactorial aspect comes from. And I think that’s why no one’s really jumped on this idea of the consistency and explaining the consistency. It’s been tried, but no one’s actually succeeded really focusing on the consistency side of things, which is why I focused on it. I realized that as the disease is consistent itself, it has a consistent pattern. There needs to be this aspect of explaining the consistency of the carcinogens, and that just maybe looking at that consistency will likely draw us closer to the underlying mechanism driving the disease.

Robin Daly
So, if you were to look at the point at which a bad infection turns into cancer from your perspective.

Mark Lintern
Where is that? Yeah, I think we need to define what we mean by infection, because I think most people, when they view an infection, it’s of a traditional type of infection. So you get a rapid onset of bacterial or viral infection, maybe, and it’s noticeable. It happens very quickly. And then maybe you’ll have sepsis because the infection has progressed so rapidly. In regards to cancer, it’s not, we’re not looking for, or we’re not looking at a rapid infection. It’s more a slow-growing opportunistic infection that is locally contained. And that only arises, I’m suggesting, from the ability of the carcinogens to damage the terrain of the tissue. So once consistent or chronic inflammation occurs, within that tissue environment, and cells cannot repair that environment, then you have an opportunity for pathogens within the microbiome, within that tissue, if it’s prolonged enough to benefit from the immune suppression and the excess lactic acid and iron overload. And they will then utilise that in an opportunistic moment to invade the vulnerable cells that are damaged and may be able to then sustain themselves within those cells intracellularly. They’re not necessarily gonna go and cause huge infection throughout the rest of the body because the rest of the immune system of the body isn’t necessarily weakened. We’re not talking about immunocompromised patients here. Right. Although, obviously, that plays a role in cancer. We see that later on with other studies showing that immunosuppressed patients are more susceptible to cancer because their immune systems are suppressed. But I think this is where the confusion sometimes lies is in that when we mention infection, people are assuming that it’s gonna be because the immune system is suppressed or can’t fathom why healthy people who have a strong immune system would get infection or allow an infection to cause a disease. It’s not a traditional infection. It’s an opportunistic pathogen within tissue that normally works with the microbiome at that moment in time and is commensal. But then is benefited from the damaged terrain caused by the carcinogen or whatever toxin it is causing the damage, sustained damage to the cells. And it’s a localized intracellular infection within that tissue.

Robin Daly
Okay, so a couple of important words there, commensal and intracellular, you just define both of those to make it quite clear.

Mark Lintern
So a commensal microorganism is one that works almost synergistically with your cells. So it’s not causing damage, it’s living harmoniously with your tissue. But then it turns into an opportunistic pathogen when the environment supports its transition into a parasitic entity that can take advantage of the damage to cells. Right. So intracellular simply means within cells. So this is a particularly, a lot of the time we see infection occurring or pathogens being extracellular, so surviving between cells, but particularly intracellular pathogens will invade the cell specifically and survive and thrive within the cell itself.

Robin Daly
So that’s very important. That’s a kind of characteristic of the mechanism you’re describing.

Mark Lintern
Yes.

Robin Daly
Yeah. Okay, good. So, now we’ve got a way to begin to make sense of the random, unpredictable side of cancers. You’re saying there’s a consistent set of conditions that they all generate that set a scene for Valergen to successfully gain a foothold inside ourselves.

Mark Lintern
Yeah, so this is essentially the initiation stage of carcinogenesis, of which there are three. So that’s an important stage that scientists are trying to explain how the initiation stage of carcinogenesis occurs, so how cancer is formed from a carcinogen, because at the moment it’s not understood how that occurs.

Robin Daly
Right, okay, so I think at this point, in terms of mechanisms, you’ve got a coherent story to tell of how cancer begins, carcinogenesis, and how it develops. So I’m just wondering if you could now give us a very top level description of cancer, all the way from the first occurrence of the damage, whatever it is, right the way through to metastasis.

