Is Cancer More Than a Genetic Disease? Mark Lintern on The Cancer Re-Solution

In this episode of The Integrative Continuum, Dr. Richard Rocker sits down with Mark Lintern, independent cancer researcher, multi-award-winning author of The Cancer Re-Solution, and creator of Cell Suppression Theory.
This is a deep and thought-provoking conversation about cancer theory, the dominant genetic mutation model, metabolic theory, terrain, infection, immune dysfunction, mitochondrial health, inflammation, microbiome disruption and the biological environment that may allow cancer to develop and progress.
Mark shares the personal story that led him into cancer research, including his own cancer diagnosis and the loss of a close friend. That journey eventually led him to spend years studying the scientific literature and developing Cell Suppression Theory, a model that asks whether cancer may be better understood not simply as a disease of damaged genes, but as a disease involving altered cellular terrain, intracellular pathogens, immune disruption and failed biological regulation.
In this conversation, we discuss why cancer theory matters. The way we understand a disease determines the questions we ask, the treatments we prioritise, and the possibilities we can even imagine.
This episode is not about giving individual cancer treatment advice. It is about asking better questions, challenging assumptions, and encouraging deeper thinking around one of the most complex diseases of our time.
We explore:
•Why Mark began researching cancer
•Why the origin of cancer is still debated
•The limitations of the somatic mutation theory
•Why cancer research can become siloed
•The importance of biological terrain
•What Cell Suppression Theory proposes
•The possible role of intracellular pathogens
•Fungal organisms, biofilms and immune evasion
•Sugar, glucose metabolism and the Warburg effect
•Ketogenic diets, fasting and metabolic flexibility
•Why cancer nutrition is not one-size-fits-all
•The microbiome, gut permeability and systemic inflammation
•Mitochondrial dysfunction as both cause and consequence
•Iron, lactic acid and chronic inflammation
•Conventional treatment through a wider biological lens
•Why uncomfortable questions are essential for scientific progress
•How patients can balance hope with responsibility
This is an important conversation for patients, clinicians, researchers and anyone interested in cancer biology, integrative medicine, functional medicine and systems-based thinking.

DISCLAIMER
This podcast is for educational and informational purposes only. Nothing discussed in this episode should be taken as personal medical advice, diagnosis, treatment guidance, or a recommendation to start, stop or change any medical treatment.
Cancer is a serious medical condition that requires appropriate assessment and care from qualified medical professionals. Anyone with cancer, suspected cancer, or concerns about their health should consult their GP, oncologist, consultant or qualified healthcare team before making any decisions about testing, treatment, diet, supplementation or lifestyle changes.
The views shared by guests are their own and are intended to encourage discussion, critical thinking and further research. This conversation is not intended to replace conventional oncology care or the advice of a qualified medical practitioner.

GUEST INFORMATION
Mark Lintern is an independent cancer researcher, multi-award-winning author of The Cancer Re-Solution, and creator of Cell Suppression Theory.
Website: cellsuppression.com
Substack: The Cancer Vigilante
Book: The Cancer Re-Solution
Free PDF / theory synopsis: Available through Mark’s website
Additional interviews and resources: Available through Mark’s website

HOST INFORMATION
Hosted by Dr. Richard Rocker
The Integrative Continuum Podcast

Website: https://rockerclinic.com/
Instagram: https://www.instagram.com/drrichardrocker/
Facebook: https://www.facebook.com/RockerClinic
LinkedIn: https://www.linkedin.com/in/dr-richard-rocker-589127/

Transcript

SPEAKER_01 0:00

You've landed at the edge of what medicine has known and what it's becoming. I'm Dr. Richard Rocker, and this is the integrative continuum of biology, energy, and human potential. In each episode, we explore how quantum biology, frequency medicine, and ancient healing systems are transforming our understanding of health. This is where mitochondria meets meaning, and blood work meets bioenergetics. Subscribe now and join me on the frontier of integrative healing, where science and soul are no longer separate. Welcome to the Integrative Continuum. As always, this podcast is about exploring health, medicine, biology, and human potential with curiosity, open-mindedness, and a commitment to standing by the truth as I know it and as I continue to learn it. Today I'm joined by Mark Lintern, an independent cancer researcher, multi-award-winning author of the Cancer Re-Solution, and creator of the Cell Suppression Theory, or CST. Mark's work has attracted considerable attention because it challenges the dominant genetic mutation model of cancer and proposes a different way of looking at the disease, not simply as a genetic malfunction, but as a suppression-based response involving intracellular fungal pathogens, altered cellular terrain, immune disruption, and failed biological regulation. After his own cancer diagnosis and the loss of a close friend to the disease, Mark spent nine years immersed in the peer-reviewed literature, developing a model that he believes accounts for all 10 Hannahan and Weinbark hallmarks of cancer, as well as more than 20 additional features of the disease. In 2023, he presented his theory to a panel of 10 international cancer experts before a live audience of over 200 medical professionals, receiving an average confidence score of 7.9 out of 10. His work has since won multiple awards and has attracted serious institutional engagement, including a pilot study in development with the cancer charity Yes to Life and the U.S. biotech company Ultra Botanica. This is an important conversation, not because we are here to give individual cancer treatment advice, but because cancer theory matters. The way we understand a disease determines the questions we ask, the treatments we prioritize, and the possibilities we can even imagine. Mark's work asks a bold question: What if cancer is not only a disease of damaged genes, but also disease of cellular suppression, altered terrain, infection, immune dysfunction, and disrupted biological communication? Because every treatment approach is shaped by an underlying theory of what cancer is, this conversation has real practical relevance. It may help patients, clinicians, and researchers think more deeply about the assumptions behind cancer care, while always encouraging people to discuss any decisions with their qualified medical and oncology team. It is a pleasure to welcome Mark Lintern to the integrative continuum. Welcome, Mark.

SPEAKER_02 3:32

Thank you, Richard. It's a pleasure to be here. Thank you.

SPEAKER_01 3:35

Great, great. Yeah. Very, very happy to have you here. As I was telling people in the opening, your book, The Cancer Resolution, as you can see in your background and as I have here, fantastic book. I'm absolutely enjoying your book and the way you write and do your research, and highly encourage people to check that out. So, Mark, for listeners who may not know your work, can you tell us what led into your cancer research in the first place?

SPEAKER_02 4:04

Yes. It's a very different journey than most. So my background first and foremost, I'm a graphic designer by trade. And it was a very long time ago I developed cancer myself. I was lucky I had it surgically removed, but that started me on a journey of research because I wanted to understand which particular DNA mutations had caused my cancer. My uh GP and my oncologist couldn't tell me. So I just wanted to, you know, try and work out if I could prevent it from coming back. Um and that was fine. I carried on with life, no problem. But then a friend of mine got cancer, Sam, uh, cervical cancer, and um I thought I'd already done a bit a little bit of research, so I'll delve into the research again to see if I can just help her get through this period. Um and unfortunately she passed away after a year, but that year led me down quite a bit of a rabbit hole. Um, initially, really starting off um my curiosity by identity it opened the door to different theories of cancer and the concept of realizing that actually the origin of the disease is still up for debate. Um, I mean, there are approximately at least, well, at least nine credible theories of cancer at the moment. Um, that number varies, varies depending on how much um validity you apply to different theories and how you uh assess them, but there are a number of theories out there, and it is uh um an open-ended question at the moment because none of those theories approve it. And that drove my curiosity because we're told, and I was under the impression initially that cancer was a genetic disease, and it still may be. Um it's just we're currently at the theory stage of uh evolution in terms of the scientific analysis of this incredibly difficult and complex problem. However, it's presented in the literature as if we've moved past the theory stage and we've already acknowledged and identified what the origin of cancer is. So we've moved into a territory where we elevate the uh somatic mutation theory above all other theories, as if that's fact. And yet it hasn't been proven, um, which I'm I think is a serious, serious problem. Um, because we're not getting the results that we were hoping for by targeting uh genetic mutations in the way we have been in the last five or so decades. So that for me just emphasized that there was a potential issue there. I mean, that cancer could be caused by something in addition to um genetic mutations, they could both work in synergy with something else. But at the very least, it it led me down a path thinking which which was that something else in addition must be involved because we're not making as much progress as we would like. Um and then after Sam's death, um I discovered the metabolic theory and various other theories, and I was just very upset at the time. Um I didn't want to uh you know Sam's death to be uh in vain. So I thought I could carry on with my research and just document the information I already had just to help anyone else I I knew who would possibly develop the disease. They could read this and then realize that there's there's other things they can potentially do and research to give them hope. Um but then that led into eight years of research and a eureka moment for me um that made me develop a brand new theory and identify a different mechanism through a different paradigm.

SPEAKER_00 7:49

Yeah, yeah.

SPEAKER_01 7:51

It's you know, you you said the standard uh cancer treatment has gone beyond the theory stage, like we we have it all sorted out. And I always think, you know, when I hear this phrase the science is settled, uh it really kind of annoys me because I I don't think the science is ever settled. And we should be asking questions. And through asking questions, we can help to uh, you know, test those theories out, which uh you definitely have been tested out with your, what was it, six to eight hours in front of the uh, you know, the cancer oncologists and the like. So I think that is important that we never forget that. I think you bring that beautifully in your book. You you bring a lot of questions out that really makes us think. And this is really what we need. So when we're when we're talking about making us think, you're not originally part of like the conventional oncology establishment or even a medical background. So do you think that helped you to see things differently?

SPEAKER_02 8:58

Absolutely, I do. Um, there's a huge creative element to problem solving. Um, that that's number one. I mean, Einstein did I love this quote by Einstein. He said, um, logic will get you from A to B, but creativity will take you everywhere. And that there's that aspect of it, and with my design um background, it's taught me to really question my thought process. Because whenever we we're tasked with a design problem, it is you don't lead with your initial um idea that you think and feel would be the actual solution to any particular problem. You force yourself to adopt um some more research and adopt a completely different way of thinking because we've got to come up with original ideas. We can't plagiarize any sort of design that's currently out there. So it's a constant uh mindset of always looking for something new and always challenging your own perspective. And I think that really helped me try to consider something new. I wasn't afraid to kind of make mistakes because we constantly make mistakes all the time in graphic design. That's what one of the reasons why, you know, sometimes we may stumble across something, and then that forms part of the design. At the end of it, we might say, Oh, yeah, we planned that out, but really we didn't. Um, but it's a it's it's a creative process. You've got to allow yourself to make mistakes. And I find that in the medical industry, I think a lot of it's built on reputation. Um, and I think there's a fear of making mistakes in the medical industry. Um, but on the other side of that, well, because of that, um, I haven't got a reputation as of any sort in the medical industry to lose. So I'm quite happy to ask questions which may seem um rather ridiculous at the time, but these have led me down different rabbit holes uh that have then allowed me to see things from a different perspective. The other thing is um I think there is an issue with uh a medical education in the sense that it can be institutionalized. Um and I don't think it encourages necessarily uh creative thinking as much as it would do in the background that I come from. So you get what I've seen in the research is you get a lot of um, I mean, obviously, med um uh medical science is incredibly complex. So I can understand why everything is is siloed as the way it is, but but these medical disciplines don't necessarily talk to each other. It's almost frowned upon to wander into another area or another discipline. Um and I think that's an issue because what what I've seen is there isn't much crosstalk, and cancer is incredibly complex and multidisciplinary, in my opinion. And there's a huge benefit to be able to not have any fear about going into and questioning the different disciplines and drawing on information on a broad spectrum to see how everything fits together. And I think that's been the advantage for me as well. Um I'm not constrained to one perspective. Uh I've been able to um go where my mind pleases, basically.

SPEAKER_01 12:11

Yeah, yeah, that's good. Um there's two things that you said, you know, you you mentioned fear, and um you always wonder that people are gonna go, well, what would they be afraid of, you know? And so do you think is is it more of an egotistical thing? Is it a financial thing, or you know, maybe is it is it combined? If somebody's doing research, we know that often grants are made, and is it uh if you don't follow along this line, you're not gonna get your money. What what have you noticed?

SPEAKER_02 12:46

Yeah, well, it's a mixed bag. Um I've come a lot of across a lot of really leading scientists who uh I've got incredible respect for, and they are incredibly humble. They've spoken to me and they've they've they've they've expressed their um gratitude for what I've done. And it's really nice to to have that sort of response. But then I've come across people, you can tell the ego kind of dominates in that situation, and they might appear um a little bit offended by the fact that I'm from outside the field and they've got a particular view, and of course that that there's that reputation side of things, so there might be a little bit of ego going on there as well. Um, but also financial financial side of things, um people have to earn a living, and it's very difficult when you've been, you know, for decades um convinced that you your field is correct and you've been pursuing that avenue. Um to then question that you you're almost questioning um your livelihood in a way. Um that is a scary path to take. So I understand why there's hesitancy. Um but but also it just takes time for people to adapt to new ideas as well. So th there's that. And especially I think because I'm from outside the field, um, there is that extra uh amount of hesitancy.

SPEAKER_01 14:10

Yeah, yeah. Yeah, it's it's almost it's almost like that uh, you know, I could I I can understand being in your shoes because yeah, you will get some people where the ego comes into it and they're go, well, what do you know? You know, who who are you to tell me this uh with your with your background? And what I found what I found going through my medical uh career, if you want to call it that, is the people that I've learned the most from and I got the most beneficial information from has always been the researchers. It hasn't been the doctors, it's been the the people that are in the field that are digging in and researching. They're the ones that are figuring it all out, the researchers, the scientists, and they're just telling the doctors what they found. So it depends who you're listening to. I think that plays a big part into it. Yeah. So um and if we look at modern day uh doctors, uh a lot of them are so busy they don't really have time to research. So they might be just looking at headlines, or uh they might just be looking uh at the drug rep who comes by and uh gives them maybe a very one-sided look at something and not outside of that. And I think we s I think that happens a lot uh in these days. Uh and I'm sure you've you've come across that multiple times. Yeah.

SPEAKER_02 15:34

Um I think it's the system. It's just it's it needs to change because it doesn't work in the favor of the doctors because, like you say, they're far too busy um to be able to spend the time to do the research. Uh so that that does need to change.

SPEAKER_01 15:49

Yeah. And the other thing that you mentioned uh about the things being siloed, um, this is something I've referred to too many times that uh essentially medicine has become very reductionist. And uh we have all these hundreds and thousands of specialists uh that are focusing on a minute aspect of health or a minute aspect of a cellular function or that and it's it's great, it's fascinating. I I I love it, but who's who's taking all of that stuff, who's putting it all together to make a system that works, right? And uh and this is what I really like when when I've been reading your book there, and I see you building up that perfectly, taking not just one theory, but multiple theories, uh, and finding, hey, uh where where is the answer here? What can we do that uh actually is going to help people here? So that's great.

SPEAKER_02 16:42

Um, yeah, just on that point, sorry to interrupt.

SPEAKER_00 16:47

Yeah, go ahead. Yeah.

SPEAKER_02 16:49

That that was the issue that I came across when I discovered the different theories of cancer. Um it's it's really in important to be looking at different things from different perspectives. But what I found was the proponents of different theories were quite staunchly in favor of just pushing that particular theory. And it seemed it seems to get to the point where it's it's not about presenting truth, it's almost about sometimes just trying to prove that that theory is correct. Um what I've tried to do is you know, I I was on board with the metabolic theory, and I I am still on board with the metabolic theory. It's the most um it's the the most established theory with the most explanatory power I can see at the moment. Um, however, there's there were still some contentions with that theory. So I couldn't wholeheartedly jump in and and champion that theory alone. And that's what led me down this different path. So I've always tried to, and because I've not got a medical background, um, I've had to rely on the evidence. So I've had to be as objective as I can be, and I've had to take a stance of, you know, asking questions and never, never stating anything as fact, because that's not how science works anyway. That's how I thought science operated. But um, so I've tried to to follow that principle. And I'm not saying with my theory that I'm particularly right, I'm just saying, and this is what what I thought scientists, you know, ha and most scientists are like this, but I'm just I'm just trying to say that all the evidence is out there, I've done a broad look at the evidence, and and a huge bulk of this evidence is pointing down an avenue where where is that's been overlooked. We haven't really looked at this particular section. It just seems as if everything's pointing towards this, and it can almost beautifully explain the disease almost in its entirety. Um now, again, that's not saying that I'm right, it's saying that here's a cor many, many correlations that almost turn into a bit of a signal, really, when you when you put them together, that's worth investigating. It's absolutely worth investigating, and that's where I I leave it. Because that's to me, that that's what science is. You need to bring other people on board so they can investigate it further and find the holes if if there are any holes in it. And then, you know, there's this to and fro, isn't there? Um, between trying to find out what the actual truth is. And I think that's that's really been what I've been trying to go for. It's not, I I don't really care if I'm right or wrong. In fact, um if I'm wrong and I try and push that my particular view, that's not gonna benefit me. It's not gonna benefit my family and friends or anyone around me. Uh, because I'm gonna be pushing something that could be damaging to them.

SPEAKER_01 19:29

Yeah, absolutely. Well, as with anything in life, we we learn the most from our our errors and mistakes. Um I don't think everybody gets it right all the time. It's uh this is what it is. That's how it works. So, yeah, absolutely. Okay, let's get a little bit into some of the theories. So for decades, cancer has largely been explained through the somatic mutation theory. So the idea that cancer is primarily driven by uh accumulated DNA mutations. So, what do you think that model explains well and where do you believe it may fall short?