Mark Lintern
Okay yeah so we’ve covered the initiation stage of carcinogenesis so let’s assume that we’ve had chronic inflammation for a long time, the immune cells have been suppressed, lactic acid overproduction is in full swing, we’ve got iron overload, the immune cells at the site of damage are finding it difficult to help repair that tissue damage because it’s ongoing as chronic and this lactic acid iron overload is suppressing them. Now this provides an opportunity for the lactate and the iron and they essentially invade the cell successfully, this may not happen all the time obviously it’s opportunistic in nature. Now there are various mechanisms they use to do that and I’m obviously just going through very simply but particular pathogens can use particular receptors such as the HER2 and they are absorbed by the cell through these particular receptors and there’s also many different mechanisms involved but once the pathogen is inside the cell there are many aspects of further immune invasion they can apply through providing toxins or metabolites of their own, they can also manipulate the cell to produce something called PD-L1 which is an expressive protein that allows the cell to evade immune detection which is very paramount to the ability of cancer cells to evade immune detection, that can be instigated by pathogens, intracellular pathogens. So as we described a little bit earlier with the Wahlberg effect, the Wahlberg effect is a response to pathogen or infection, pathogen invasion, so all this all the while we’re having this invasion occur intracellularly by these pathogens, the Wahlberg effect is in play and once inside the cell the particular pathways that are involved in mediating the glycolytic pathway or the Wahlberg effect, the energy switch that we see can be controlled and suppressed by the intracellular pathogen itself. Furthermore there are many different mechanisms that this cell can deploy one of which being cell death apoptosis, these intracellular pathogens have also been shown to suppress this cell death mechanism. So already what we have is now the inability of the cell to die and the growth receptors have potentially been stimulated and further immune suppression is on the cards because the pathogen has initiated several methods of further suppressing the immune response.

Robin Daly
So these are all hallmark behaviors we’re talking about.

Mark Lintern
All Hallmark behaviors and at this stage you have essentially the cell has lost control. It’s now working on autopilot in order to try and defeat the pathogen, but it cannot commit cell death. So you now have the proliferative state in that glycolysis is sustained and cells are likely to proliferate and not die as they should because they can’t. The pathogen is suppressing that process. And because you have this process, you have an extension of glycolysis occurring, which results in a continued production of lactic acid. Now that has many detrimental effects, which can lead to the cells around the damaged tissue losing their integrity. So the suppressive signals that you normally get from cells around other cells that would normally prevent them from growing become lost quite simply because the lactic acid is corrosive. On top of that, lactic acid is a stimulatory factor for blood vessel growth. This is one of the key aspects of the tumor is that once it grows, proliferates out of control, it loses its blood supply because it grows too fast for the blood supply to accommodate this. But lactic acid production itself is a stimulatory factor for angiogenesis or the growth of new blood vessels. This is a normal mechanism we have in our biology that allows us to improve our blood supply. So for instance, when we sprint, we produce excess lactic acid, so athletes will push themselves and when they do push themselves and they’re using glycolysis to a greater degree, they’re producing more lactic acid. And that’s not beneficial for the athlete. So the body responds due to the increase in lactic acid in order to facilitate more blood vessel growth so that more oxygen can be provided to those cells to enable oxfos to occur, which provides more energy for the athlete. So this constant control by the pathogen instigates its overproduction of lactic acid and then allows new blood vessels to grow. So these blood vessels then grow towards the cells in a haphazard manner, as we see, dependent upon the level of lactate being produced, dependent upon the level of control the intracellular pathogen has in any particular cell at any given moment in time. So from here, we have a situation now where it’s chronic even more so than the early stage of cancer. So the cell is being constantly damaged all the time. This kind of explains the random damage that we see occurring. We have toxins coming from the pathogen, free radicals being produced in a battle between immune cells and the cell itself, a lot of other factors such as e-cadering, which I can go into a little bit later, which are junctions on the cell that enable cells to adhere to each other. So these pathogens can reduce e-cadering, essentially, which allows cells to break away from each other, which is very interesting. So you can now imagine you’ve got this corrosive environment occurring and you have a mass of cells.

Mark Lintern
So you’ve got iron overload, you’ve got lactic acid being produced and now you’ve got more immune cells being drawn to the tumor mass and these immune cells can’t get access to the pathogens that are within now the tumor mass because they’re being protected, essentially, by the overproduction of iron and lactic acid in the surrounding tissue. So you have these macrophages and immune cells that are becoming senescent or they’re being blocked from doing their normal job, they’re being stopped, essentially, and they’re just sitting there around the tumor and unable to attack the pathogen cycle, it’s protected. So you have ongoing now damage to the cell, mitochondria within the cell are getting damaged as well. Now, the interesting thing here is that when mitochondria are damaged beyond a particular degree, which will occur over a period of time, you’ve not been able to kill the cell through apoptosis. They instigate a system of signaling called retrograde signaling, where they signal to the DNA contained within the nucleus to try and transform the cell in a defensive response, essentially. Now, this signaling can instigate the transition of a normal or regular cell into a cancer stem cell through what is called an epithelial to mesenchymal transition. So what you essentially have with all this pathogen is damaging the cell over a long period of time with this whole battle of trying to kill the cell itself through free radicals and toxins. And that results in excess damage now to mitochondria and the DNA in the nucleus, which explains the random DNA damage that occurs, but also explains the transition to a cancer stem cell, which turns the disease into a deadly form. And from here, cancer stem cells are a lot more resistant to chemotherapy and various other drugs. We also have the instigation of blood vessel growth and the lactic acid can make the blood vessels leaky, essentially, because it’s so corrosive. So after a long period of time, you will have cells that end up breaking away, cluster of cells breaking away into the bloodstream because of the corrosive environment that’s been caused. These cancer stem cells break away with cluster of other cells. And the last-ditch effort that the immune system has against trying to affect these cells is to produce a sticky protein called Galetin-3, and we find a lot of metastatic cancer cluster cells that are traversing through the bloodstream are surrounded by this sticky protein called Galetin-3. This sticky protein allows the cancer cells to adhere to other cells within the body at a distant site. Now this Galetin-3 is an antimicrobial protein being produced, essentially. It has many other functions, but one of its functions is as an antimicrobial protein. So in a sense, the body is trying to rid itself of the intracellular infection, is unable to do it for various reasons. And things like Galetin-3, the creation of cancer stem cells, enable the metastatic process to occur at a distant site. And the infection travels with the cluster of cells, allowing the whole process to begin again at a distant site, and there you have metastasis of the disease.