SPEAKER_02 20:10

Um very good, very good question. It's what does explain well? No one's actually asked me that question before. Explains well, I would say um there are a number of common mutations that occur. And those we see that there are there is an effect with those mutations. We see a a huge increase in risk um through those mutations. Um and there are a number of one or two drugs that have provided a quite substantial benefit, like Glevec, for instance, um for non-Hodgkin's lymphoma. Um but by and large it I'm more in the field of it doesn't really explain anywhere near as much as I would like it to. Um because the impression I'm I'm getting is that it it is the theory that explains what cancer is. However, the more I've researched, the more it it doesn't seem to explain. So there's a huge issue I find with that particular theory. Again, it it could be that um cancer is a genetic disease, but it's just far too complex for us and our technology to fathom at the moment. So that might be something down the line. However, the evidence um building against the theory, the contentions that exist are numerous and they shouldn't be ignored. So that needs to be looked at. So one or two things um just to highlight, and that is that there's there's been tissue found with cancerous mutations, uh the healthy tissue with cancerous mutations, and those mutations don't give rise to cancer. And then you have um Tumours that do not harbor any of the expected driver mutations at all. So the question there is what in particular is driving that particular type of cancer if it's not going to be those mutations. There's also a recent study of around 7,000 tumor samples that identified around 1.7 or 2 mutations on average, which is far too few for cancer to develop. And then you have the nuclear transfer experiments where they transferred the cancerous nucleus into a healthy tissue, healthy cell, and we didn't get an abnormal growth. But when you transfer the cytoplasm into healthy tissue, cancerous cytoplasm, we then get cancer growth. So that suggests that it's not the nucleus, it's not the DNA within the nucleus that's causing this mechanism of abnormal growth. It's something in the cytoplasm. And then Professor Paul Davies mentioned this a while back in 2013 in his presentation of the ativistic theory. He highlighted that around 80% of the studies that support the systematic mutation theory are cannot be replicated. That is, you know, they're incorrect. So a lot of the science being produced and what we think is correct about the disease is later retracted because it cannot be replicated. So there are huge, huge contentions. And one more final one would be the randomness of DNA damage that occurs. So we have a consistency to the disease, which is the hallmarks that occur. So each solid tumour follows the same pattern. And this was a big thing for me. The metabolic theory actually identifies this consistency with the Wahlberg effect that occurs in all cancers or thereabouts. But with genetic mutations, we're expected to believe that utter randomness, not just from patient to patient, but from within the same tumour, there's the heterogeneity is quite incredible within the same tumour. So the question is, how how could so much random uh damage to the DNA um cause the consistency of the disease even within the same tumour? It just it doesn't quite add up from a consistency and a um uh a problem-solving perspective. So all those combined, um, yeah, it led me to to really start questioning the established view.

SPEAKER_01 24:41

And and what and why do you think this mutation model has remained dominant for so long?

SPEAKER_02 24:48

Um, consensus, I think. Um, well, I think initially the the idea was good. It you know, it was very plausible. It started i in uh the 1960s, just after um Watson and Crick identified the structure of DNA. And it was very plausible. It's very plausible to think that the mutations, because there are plenty of mutations in cancers, those mutations could drive the disease, being as though um DNA pretty much can drive all different mechanisms within the cell, you know, it's it's almost the blueprint, you could say, uh, for want of a better phrase. So naturally, um a lot of funding came in through that route. Um and it's it's the God particle, isn't it? You're it's the ability, it's the it's the excitement of possibly amending how or creating design of DNA um to eradicate disease, I think initially would be, but that there's other things that you could do with that that are exciting. So it just garnered a lot, a lot of interest, a lot, a lot, a lot of uh investment. And when you have a huge amount of investment, you essentially have a juggernaut, you then consensus follows. And when you have that juggernaut of investment, it then becomes hard to actually question that paradigm. So it becomes the established paradigm, um, especially when your your your um career depends on it, your your earnings depend on on that. And it's it it must be very hard. I really respect the scientists who haven't gone down the genetic route and are looking at the metabolic theory, the cancer stem cell theory, and the different theories, tissue organization field theory, because there's less money in that field. Um so it's a combination of those things, really.

SPEAKER_00 26:37

Yeah, yeah.

SPEAKER_01 26:38

Okay, so we're talking about mutations. So how do you distinguish between mutations being a cause of cancer versus mutations being a consequence of cellular stress or disease progression?

SPEAKER_02 26:55

Um that's a great question. Well, as far as I I'm aware, there's there's different types of mutations. And in a particular, uh scientists have identified the driver mutations, which they categorize as the ones that are actually driving the particular mechanism uh of cell proliferation of apoptosis. So there's specific detailed hallmarks that drive angiogenesis, for instance, um, that actually enable the tumour to grow. Um there are many other side mutations, of course, that may affect the ability of the immune system to function. Uh, but generally it's the driver mutations um that are the key uh mutations that we're looking, or we should see a pattern in, but we don't. We see that they're random and non-existent in quite a number of cases.

SPEAKER_00 27:47

Yeah, yeah. So okay.

SPEAKER_01 27:52

So do you think with modern oncology that it's become a little bit too much focused on the tumor itself rather than the biological terrain that allowed the tumor to emerge? I know this is a big contention between various groups.

SPEAKER_02 28:10

Yes. I think it's got to the point where we can't see the woods for the trees. So terrain for me is absolutely everything. That's health, that's mitochondrial function, that's cell signaling, that's just your body working as it should do to repair, regenerate, and working out optimum. As soon as you start compromising that in any particular way, not only are you causing damage that can then be copied into other cells and generate the wrong type of proteins, um, the loss of signaling, but you're also opening the door to additional problems such as um infection into the into the wound. And it just complicates things. So yes, it's it's it's terrain for me is everything. Um and what I felt was when I started initially doing my research was that scientists, yes, they're siloed, but I I felt like they'd done enough uh research across all uh aspects of um of the medical spectrum that you should we should be able to identify if we step back and look at it from a distance what the patterns were. So that's really where I I went down that particular avenue. And I think that's what really needed to be done. No one's really stepping back and looking at it holistically um across the board to find connections. Uh and yes, I do think the problem is that because things are so complex, we can focus on the really mignust aspects of the cell itself, even biophysics. That's that's another realm in itself. Um, but if you do focus without coming back, then you know you lose sight of the overall picture, and I think the overall picture really matters.

SPEAKER_01 30:02

Yeah, yeah, absolutely. So you've you've developed or coined a phrase the the cell suppression theory. So for somebody who hasn't heard about it before, can you explain that in simple terms?

SPEAKER_02 30:16

Yeah, I'll I'll explain it through cell malfunction, just the difference between uh so basically I I believe there's a fundamental flaw in the way that we're looking at cancer. When you look at all the other theories, established theories, say there's eight, they fundamentally make an assumption that the cell's malfunctioned. And then everything, every reasoned question uh and avenue of investigation follows from that assumption. Because every theory is looking at what part of the cell is damaged, what part of the cell is uh in broken, and what and how that is generating the disease. So the cell is malfunctioned, that's the problem, it's gone rogue, it's now no longer um part of the body. So we've got to attack the cell. I believe that's that's an issue because when you focus on the cell and blame the cell for being the problem, you don't that that prevents you from looking elsewhere at other external uh effects. And one of those effects I'm I'm suggesting is is pathogens. Now, um, so I've put forward a paradigm, which is actually that our cells aren't going rogue and they aren't malfunctioning, they're actually doing what they should be doing, and that is responding to a stubborn intracellular infection. This switch that we see to the in the uh Warburg effect in the energy system is a response by the cells, by the infected cells, and the cells around the infected cells that aren't actually infected. They're all collectively working together and they're responding, triggering the Warburg effect, in order to target the pathogen. And the pathogen, the issue is the pathogen is sustained within that tissue for various reasons because the the um terrain is damaged far too much that's it's allowed the pathogen to gain a foothold. And in that moment, the immune system has been suppressed because of the damage to the tissue, the iron overload that occurs, and the lactic acid that occurs. So we have this element where the pathogen locks in the Warburg effect because it's sustained within the tissue and the it the immune system and the infected cell itself and the surrounding cells aren't able to actually eliminate the pathogen. And because the pathogen is sustained, we have this lock in this process, this proliferative state. So for me, it's the pathogen is suppressing the pathways within the cell and the tissue, surrounded tissue, in order to survive. So it's blocking the cell death mechanism, it's forcing the cell to shift to this Warburg metabolism, because it's suppressing certain uh defensive mechanisms that the cell is trying to establish um in order for it to survive. So that's where the suppressing aspect comes from. Because I want to make a little distinction, because when I do talk to other clinicians, they often say, well, infection, we we accommodate that anyway, because viruses and bacteria, we highlight that they cause cancer. But when you look at those particular theories, they're not talking about the novel mechanism of suppression by active suppression, by the pathogen that's hijacked the cell. They're not talking about that. They're talking about the pathogen damaging the DNA. So the virus damages the DNA, the bacteria damage the DNA, and then the mechanism or the origin of cancer is the DNA mutation or is the mitochondrial damage. That's the mechanism. I'm saying that's not the mechanism. The cell is trying to do what it should do, it's not the enemy. We should be supporting our mitochondria to target the actual pathogen itself, not attack the cell. And if if I may go on a little bit further, just to illustrate my point with the immune system, the immune system is having a really difficult time trying to identify the tumor. Um and immunotherapies have a really difficult time too. I mean, some work really well, but not for everybody. And then you get hyperactive disease in others. So it's it's uh a double-edged sword. And the question is, why is the immune system not able to see the tumor? And there's there's a couple of other mechanisms, PDL, one-up regulation and various other things. However, one of the main points I'm making is that um a tumor is not completely uh, not every cell in the tumor is infected with a particular pathogen. You only need a small number of infected cells to elicit a huge response in the surrounding tissue because they all work together. So non-infected cells will switch to the Warburg effect. And then what you have is these cells are locked into that Warburg-like metabolism because it is an anti-infection response. So you have a load of thousands of regular cells doing what they should be doing. They're not the enemy. So the immune system doesn't see them as the enemy because they're actually trying to eliminate the pathogen. They're regular cells doing a regular, their regular job. So that's one of the main arguments I put forward for highlighting why the immune system has difficulty in identifying uh and attacking the tumor, because in effect, you're asking it to attack self. Self-cell. So yeah.

SPEAKER_00 35:40

Yeah, yeah.

SPEAKER_01 35:41

It's interesting. Um there's so many, there's so many thought processes and in theories in regards to tumors, and um, I've heard many things that it's uh it's a sack, and it's a sack that may contain toxins, or I've heard that it may contain some kind of infections in that, which which means that uh you would want to be very careful about damaging that sac, because if there was an infection in there, then all hell could literally break loose, right? And I suppose that's why when they're doing surgery on certain tumors, they go, well, this is just simply too much of a risk here. So then with your theory, then, then if there was an infectious process, then wouldn't it make more sense to treat the infection to make the environment less ha ha habit you know habitual for these infections?

SPEAKER_02 36:39

Yes. So that's that's primarily the approach that I would argue that needs to be taken and uh added additionally to whatever metabolic approach or if you if chemotherapy, whatever it is you you are are using off-label drugs, even, because one of the main things I've found in the research, only really because I'm looking at it from this perspective, is that you look at the number of off-label drugs that are being used and trialed and tested, and they're all also antifungal. So the additional property they have is that they're all antifungal. So I'm finding this coincidence across all different aspects of infectious behavior and the uh the treatments that we use that's that's that's worth looking into. So I'm not saying, you know, there are different drugs will work in obviously um different ways, and they they can be directly targeting the metabolism of the cell. However, there's this there there's this feature of all of them being antifungal. And so the question I would ask is are we inadvertently having benefit because we are actually targeting the fungal pathogen that I say is potentially driving the disease? Now, that's not to say it's going to be as easy as that and use, say, itrachonazole, a broad spectrum antifungal drug, and you're gonna clear up the cancer. There's a number of issues because the immune system is already primed not to identify fungal pathogens, for one, and you need the immune systems with a drug like itrachonazole because it's um a fungostatic drug. It doesn't kill fungi, it inhibits the fungal pathogen. It's not fungicidal. Um, so what you need is the immune system to help out. So they both work in unison. But what we find in pretty much all cancers is there's a switch from a TH1 response to a TH2 response, which is the TH2 response is primarily uh for cell repair and targeting external pathogens such as viruses outside the cell. The TH1 response is immune cells geared to targeting intracellular pathogens. So we have this mechanism at play where you have the wrong type of immune cells surrounding the tumor, and they're trying to just repair the tissue that's constantly inflamed, and they're not targeting the pathogen inside. So we need a way of if we're going to target the pathogen, yes, that's what absolutely we need to do. We need to make the the environment hostile to the pathogen, reduce inflammation, um, possibly reduce its fuel source, primarily glucose, but it can uh adapt to fat and protein as well, which is why there's this metabolic flexibility we will talk about. Um, but we do need to target the pathogen, but we need it, it needs to be in a nuanced way because it's not as simple as just giving them antifungal drug. There's resistance to those drugs, not all pathogen, not all fungopathogens are targeted with those uh antifungals as well. So we need to modulate the immune system. There's a number of things that need to be done all in one go.

SPEAKER_00 39:39

Yeah, yeah.

SPEAKER_01 39:40

Yeah, it it's interesting when you talk about the fungal aspect of things. The first time I came across research was that was by an Italian researcher. Uh I'm not sure if I'm pronouncing it right, Simonocci, or uh he wrote a book called I think it's Clio Simoncini.

SPEAKER_02 39:59

That's how I've avoided it.

SPEAKER_01 40:00

Yeah, see, that that's probably it. Yeah, my uh apologies to the Italian people out there. But yeah, he wrote a book called, I think it was called Cancer as a Fungus, and uh and that was uh that was an interesting read there. So if if we look at that theory, um, and I know from when I'm working with patients that if somebody would have, let's say, a fungal infection, uh, a big part of it is changing the environment. And the first thing that always comes up is well, what drives fungal growth the most in the body? And it tends to be sugar, right? So we always go, well, you need to go on a low carb or uh or a no-carb diet. Um, and how have you found that uh in your research and work?

SPEAKER_02 40:45

Yes, um, there's definitely a correlation between reducing the amount of um uh sugar intake you have, uh, normally synthetic um refined sugar is the problem. And the same with infection. So if you look at infection studies, whenever you do a fast of any kind, you reduce the fungal burden within the body. This is a well-known phenomenon. Um, primarily because they do, they feed on those sugars. Um, and the problem as well is the biofilms that they generate. So it's very difficult to target them when they're within those biofilms. So that that's that's why I would argue that obesity is is linked to higher rates of cancer, apart from the fact that you have glycation occurring in environments where you have a lot of glucose within the bloodstream, which is going to cause its own problems. Um mainly because you are feeding these pathogens over a long period of time, they're establishing themselves within tissue. And then if you've got constant inflammation, uh those pathogens are sitting uh and waiting for that opportune moment for the signals of that inflammation in order for them to transition into a pathological state, the hyphal form and invade cells and tissue. So they're incredibly intelligent and it is it is about um it is largely about sugar. Um, but having said that, there are a that there is research that highlights that just you know, you can't just starve the body of sugar because your cells need sugar, your brain needs sugar, and and the bloodstream uh regulates the amount of blood uh sugar you have within the bloodstream to a a specific level. I think the issue is not the fact that you you your blood is still supplying sugar to the body, it's the fact that people are overconsuming the sugar. And then that allows the the tumour, because it's a its metabolism is such that it's relying on glycolysis, it actually requires, in order to generate more cells, more um glucose to produce more of the metabolites needed to generate extra tissue. So, and simply because glycolysis absorbs a higher rate of glucose for every ATP molecule molecule it produces. So, yes, um cancers definitely require a higher rate of glucose. We see this with the PET scan, and that feeds into the survival of pathogens within the body. So the two go hand in hand, in my opinion.

SPEAKER_01 43:23

So then so then with that logic, if we look at different uh dietary types, then there's an awful amount of positive research on a ketogenic diet and being in a state of key ketosis can help a lot of people with very serious conditions. So, how would that play into into a situation like this?

SPEAKER_02 43:47

Yeah, you see uh the research does seem to show that there's there is um a very good benefit. And even with chemotherapy, um, because you're strengthening the immune system as well. You're because one of The other things I found was because the uh surface structure of fungi can uh be primarily carbohydrates, 90% carbohydrate in structure. Um if you consume a lot of glucose and carbohydrate, it's flooding through the body. The the the neutrophils actually find it difficult to differentiate between um the carbohydrate structure of both. So it can suppress the immune system in that sense. Um but sorry, can you can you um remind me of of the question again? I went off a little bit of time.

SPEAKER_01 44:35

Yeah, we were just talking about a ketogenic diet and and being in ketosis and how that may uh help the uh the environment, the um, you know, the terrain and being able to uh help somebody with uh, let's say a metabolic uh process, whether it's obesity, cardiovascular disease, cancer is uh as the big top three.

unknown 44:56

Yeah.

SPEAKER_02 44:56

So if you want to look at it really simply, and you'll know better than I do, but there's there's essentially two states within the body, an anabolic and a catabolic state. And the ketogenic diet gets us into that catabolic state. Um so the anabolic state is when food is abundant, like in a business, you know, the economy is booming, you take on a load more employees, but then you get to grow those employees, that business grows to a size where you actually have a number of jobs that aren't really doing much. And it's the same with the cells in your body. You're accumulating, you're storing fat, you're storing more food, um, and you're generating more cells because the times are good, but then those cells become maybe senescent or uh they don't function as well, less mitochondria, or the mitochondria don't function very well. So when you enter into a state of ketosis, you enter a catabolic state, uh, or you're trying, uh you're trying to get yourself in a catabolic state. And that's like in the business world when the economy dips and there's less money going around. So you have to um what's the word? You have to economize, you have to make your business more efficient. So you you get rid of the the lesser efficient stuff and you reduce things down. And it's the same with the body. So we have autophagy, mitophagy occurring, um, and this is where the body actually recognizes that there's less food coming in. So in this state of fasting, you could say, or a ketogenic state, uh the body is trying to conserve energy. So it it breaks down the inefficient cells uh and uses that those nutrients to um you know improve the mechanisms, the functionality of the rest of your tissue, your immune system. Uh, and then you have uh mitochondrial biogenesis occurring. So you have this process of renewal effectively in your mitochondria, in your immune system, and you eliminate a lot of the inflammation that occurs in the body because you're getting rid of those cells that generate the inflammation because they're not working as efficiently as they could be. So that in itself is a fantastic um, you could argue, medicinal process that allows your body to regenerate. Um, but also it's it's cutting back the glucose that is available for the tumor, and it's cutting back the glucose that is available for um pathogens to survive and thrive within uh biofilm and within the tumor itself.

SPEAKER_01 47:17

Yeah. So so then really the modern day the modern day food pyramid, um, which is slowly being changed, is really not is really not serving us uh in that process of helping the to build the terrain uh at all, really. When when you look at uh the classic U.S. food pyramid, uh I think it would they had six to eleven servings of grain-based carbohydrates as a base of a healthy diet, which somebody who studied nutritional biochemistry, I just think that's funny, uh ridiculous funny. But um I don't see how anybody can um build a proper terrain with a diet like that. And even when it comes to digestibility of foods, um we have to be able to digest and break it down to assimilate any benefits from that. So I think the whole diet wars out there right now has got a lot of people confused. Um and as I say, a lot of people are looking at uh philosophical ideologies instead of looking at biochemical sense on how things really are.