Robin Daly
Wow, what a story, but you’ve got some reasoning behind every step of the way, which is interesting, because that’s really not been something anybody’s been able to put forward at all. Okay, so there’s one question that remains, and I imagine it preoccupied you a lot, but, and that is, well, what exactly is the Kalpra then? What’s the pathogen, the microorganism that’s causing all the trouble, or indeed, is it our whole assembly of culprits? Maybe to start us off on this subject, can you tell us what potential pathogens were under consideration?

Mark Lintern
Well, you’ve got parasites, you’ve got bacteria, fungi, viruses, and there’s a lot of information in the literature about viruses and focusing on bacteria. But there doesn’t seem to be that much associated with parasites and fungi. But as I’ve gone through the whole process, my initial research was focused on what was most prominent in the scientific field, which was initially viruses.

Robin Daly
Okay.

Mark Lintern
And so we have a number of oncogenic viruses that can invade the cell and produce DNA damage or manipulate DNA, manipulate the P53 gene and various other aspects of the disease. And these are seen as being the driving mechanism of cancer. But the problem I found with several of these, in particular bacteria and viruses, and even parasites, because parasites are normally rather large and quite easily identifiable and not found to be present in all, particularly all cancers, is that viruses and bacteria can’t explain the disease as well as fungal pathogens can. So the evidence has channeled me through this process of looking at viruses, looking at bacteria, and then coming across anomalies and inconsistencies that can’t or contradict the theory that bacteria and viruses in particular can call are the underlying mechanism of driving disease. Now, that’s not to say they’re not involved. Clearly they are. It just depends on what capacity they are involved.

Robin Daly
So here we’re back into this multi-factorial territory again where they appear to be some of the things that cause cancer along with lots of other things, but you’re saying that maybe their role is different to being the actual cause.

Mark Lintern
Yeah. So because how infection is currently viewed, it’s accepted that around 20% of cancers are caused or triggered by infection. It’s based on this multifactorial cell malfunction concept. So the infection goes in, damages the cell, and then it’s the damage to the cell caused by the infection that then drives the disease. It’s not the infection or the pathogen per se. However, the way that I’m looking at it is that the evidence seems to congregate on fungal pathogens being the underlying driver of the disease through a mechanism of active suppression within the cell, surviving intracellularly within the cell, blocking the cell death mechanism, controlling the energy system of the cell to instigate the Wahlberg effect or sustain the Wahlberg effect in order to sustain access to nutrients contained within the cell and being absorbed by the cell.

Robin Daly
So, something I learnt about from you, which I wasn’t aware of before, was the kind of relationship between fungal cells and our own cells, which is an interesting one, which gives them some of the abilities you’ve just described, I think.