SPEAKER_02 48:28

Yeah, well, I expect, you know, you look back at our ancestors and they will have been in ketogenic states at some at certain points and fasting at certain points because they couldn't actually get access to the abundant food that we have now. So the body goes through this cycle of um this this catabolic cycle it needs to go through. Um and that makes it more metabolically flexible uh and efficient. So, you know, it's it's a natural process. And I I think we've lost that because we've got access to food 24-7 whenever we want.

SPEAKER_01 48:59

Yeah, yeah, yeah, absolutely. And uh and uh yeah, and to so many different foods, if we can even call some of them uh uh foods, you know. I've heard people saying, oh, you need to have such an array of different foods. And I remember one person saying it was something, it was an unreal number. It was something like, oh, you have to expose yourself to like 200 different foods. And I'm like, I don't even have 200 foods at my doorstep unless you want to include processed uh and ultra-processed, which I don't really would call foods to begin with. So um I think we've made things a little bit too complicated. Uh, and I think diet and nutrition is actually a lot simpler than people uh believe it to be.

SPEAKER_02 49:42

And uh Yeah, so the ketogenic diet isn't just about, you know, starving the cancer of glucose. That's the point. There's there's other mechanisms going on within the body um that are regenerative and beneficial on a number of different levels. So it's not just about the sugar. But the other thing is the ketogenic diet can be can be very good and very beneficial, but it's not the answer to everything. Uh, and that's what kept me moving forward with um looking beyond the metabolic theory uh with a number of contentions that were there. Um but like for instance, prostate cancer, you would want to be careful about how you you you diet with prostate cancer because um it isn't driven by the Warburg effect initially. So this is one of the one of the big contentions with the metabolic theory. It's actually driven by um uh oxifos and fatty acid oxidation, or it appears to be. Uh glycolysis is the base um metabolic rate of healthy uh prostate cells is actually an regulated form of glycolysis in conjunction with fatty acid oxidation. So yes, that that there's a different explanation. I think I'm the only person who's actually provided an explanation for prostate cancer because I I show that the abnormal metabolism of prostate cancer, which doesn't map onto the metabolic theory Warburg paradigm, um is easily explained through infection. So that's that's the beauty of what I'm I'm I'm saying there. But just the point is you can't just go and and say um obviously a ketogenic diet is beneficial for all cancers because it's not you've got to you've got to understand the nuance uh and the base metabolism of any particular cancer at any given moment in time. Most of them are affected in that way. However, there's just one or two. Breast cancer, I think, is another one.

SPEAKER_01 51:36

Yeah. So so based on that, different cancers uh may react differently. So does your cell suppression theory apply to all cancers, or do you see it as more relevant to certain types than others?

SPEAKER_02 51:49

No, all cancers. So Robert Schroutzman has has done the research in 2017 and he overturned the notion that tumors were sterile, free of microorganisms. So he found that bacteria and fungi exist intracellularly within all cancers and all tumors. So that's the first big thing. Um the second big thing is that the cell is doesn't appear to be broken, malfunctioning in the sense that the metabolic theory suggests, in that it's reliant on glycolysis. So it's just reliant on glucose and glutamine effectively. Um that's the argument there, because a lot of people are showing, a lot of scientists are showing, and there's a lot in the literature showing that you can actually regulate OXFOS and certain cancer stem cells are operating using OXFOS, and like I say, um so is prostate cancer. So it seems as though the cancer cell is metabolically flexible. So that's one big question, Mark, over the metabolic theory. But also you've that's gotta really factor in if you're thinking about what treatments you're gonna be utilizing. And the way I explain that is that um the pathogen within the tumor can actually adapt. It can adapt to glutamine and fat. It upregulates particular pathways, um, and it does this within when it gets um absorbed by an immune cell. It rapidly upregulates, say, the glyoxalate pathway, which allows it to convert fat into glucose. The pathogens always trying to convert back into glucose. I mean, there are a number of pathogens that are lipophilic, so they they'll consume fat, such as malaasia, which has been implemented in pancreatic cancer and breast cancer and a number of others. Um, but primarily they're they're they're glucose-loving. But if you do cut off the glucose supply and the pathogen isn't eliminated and the immune system isn't able to get in there, what you then have is uh a cell working on autopilot, because that's what cells are doing when the pathogen's in control. The pathogen has blocked the cell death mechanism. Now the cell cannot die. So it's literally just trying to rebalance because our tissues are constantly always trying to reach homeostasis. So the pathogen is absorbing the nucleotides, the glutamine, whatever compounds are inside the cell and in the surrounding tissue in order to thrive itself. And the cell is then forced just to balance those off. So if the um the cutting of the glucose isn't quick enough, or the pathogen can easily adapt, and the and the cell is also absorbing glutamine uh through substrate level phosphorylation um to allow ATP to occur, then the pathogen will sequester that glutamine and convert that through glucode neogenesis um into glucose. And the same with fat. So it's understanding that there is this metabolic flexibility and the pathogen being present and in control of things explains why that is able to occur.

SPEAKER_00 55:00

Yeah, yeah.

SPEAKER_01 55:02

Yeah, it's it's fascinating when you look at it, and I think um you explained that very well with the uh with the glutamine. Because I think there's some misconceptions there as well. When people go, Oh, that's an amino acid, so therefore maybe we shouldn't be eating any proteins. And it is there any truth to that, or have you found that the diet type uh varies depending on the stage of cancer that you're at?

SPEAKER_02 55:30

Again, it's I wish there was an easy answer. It's it's incredibly nuanced because I mean you can check the metabolic profile of particular tumors at the stage that they're at, can't you? Um, but there's sufficient evidence to show that actually if you supplement with glutamine, that can have a benef beneficial effect depending on the stage of the cancer and what its uh its metabolic profile. So the reason for that being you're the glutamine is supporting the um the stomach lining, repairing the gut, so you so you're reducing the inflammation going into the bloodstream from the gut and the toxins that are going into the bloodstream from the gut because you're gonna have a dysbiotic microbiome.

SPEAKER_03 56:11

Yeah.

SPEAKER_02 56:12

And also um your immune system relies on glutamine as well, heavily uh in order to function properly. So by supplementing glutamine in certain circumstances, and I'm not a clinician, so please do not take any of my uh my instructions at medic as medical advice, you can actually benefit the tumour. Uh sorry, benefit um the patient and reduce the tumour. Because arguably the tumour will only absorb a certain amount of glutamine. It's not going to increase exponentially the glutamine if there's more glutamine available, it can only grow at a certain um certain speed. And then the pathogen can only access the glutamine to a certain degree. But if you're also uh enabling the immune system and if you're able to then transition from a TH2 to TH1 response, uh then and you're making the immune system, you're optimizing it. Because the problem is a lot of patients are glutamine deficient because uh when the tumour is actually absorbing a lot of glutamine, our bodies can it becomes um semi-essential because uh the amount that we're producing is not enough to sustain the optimal function of the immune system at that point. And that's when you start to have a problem, really. So, yes, it the nuance is you can actually optimize the immune system with those amino acids or that amino acid in particular. Um, so it's not a one size fits all, it's it's really trying to understand the nuance.

SPEAKER_01 57:39

Yeah, yeah, absolutely. And uh we very much uh especially in uh in functional integrated medicine, we always talk about uh healing the gut. Uh and like you said, when there is a a diotic um stage uh that leads to kind of more of a full-fledged intestinal permeability that you can't really get somebody better until you until you heal that. Um so there again, we have to look at well, what causes the intestinal permeability, what causes the dysbiosis in the first place, what lessens the mucoal mucosa lining to protect the, you know, from leaking into the bloodstream. And yes, there can be pathogens there, but then there's also the inflammatory reactions, right? It's again, we're back to the foods that we eat, uh, the toxins that we're exposed to, the medications that you're taking, uh, the stress that you're under, and who doesn't have stress in this day and age, you know, there there are all loads of stresses. So it's it's always a multi-layered approach, isn't it?

SPEAKER_02 58:48

Oh, absolutely. Absolutely. Um, the body's an ecosystem. And the heart of it, I think, is the microbiome. We don't touch on it enough. Um, I mean, the microbiome produces a number of metabolites that we actually require. It removes the uh toxins that we absorb uh can be effectively. The bacteria also combat the pathogens if so we keep the bad bacteria and and fungi in check. Um, but this is the other thing. Part of my research um was showing that if you have a dysbiotic microbiome, not only you are you getting um inflamed gut and um leaky gut, but candida within the gut, when they overgrow to a certain potential, they can cause inflammation and disease to occur in a different part of the body. So there's one particular study which was showing that they caused a massive amount of inflammation in the in the lung and disease in the lung. This was directly from interacting from the gut. So you've got to realize that they the the health of the microbiome or the health of the human being really follows the health of the microbiome, in my opinion. Um because I mean there's there's been studies showing that fecal transplants, for instance, uh appear to be quite effective in in a number of uh diseases um and helping the microbiome come back to um good health. But just just simple studies that done that are done in rats when you look at um you feed a particular one set of rats a particular diet on the same diet to another particular group of rats and they have a different microbiome, you get obese rats jet being generated, and other rats, you know, they're they're perfectly healthy in terms of uh weight. And then you switch the microbiomes over and they switch their weight dimensions. Um and that's purely down to the type of bacteria that are present that are feeding off of maybe the glucose that is present, so less of it is being absorbed by the person themselves. So that we that we still don't know enough about the microbiome, but what we are learning is pretty incredible, and it's it's integral to our uh our health as well as looking after our hormonal balance and everything else um within the body. It's an ecosystem.

SPEAKER_01 1:01:06

Yeah, yeah, absolutely. Yeah. I think we're just scratching the surface on what we know about the microbiome and and bacteria and probiotics and the like. And I think it's almost it's almost like this big messaging system that affects the signaling inside of the body, uh, essentially. Um and when we go back to the diet, um what throws the gut out the most? You know, uh that's what I when I work with patients. I'm going, well, you know, how's your digestion? Uh and are you bloated? Are you gassy? Uh and if so, what what what have you been eating? How what what do you notice when you eat that that triggers that? You know? And I think uh listening to our body is something that we don't do enough. Uh, or sometimes some people are ignoring the message that it gives to us, and we have to kind of tune back into that again. Yeah. Um You mentioned um the microbial environment. Let me just get this in my head. So there's a microbial environment of the tumor. So could that be one of the missing pieces in why tumors behave differently between patients? May act one way in one person and different in another.

SPEAKER_02 1:02:21

Yes, I believe so. So it's not going to be one fungal pathogen, and it's a combination of viruses, bacteria, and parasites working together because you never have an infection of one particular microorganism. That's it. They work in synergy. So that super complicates uh things. Plus, different fungal pathogens will have um uh will operate differently and they'll produce different metabolites, they'll affect DNA differently. And it's all those, it's that um complexity of the multitude of DNA uh mutations that occur, the damage to mitochondria that occurs. So, I mean, there are there is obvious damage to going happening to the cell. But if you're damaging a random array of uh chromosomes or uh DNA genes, you're gonna get really um a plethora of random um responses, uh random proteins being produced that are just gonna go on and cause further information to in all different organs and different areas of the body. So, yes, it's the for me, it's the pathogen that's causing a lot of the randomness because you've got to imagine that this has been going on for a long time, the pathogen has been present for a long time, and it produces reactive oxygen species, the cells produce reactive oxygen species. Um, it's producing genotoxic metabolites. We have acetaldehyde, all sorts of um uh mycotoxins are being produced in order to eliminate the immune response and damage particular aspects of of DNA. So that's been going on for a very long time, and that's why it's random for me, and that's why things can can operate or seem to appear different from one patient to another, even though they've got the same uh cancer, and even within the same tumour of the same uh the same person as well.

SPEAKER_00 1:04:06

Yeah, yeah.

SPEAKER_01 1:04:08

Um going back to the mitochondria, um so do you see mitochondria dysfunction as a cause, a consequence, or both?

SPEAKER_00 1:04:24

I think it's both.

SPEAKER_02 1:04:26

However, I'm I'm moving more towards sixty percent, forty percent with the microbial interaction. So mitochondria in the terrain need to be damaged to a degree that enables the pathogen to take control. Whether or not mitochondrial damage on its own could actually be the driver, I'm open to that. Um, however, there's a number of studies that kind of challenge that perspective. Um, you could argue senescent cells are the result of mitochondria becoming um uh dysfunctional to the degree that they don't really work anymore. Um, but um oncocytomas are benign tumors, and they they literally uh have this completely dysfunctional mitochondria, so they can't function, use utilize and they can't utilize oxfas. But because because they're reliant on glycolysis, as the metabolic theory suggests, is the underlying mechanism that drives cancer, the mitochondria dysfunctional, so reliance on glycolysis drives proliferation, that doesn't occur with oncocytomas, which have dysfunctional, really dysfunctional mitochondria. So there is a question there for me how dysfunctional, can the dysfunction of mitochondria actually drive this mechanism? Because mitochondria are also involved in apoptosis, the cell death mechanism. For me, it's working out where at what point would the dysfunction Function to the mitochondria prevent apoptosis from happening. Because as far as I'm concerned, past a certain threshold of damage, apoptosis is triggered. And that would combat the fact that the mitochondria are dysfunctional past a certain point. Because I'm even arguing that senescent cells and those benign tumors, they have a microbial, a small microbial constituent that is affecting those tissues. I think in terms of the oncocytomas, that the pathogen has damaged myocardias so much that it's actually now detrimental to the functioning of the tissue, so that it doesn't grow. Because there's a number of papers that highlight that oxfas is required, a certain level of oxfos is required for proliferation to occur. So I'm gearing towards really, it's more, and I'm putting my flag in the ground here. So they're not using the oxygen to generate energy, because they are allowing glycolysis to do that to generate the ATP. That allows the defensive mechanism, the mitochondria, to then target the pathogen, utilising that oxygen indirectly and directly. So in a long-winded way, I'm edging much more to the fungal pathogen being in control. And when you kill the fungal pathogen, that relinquishes control. And then the mitochondria, regardless of how damaged they are, will either bio regenerate from healthy mitochondria being fed in from healthy tissues in the periphery, or they will trigger apoptosis because they've been damaged past a certain threshold. And we see this, this is one of the other things, uh, one of the other contentions, is that we see that if you give natural compounds to cancer cells, they they trigger apoptosis. So honey or even silver, it triggers apoptosis, which suggests that cell death mechanism isn't damaged beyond repair, which is really what the meth metabolic theory is is suggesting. That's why it shifts over to glycolysis because uh and the cell doesn't die because mitochondria damage too much for that to happen. But quite clearly it it can be instigated, which suggests to me that there's a suppression or suppressive mechanism going on, and that would be for me the pathogen blocking that cell death pathway.

SPEAKER_00 1:08:29

Okay. Okay.

SPEAKER_01 1:08:31

So then to kind of sum this part of the topic up. So from a systems biology perspective, what uh for our listeners, what are the upstream conditions that would make cancer more likely?

SPEAKER_02 1:08:48

Anything that generates chronic inflammation damaging the tissue, weakening the immune system. Because the consistent I was always trying to explain the consistency of cancer. So you've got a number of different carcinogens. They all damage cells and tissue and DNA in completely different ways. Really random, yet they somehow manage to generate the consistency of the disease. So, what is the consistency with all these different carcinogens? And for me, it was four four things: weakening of the immune system over a prolonged period of time, chronic inflammation, which opens the pores to the cell and the tissue, which allows fungi to gain greater access. Um, lactic acid overproduction, because whenever you've got inflammation, you the cell switches to the repair mode, which requires glycolysis. So you've got overproduction of lactic acid and iron overload. Past a certain point of inflammation, the cell and the tissue cannot store enough iron for any length of time and it gets released. Now, the lactate, lactic acid, and the iron feeds the pathogen. It's like rock, both are like rocket fuel. The pathogen senses the local environment when it senses enough lactic acid past a certain threshold, it realizes that's almost telling it that we have an inflamed situation and the tissue is vulnerable. But at the same time, the lactic acid and the iron overload suppresses the immune response at the site of damage. So you've got this now niche where pathogens can take advantage of this inflammation. So it's anything that generates, doesn't matter what it is, which is why so many different things appear to be able to cause cancer, and that's not the same as an origin. The origin is the fungal pathogen, I'm saying. So the fungal pathogen gets into the cell, you provide it with that opportunity to access the cell because of the prolonged inflammation that you uh are providing it with whatever toxin, pesticides, lack of nutrients is generating the weakness to the immune system and the tissue. So the tissue is no longer able to function optimally to resist the invasion. But the key thing is the pathogen needs to be present in the tissue as well in sufficient number. If the microbiome's okay and there isn't that pathogen present, it doesn't matter if you're gonna have the mutations or you you have um the carcinogens, um, you're not gonna get cancer. And that is how I also explain um the inconsistency of that, because you can still take a number of these carcinogens or you can have the particular DNA damage, but it's not 100% guaranteed that you're going to get cancer. For me, it's because you haven't got the fungal pathogen present in sufficient number within the tissue at the time, or you have. It's the pathogen that differentiates the inconsistencies in what we see between patients.

SPEAKER_01 1:11:38

You you mentioned you mentioned iron overload. Uh, we hear a lot about iron these days, and there's there it seems to be a very debatable topic for for a lot of people. So is there truly an iron overload, or is there, would you say there could be more of an iron transportation issue?

SPEAKER_02 1:11:59

Um a bit of both, I think. Because, you know, um iron is highly reactive. Um when when there's a difference between transportation and iron being freely available. So I think it's the it's the freely available iron that I'm talking about. Okay. So excuse me, with with inflammation, you have a process called um anemia of inflammation. So the body knows that iron is highly reactive, and it also knows that iron is like rocket fuel to pathogens. So it instinctively um sequesters iron away into um iron proteins, storage proteins, and the immune system does that too. So the whole goal of that is when you have an acute infection, you remove the iron, which could facilitate infection, to then allow uh the repair process to establish, eliminate the pathogen if it's path the pathogens present, and then you release the iron because it's required for cells to grow. Um, you know, mitochondria, uh you know, many different aspects of the cell require iron. So in that acute process, that's fine. But after a long period of time of prolonged inflammation, um you cannot sequester the the proteins that absorb the iron to sequester it away so the pathogen can't get access to it, become saturated. And the cell, the tissue can no longer hold it. So now you have this freely available iron, which is damaging, and the pathogen can get access to. And the pathogen requires the iron in order to grow. So, like I say, it's like rocket fuel. Um, so in that situation, iron's bad, bad in the sense in chronically inflamed tissue. So it's a dual-edged sword. You really need iron to survive.

SPEAKER_03 1:13:52

Yeah.