Mark Lintern
Yes, I think so. If I want to be really reductive about it, obviously human biology is a lot more complex than this, and life is a lot more complex, but you can look at it from this perspective. There are essentially two types of cell that make up all living organisms. It’s more nuanced than that, but you have bacteria which are prokaryotic cells, and they are single-celled organisms. Then you have eukaryotic cells, which make up all the rest of the life forms on the planet, essentially, so animals, humans, insects, plants, and fungi. Now eukaryotic cells are different in the sense that they’re bigger, they’re more complex, they contain more organelles, which are structures within the cell that do various different jobs, ribosomes, and what have you. They’re like factories within the cell, where a bacterial cell doesn’t contain mitochondria, for instance. It doesn’t contain all these other organelles that eukaryotic cells contain. Fungi, in particular, are eukaryotic, as are human cells. They’re eukaryotic, so they contain a nucleus, they contain mitochondria, and other organelles. Fungi are more closely related to human cells than they are plant cells. With that in mind, there’s a shared homology, a shared ancestry, a shared pathways between fungi or fungal cells and human cells. This is explained by the fact, or this is highlighted by the fact, that the antifungal drugs we have are extremely toxic to us. Not only do they affect fungal pathogens, particular pathways in fungal pathogens that they target, but because we share similar pathways, they target the same pathways in us, which makes them extremely toxic. Whereas antibacterial drugs, they tend to target factors of bacteria that are bacteria that aren’t contained within us, within our eukaryotic cells, so they’re not as toxic. They were near as toxic.

Robin Daly
Thank you. And where do viruses sit in that?

Mark Lintern
Viruses aren’t essentially living or are on clusters living because they require they require to invade another cell in order to propagate they can’t propagate themselves. So they they’re and they’re generally um they do not contain mitochondria they are essentially similar to exosomes in the sense that they’re a package made up of um RNA uh which is essentially code you could say code that allows the virus to propagate itself once it invades a cell it will tend to release the RNA or any DNA that it has as well into the cell um and change the format of the cell in order to produce more virons which are baby viruses.

Robin Daly
Okay, so what you’re saying then is that fungi are in a very different class to these much simpler types of organisms, and this means they can… well, first of all, they’re similar to ours, and so there are difficulties in trying to get rid of them if they’re around, but secondly, they have the ability to affect us in ways that the simpler cells maybe can’t.

Mark Lintern
Absolutely. It’s just the shared pathways, the ancestral pathways that they both have that just allow them to navigate the immune system and human cells probably more proficiently than bacteria can.

Robin Daly
So you’re saying that once a cell gets infected with a fungus that it can actually produce some of the kind of behaviours you’ve been talking about, it can actually manipulate the cell because it’s a complex enough organism in itself to get the cell to behave in the way it wants it to.

Mark Lintern
Yes, but that’s not exclusive to fungi though. So bacteria as well. These microorganisms are incredibly complex and intelligent. So bacteria as well as fungi can suppress particular pathways within the cell. So tuberculosis can suppress the cell death mechanism. So it’s not a case of one size fits all. It’s essentially trying to work out which combination of pathogens essentially could be the underlying mechanism. And I’m not saying that it’s definitely going to be just fungi necessarily. I’m just saying that the evidence that I’ve consumed over these last eight years is pushing me down that route just because of the way that the cancer cell operates. It’s very reflective of the way slow growing fungal pathogens operate. And there’s many there appears to be many more consistencies with the fungal pathogen than the bacteria. Now bacteria and fungi can live synergistically. Certain combinations of bacteria and fungi work together in particular situations. So there’s going to be an effect with bacteria as well. But patients undergoing chemotherapy are subject to infections and one of them being bacterial. And then most bacterial infections are rapid in their progression and viral infection as well, which is probably why we focused in medicine on bacteria and viruses more so than fungi, because fungi are also very difficult to detect. This rapidness means that cancer patients going through chemotherapy will be given antibiotics to prevent those infections. Now what we see in the literature is that despite this, we don’t see cancers being cured by these antibacterial drugs. And on top of that, there does seem to be a relationship with the longer these antibacterials are used with cancer patients, it aids the progression of the disease. Now that can be through various mechanisms. The antibacterials can be killing the beneficial bacteria within the microbiome, which could then aid the disease, irrelevant of whether fungi are present, or that in itself would aid the fungal pathogen, because it has less competition from the beneficial bacteria that would normally control it or can take. But also antibacterial drugs will affect mitochondria, because mitochondria appear to have a bacterial ancestry, so they are affected. So you’re damaging, potentially damaging or restricting or inhibiting the metabolism of a cell anyway.

Robin Daly
themselves, right?

Mark Lintern
Yeah, there just seems to be a lot of evidence in favor or largely in favor of a fungal pathogen being the underlying mechanism driving this suppression of the cell, which then leads to a tumor mass and the corrosive environment and the corrosive environment where immune cells are unable to defeat the pathogens that have taken the opportunity to invade these cells.

Robin Daly
Okay, well look, I know in your book that’s coming soon, you’ve built up quite an array of evidence to support your leaning towards fungi as being the culprit here, and we can’t go into all the detail of that now, but maybe it’d be nice to make a start now on, well, what does this mean exactly about the way that we look at cancer, the way in terms of managing it, of treating it? Bacteria viruses, at least on the radar of orthodox medicine as some part of the picture in some cases, I haven’t heard fungi mentioned ever in relationship to cancer, it was in mainstream circles, so yeah, how does this affect the way that we look at treating or containing the disease, do you think?