SPEAKER_02 1:13:52

But too much iron in a situation where you are overloaded with inflammation and you have a high uh pathogen fungal burden, that's gonna have a negative impact. That's gonna it's gonna become pathological.

SPEAKER_01 1:14:05

Yeah, yeah. So do you think for somebody in that situation, do you think that uh let's say going down to the local blood draw place would be a benefit, giving a pint or two of blood?

SPEAKER_02 1:14:18

That's interesting. That's uh a very good question because um what we see is there's a difference between men and women in terms of how often they get cancer and uh who's more likely to die from cancer. It's men. Uh and one of the reasons, one of the many reasons of that that is, is because women obviously lose a a certain amount of blood each month. So, yes, there's this factor that the iron is less available and it's only it's being used more efficiently more efficiently in the female body. Um there's another other issues as well. The X and Y chromosome, I think it's the X, I can't remember which which chromosome it is now, but one of them, I think it's the X, um uh codes for immunity. So men have um a reduced uh or less aggressive immune system because of that, where women have a more aggressive immune system. And that's one of the reasons why women, I think they suffer a little bit more from autoimmune disease. But that more aggressive immune system can also also eliminate the pathogens that I say are driving the disease, which would translate into why women have a reduced um rate of cancer and a reduced rate of dying from the disease.

SPEAKER_01 1:15:30

Yeah. So I I I guess the guys we've got to fight a little bit more and get a few more bloody noses, don't we?

SPEAKER_03 1:15:37

That's why we're not doing it.

SPEAKER_01 1:15:43

What's your opinion? And I and I I have an idea what you're gonna say, but your view on conventional cancer treatment such as surgery, chemotherapy, radiotherapy, immunotherapy, targeted drugs.

SPEAKER_02 1:15:58

Surgery is one of the best um interventions we currently have, isn't it? It it it accounts for the bulk of the survival figures that we have. So yes, I would always argue for surgery where it's needed. However, then again there's always a nuance there where there's the danger of releasing whatever contents of the tumour into the bloodstream. So you would need an adjunctive um uh you know treatment response for that.

SPEAKER_03 1:16:32

Um radiotherapy.

SPEAKER_02 1:16:36

Again, I'm not an expert on this, but I think this damages the tissue more than it should do. It raises, I think, glucose levels, it it does a lot of damage that can be ongoing and it can you know suppress the immune system. So I I think that tips the balance in favour of the pathogen for me. I think it can work in in targeted certain situations where it needs to be, um but I I I think it's more damaging potentially um than it could be. And similarly with chemotherapy chemotherapy has its place. And uh Robert Dr. Robert Gatenby highlights that he's been looking at reducing the dose dosage of chemotherapy and showing that low-dose chemotherapy can actually work really, really well uh for longer periods of time with less toxicity. Um and you it and I mean we can always combine these things with chemotherapy, but for me, chemotherapy, while it's very good at targeting the regular cells, and it's it's good at shrinking the tumour initially, so it might be really good for shrinking the tumour initially uh and then it can be resected, removed via surgery. That that that can be a good strategy. However, for me, the prolonged use of chemotherapy I think is an issue because you're damaging the mitochondria, which are your defense mechanism, you're reducing the quality of the immune system, you're damaging tissue further, causing further inflammation throughout the entire body, and it targets fast dividing cells. Cancer stem cells are not fast dividing, and they have uh efficient efflux pumps and the ability to pump out toxins. So, what often we see occurs is the tumour comes back because it develops resistance. Why does it develop resistance? It shrinks dramatically, so it looks great, but you have um this element of cancer stem cells that then regenerate the tumour because they have to regenerate the the tissue a lot quicker than before, because they're associated with that dying tissue. But also, part of the way that chemotherapy works, in my opinion, and it's documented within the literature, is that it produces a lot of reactive oxygen species. And it does that by damaging mitochondria. So it's the same with any toxin entering the cell, isn't it? Mitochondria will all react and produce reactive oxygen species. Excuse me, I might have to get a drink of water in a moment.

SPEAKER_00 1:19:07

No problem.

SPEAKER_02 1:19:08

Um during that process, you're as you're damaging for mitochondria in every successive then chemotherapy treatment, you've got fewer mitochondria that are uh efficiently able to produce enough free radicals. So my argument is that initially your your the free radicals that are generated en masse by the initial chemotherapy is actually able to combat and kill the pathogen, the fungal pathogen present, or at least weaken it. But then the fungal pathogen upregulates its antiox antioxidant mechanisms. The cell is doing that as well because the ROS is so widespread and damaging. The mitochondria being reduced. So the next phase of chemotherapy and the next progressive phase of chemotherapy, fewer mitochondria are producing fewer reactive oxygen species while the fungal pathogen is upregulating its antioxidant defense. So it gets to a threshold where you can't produce enough free radicals in order to combat the pathogen, and then of course you're stimulating the cancer stem cells.

SPEAKER_00 1:20:07

Yeah, yeah.

SPEAKER_01 1:20:09

Um historically, many important shifts in science become uh really, as we said in the beginning of the podcast, is uncomfortable questions. Uh do you see your work in in that tradition?

SPEAKER_02 1:20:29

Asking uncomfortable questions.

SPEAKER_01 1:20:31

Yes.

SPEAKER_02 1:20:32

Absolutely.

SPEAKER_01 1:20:34

The biggest shifts in science began become began with uncomfortable questions.

SPEAKER_02 1:20:39

Absolutely. Um because we have the uncomfortable question really is have we misunderstood the underlying cause of cancer? And are we um like a juggernaut, are we going, are we pursuing the wrong, are we pursuing a path that is not as uh effective as it could be, if I want to be politically correct? Um so the uncomfortable question is that the majority of the cancer industry are on this juggernaut. And at some point they've got to ask themselves the uncomfortable question is Am I actually, you know, on the wrong path here? Do I need to transition to a different, probably more difficult path and be really honest with what I'm doing? Is it not going to get us to the goal that we want it to get it to? I don't I need to get off this train. But that's a very difficult thing for a lot of people on that train to ask themselves. So, yes, it is a very difficult question, and and and they are the questions that do change things because unfortunately, throughout history, um the consensus has been proven to be wrong. It's the only way that progress is ever made.

SPEAKER_00 1:21:51

Yeah. So so then what would need to happen for your theory to be fairly tested?

SPEAKER_02 1:22:00

Um a lot more funding for one in this area. Um there are a number of different studies that can come from um come from my research. Uh at the moment I do have a biotech company on board, and we're looking at doing a pilot, a pilot study, an observational study, uh, and hopefully that will grow into something else. But um, yeah, there's a lot of a lot of um testing that can be done with different pathogens and how they relate to to cancer and how it functions, and then the progression of hopefully different antifungal drugs potentially. Um not not just antifungal drugs or other off-label drugs, the combination use of those, um, and natural compounds, natural natural compounds, but we all know that that's very difficult to actually get the studies on natural compounds because there's not a lot of money in that can be made from those, but the very least, um antifungal drugs. Because we're going through um an epidemic, really, or even a silent pandemic, of antifungal drug resistance. And that's something that needs to be addressed because um it's becoming a real big problem. So a lot of these antifungal drugs we currently have aren't really working because of that. So to generate an antifungal drug that is both anti-cancerous as well, I mean, that's that's uh a very interesting prospect for any pharmaceutical company, I would have thought.

SPEAKER_01 1:23:23

Yeah, yeah. And I think maybe aspects that we haven't uh touched on is going more into kind of the quantum medicine realm where we're dealing with light and frequencies and the like. And we know, especially with things like red light therapy and that, that it has uh a lot of benefits to mitochondrial function. So I would assume that that's a whole other area that um could be explored a lot more than than it currently is.

SPEAKER_02 1:23:53

Absolutely. I think it's I think it's paramount. Um I've been listening to a lot of Jack Cruz's um work.

SPEAKER_00 1:24:00

I love Jack.

SPEAKER_02 1:24:03

Um so I I agree entirely with a lot of a lot of what he's saying. Um and the mechanism, um, how near thread um light works being as though it penetrates deep within the body, it's it's very interesting. Uh what I what I draw a correlation with is that uh fungi actually control and manipulate um nitric oxide mechanisms, and and that's a mechanism that mitochondria use to control the flow of Oxfos. And what we we find is that fungi can manipulate that pathway and potentially they're using that to block um uh the complex four, I think, of the electron transport chain. But where a near-infrared light comes in is it's able to knock off the um the bonds, the the bonds that that the nitric oxide have within complex five that allows mitochondria to function um more efficiently. So for me it is it's it's about making mitochondria more efficient, which is why you have methylene blue and hyperbacoxygen therapy and any other particular therapy that improves the functionality or tries to improve the functionality of mitochondria, but especially if it's antifungal as well, because I think that's really going to benefit the process. Because really, what we're trying to do here, and the paradigm shift I'm putting forward, is we want to be supporting the mitochondria to eliminate the pathogen rather than trying to force the mitochondria to do something that we think they don't want to do or damage the mitochondria to stop them from working entirely. It's it's a supportive role.

SPEAKER_01 1:25:39

Yeah. In my in my clinic, we use um we have a red light therapy room. Uh we use that quite a lot. Uh I I use it Monday to Friday because I'm indoors all day and I got to get my dose of light. And uh if the weather's nice on the weekend, I'm out all the time. Also infrared saunas. Um, we use that a lot with uh patients here. We get uh really good results uh with that. And uh going a little bit more out um of uh uh resonant frequency device as well that uses uh proton emission because that helps to get inside of the cell. So again, it's all dealing with frequency. So this is all the quantum medicine world that we're we're getting into now, um, which I think is interesting. I think it's old, it's old technology that was maybe used in a different way way back when, and we just kind of modernize a way to do it. Um, but yeah.

SPEAKER_02 1:26:37

Yeah, it's very interesting. It's an area I'm also will be uh adding to my second edition. Um, but blue light, um melanin within the body, and it's just very interesting how we see, and Jack points this out, how we see fungi growing in and around Chernobyl, and how they uh they actually use melanin as uh a virulence factor. So one could argue when we're talking about how mitochondria produce light and potentially light being a mechanism of communication within the body and a mechanism of facilitating mitochondrial energy production. Uh, one could argue that on that premise, the fungal pathogen is an a is essentially uh stealing, if you will, the light energy that our cells actually use through regulating the melanin um that's absorbing that weight, that light wavelength.

SPEAKER_01 1:27:30

Yeah, yeah, yeah. It's it's very interesting. And geez, we could go on for for a long time about that. But yeah, I look forward to the uh is did you say your second edition or your second book?

SPEAKER_02 1:27:41

Uh second edition of the book.

SPEAKER_01 1:27:43

Second edition, upgrade it. Okay. Excellent.

SPEAKER_02 1:27:45

That's what I'm gonna be for a little while, yes.

SPEAKER_01 1:27:47

Yeah. So um, okay, so one of the most powerful things about your work is that it is it gives people a different way to think about cancer.

SPEAKER_00 1:27:56

So how do you balance hope uh with responsibility?

SPEAKER_02 1:28:03

Great question. Um yeah, it's it's never about uh trying to say that my work can uh affect a a positive outcome. You know, there's there's no guarantee without anything at the moment. As I said at the beginning, uh we're at a stage where we're still at the theory stage. But for me, it's it gives hope because it offers additional potential diff additional conversations patients can have with their oncologist or their medical team that's looking at other particular options. Um and that's just it adds to the toolkit, you know. Um and that can only ever be a beneficial thing because what we're seeing in the literature is that um antifungal drugs are now being used and studied for their anti-cancer properties. So that might be because they're they're targeting the metabolism of the cell, you could argue, but you know, there's always that antifungal aspect that I'm highlighting. Um what we see, what the beauty between my theory and and the metabolic theory is that both that that both the metabolic drugs are antifungal and the antifungal drugs are metabolic. So we're we're both really pushing down the same path. Um and the nice thing about my work is that I'm saying that things are at the we're at the the um cancer theory level of understanding and scientific research at the moment. There's no one theory that is correct, but there is a difference between the accuracy of different theories, and you can measure the accuracy. So if you're a patient coming into this and you want to, okay, there's say there's five theories or six theories that warrant you um looking at them. And the reason why you should look at these theories is because each theory associated with each theory is a different treatment. Treatments are developed from cancer theory. Yeah. So if you're ignoring a particular theory, you're ignoring the treatments associated with it. If you're ignoring the metabolic theory, you're ignoring metabolic treatments. So if you're ignoring my theory, you're ignoring the treatments that uh are are uh focusing metabolically, but also antifungal as well, that seem to have some efficacy in certain situations. So I'm arguing, how do you differentiate that? All that information. Well, you can use the hallmarks of cancer, the ten hallmarks. There's now 14, and I think a couple of months ago, um Hannah Hannah's has said some, uh at least nine more, so it's getting quite convoluted, I think. But there's there's there's ten at the moment that are officially accepted, excuse me. And what every theory is trying to do is trying to explain them all. The more you can explain, the more accurate the theory is likely to be. So you want to look at, and I've documented this within my book and my work, and I assess the theories and how many, uh, how accurate they are. So you have, unfortunately, the the um smagumentation theory has can can explain around two, just two of the ten hallmarks, which indicates everything that we said. It's it's there's a difficulty in explaining those hallmarks. There's not, there's there's no pattern of DNA genes that can explain every single hallmark. It's random. And, you know, so that suggests that lower low of a uh hallmark count suggests that genetic mutations may be involved, but they're m they're probably not the main driving mechanism. So you don't want to be targeting, you don't want to be using just those treatments. And then you have the the tissue organization field theory, which is looking at all the inflamm within the tissue. You want to reduce your inflammation as much as you can because that's a precursor to cancer, it's a precursor to the fungal pathogens you invade in the cell. That can explain around five of those hallmarks. So that again suggests that there's a mechanism that is intrinsic to the disease. So we should be targeting inflammation. We all know that, and uh all all the patient, all the umcologists are aware of that anyway, so that's really uh not a given. But then you have the cancer stem cell theory, that's explains about five, too. Then you have the metabolic theory, that explains about seven. Uh Professor Seafee would argue all ten, but I've got contention with three, so that explains about seven. Then my theory, actually, the first, the first one to coherently or better explain all ten. Plus, the additional four that have been added, I can explain those two, along with a load of other features as well. So, from that perspective, as a patient coming in, you don't want to disregard the somatic mutation theory because there are genetic mutations will have an influence over um how your tumour um acts. But you want to consider the other theories, and really you want to consider the higher the accuracy in terms of explaining the hallmarks, those theories up front and consider in combination um treatments that are associated with them targeting those particular mechanisms because those theories suggest that they're targeting something really specific and significant to the tumour. So, why wouldn't you target those? So use cancer theory as a practical tool to guide uh treatment decisions. Um I'm I I would ask oncologists to do that. And um, obviously, patients always to converse with an oncologist or your medical professional.

SPEAKER_00 1:33:03

Yeah, yeah, absolutely.

SPEAKER_01 1:33:05

So so you if you could change one assumption in cancer research tomorrow, what would it be?

SPEAKER_00 1:33:11

That cancer is a genetic disease, period. There we go. Yeah.

SPEAKER_01 1:33:18

Okay, and then so in the next, let's say in the next decade of cancer research, what do you think needs to be focused on?

SPEAKER_02 1:33:26

I think we need to equally as much as we can focus on um the other theories. Uh those those five, at least I've just mentioned myself, mind cell suppression theory, metabolic theory, tissue organization field theory, um, cancer stem cell theory. And you know, we still still got to look at the genetics, so somatic mutation theory as well. It's just share the resources around because there's so much evidence in support of these other theories that we're we're we're potentially missing something big that can really help and make a big difference in the near future if we were to provide that uh those resources.

SPEAKER_01 1:34:04

Yeah, yeah. So um so for people who want to know and understand your work uh properly, what would be a good starting point for them?

SPEAKER_02 1:34:13

Okay, so I have uh a website called cellsuppression.com. That's where you can get most of my information from. I also have a Substack uh publication called the Cancer Vigilante. So I bring up um articles on there. My most recent article is about prostate cancer, explaining the abnormal metabolism um of prostate cancer, which is something that hasn't really been done before. So those two are a really good starting point. And there's many different podcasts I've linked to on my website. I have a free PDF, uh, which is a synopsis of my theory. It's a very short explanation in layman's terms of what my theory is all about. So by all means, go on there, download that, understand the basic principles, provide that to your oncologist, see what they think. Um, and then you know, the book's available there too.

SPEAKER_01 1:35:07

Excellent. Excellent. Yeah, and we're gonna put all that information into the into the show notes there as well. So um, you know, while you were talking, I was scribbling a few things down here, and I I want to kind of give a summary. Um, so uh I'll I'll see what you think of my summary here, all right? So the body is not random. Uh cancer behavior like chronic pain, fatigue, autoimmunity, or metabolic dysfunction, it may be a logical biological response to altered inputs and altered cellular conditions. Theory determines the treatment. And if the theory is incomplete, treatment strategy may be incomplete. The terrain matters. So tumors do not arise in isolation from immunity, metabolism, inflammation, oxygenation, microbial ecology. What else we do? Hormones, nervous system signaling, environmental exposures.

SPEAKER_02 1:36:10

Stress.

SPEAKER_01 1:36:10

Uh, and overall, patients need clarity and not fear.

SPEAKER_03 1:36:17

Yeah. Brilliant.

SPEAKER_00 1:36:19

Sum it up. Okay. Yeah.

SPEAKER_01 1:36:22

Good stuff. Well, Mark, listen, um, it's been a real pleasure to have you here. I think, I think um, we skim by uh so many things. Um there could probably be a two, three, four, or five, six parts. Um, but again, we really highly encourage the listeners to check out uh Mark's book. Um, it is really great. Um uh I I love reading, and your book is really good. It really captures, uh it really captures my thought and imagination and the possibilities that can arise from that. So definitely encourage people to check that out. And as always, uh please like, share, subscribe, especially to those that could benefit from this information. And uh and that will that will really help to get the word out there. Um so again, we'll put all Mark's info in the in the show notes. And uh we wish all the listeners a good day. And until the next time and the next uh uh podcast, have a great day. Take care. Thanks, Mark.

SPEAKER_02 1:37:20

Thank you. Take care, everybody. Thanks, Richard.

SPEAKER_01 1:37:25

Thank you for joining me on the Integrative Continuum. I hope today's conversation gave you new insights and practical tools for your own health journey. If you enjoyed this episode, please subscribe. Share it with someone who would benefit, and leave us a review. It helps us spread this message further. Until next time, I'm Dr. Richard Rocker. Stay curious, stay empowered, and keep moving forward on your path to integrative health.