Mark Lintern
Well, you could look at this information and state that well, all we need to do is use an antifungal drug. Now, I want to emphasize that no one really should be drawing that conclusion because there is a danger in using antifungal drugs because they are extremely toxic. So depending on your health status and the other drugs that you may be taking any particular time, it’s always preferable to speak to a medical professional and antifungal drugs in particular will or can have an adverse effect and there are certain contraindications that can cause other complications. So I’m certainly not saying that antifungal drugs are the answer, although many studies do show that they are being used in a clinical setting in certain places, just if anything, to clear up from the infections that occur in cancer patients. But they have been shown to be quite effective and there’s now a push to utilize and investigate antifungal drugs against cancer because they’re showing that antifungal drugs, in particular, say, for instance, Itroconazole, has been shown to be effective against a broad range of cancers. It affects many different parts of the cell pathways and what have you. So there’s definitely a need to look at the antifungal drug side of things, but there’s many other aspects of the disease, many other treatment programs that, for instance, from the metabolic side of things, restricting glucose fasting and various other natural substances that not only target pathways within cancer cells, but also target fungal pathogens. For instance, you have the Care Oncology Clinic. They’re using particular off-patent drugs, Metformin, Menbendazole, various statins, and doxycycline, I think. And when you look at a number, not just those four, when you look at a number of other off-patent drugs that are being used and being studied at the moment appear to be effective against cancer, they’re also antifungal in their own right. So studies have been performed showing that they affect common fungal pathogens. So while drugs will independently affect pathways within cancer cell directly, there is also this other aspect, this other perspective that I want to draw attention to. Could it also maybe be that these drugs are actually affecting the fungal pathogens contained within the tumor? And then that’s the reason or one of the reasons why we have a positive effect against the cancer solely just because the drug is directly affecting particular pathways. Because what I found is when I came across the studies that showing that antifungal drugs have a broad effect, which incidentally, antibacterials don’t. Some antibacterials do affect cancer cells in a positive way, such as doxycycline, but that’s for a different reason other than bacteria. It’s targeting the oxfoss pathway within mitochondria. When you want to look at antifungal drugs being effective against a broad range of cancers, scientists tend to just focus on the pathways that it affects as if that ignoring the fact that it could be actually affecting a pathogen, probably because very few were actually considering that a pathogen is suppressing the cell.

Mark Lintern
So scientists are so drawn to this aspect of the cell is to blame for cancer, because it’s gone wrong. It’s the fault of the disease. So therefore we must block its pathways or when this antifungal drug, it’s killing the disease and it’s affecting this particular pathway in this pathway. So therefore that must be the reason why. But I’m saying, well, is it affecting that pathway because the fungal pathogen is actually controlling that pathway?

Robin Daly
Interesting. So it’s a completely different interpretation of the same observation. Interesting. Well look, I want to talk much more about the whole metabolic approach to treating cancer because it’s kind of developed art these days and there’s a lot known about it and definitely is helping people survive. So I’d like to go into that in a lot more detail and how this sits in amongst it. We’re out of time for this week. So that’s where we’re going to start off next time. So thanks very much again for another dive into your scientific discoveries.

Mark Lintern
Thanks Robin. Bye-bye.

Robin Daly
There’s no getting away from the complexity of cancer, indeed the complexity of human biology, but I hope in these interviews we’re succeeding in putting Marx ideas across in a way that anyone can understand. Why does this matter? Well, it’s a very different way of viewing cancer and whereas it could take years for a full evaluation, many people simply don’t have the luxury of the time to wait for the science to catch up. Fortunately, it’s clear that there are known ways of addressing the possibility that Mark is correct, that in the hands of a skilled practitioner are safe and that don’t require people to stop any existing treatment. For those of you who are in an urgent situation, I want to let you know there’s a pre-publication release of all the key chapters of Marx book available under the title Cancer Through Another Lens from the Yes To Life shop and you can access the shop 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 of the site. As always, Yes To Life advises anyone against self-medication as cancer is such a complex and individual disease so we prepared a list of practitioners who are up to speed with Mark new ideas and can help anyone with the implications of therapeutic support. For more information, contact the Yes To Life helpline by calling the number at the top of every page of our website 08701632990 or by filling out the form on the helpline page which you’ll find under the I’m new here menu on the website. Thanks so much for listening today, I’ll be picking up the story with Mark again next week so I hope you can join me again for the next episode of the Yes To Life show.