The story we tell about natural compounds

There is a story that gets told about natural plant compounds and cancer, and it goes something like this. Scientists studying cancer cells in the laboratory noticed that compounds found in certain foods – turmeric, grapes, broccoli, green tea – appeared to interfere with the molecular pathways that cancer cells rely on. The compounds seemed to slow cancer cell growth, trigger cancer cell death, reduce inflammation. Researchers documented these effects, published their findings, and a body of evidence accumulated that gave the phrase “anti-cancer properties” a degree of scientific credibility it might not otherwise have had.

The implication of the story is that these are dietary compounds that happen, usefully, to have anti-cancer effects. They are framed as nature’s accidental gift – molecules that plants produce for their own reasons, which turn out to have a beneficial side effect in the human body. The selectivity for cancer cells, to the extent it is explained at all, is attributed to the fact that cancer cells depend more heavily on the pathways these compounds disrupt.

This story is not invented. The laboratory observations are genuine. But there is a different version of this story – one rooted in plant biology rather than cancer pharmacology – that reframes what these compounds actually are, where they come from, and what they were built to do. And that reframing turns out to have some significant implications for the selectivity question and ultimately the origin of cancer itself.

To provide a little context first. You might have heard that around 60% of cancer drugs on the market are derived from plant or natural compounds. Paclitaxel is a chemotherapy drug developed from the Pacific Yew tree, or Vincristine developed from the Madagascar periwinkle – a herbaceous plant, or Irinotecan developed from the Chinese happy tree. These are however very different because they are toxic generally. The selectivity with these compounds is not so much between cancer and healthy cells, but rather cells that divide quickly – so they indiscriminately target fast dividing healthy cells as well, which is why they can damage the gut and noticeably a patients hair might fall out. Most of these toxic compounds were identified as part of the initial drive to create chemotherapy drugs – these are not the compounds I’m referring to here. We’re interested in those natural compounds that target cancer specifically without having a negative effect on healthy cells, or a far less toxic effect. How do they know to target those cells?

What plants actually produce, and why

Here is a fact that tends to get lost when these compounds are discussed in a health context. Curcumin, quercetin, resveratrol – these are not nutrients. Plants do not produce them to nourish anything. They are not present throughout the plant in the way that vitamins or minerals are. In a healthy, unstressed plant, many of them are only present in very low levels.

They appear when the plant is under attack.

Plant biologists call them phytoalexins – from the Greek for “plant” and “defender.” They are compounds synthesised on demand in response to pathogenic threat, and a primary target is fungal infection. When a fungal pathogen breaches a plant’s outer defences, the surrounding cells detect the intrusion and begin producing these compounds as part of the immune response. The phytoalexins then act directly against the pathogen – disrupting its membrane, inhibiting its growth, preventing it from spreading further through the tissue.

Resveratrol, for example – the compound found in red grapes and wine that has attracted enormous interest in cancer and longevity research – is produced by grapevines specifically when they are infected by the fungus Botrytis cinerea. It is not a component of normal grape physiology. It is an emergency response. The same is true of quercetin in its role as a plant defender, and of many of the other compounds in this group. For example quercetin is concentrated heavily in the outer skins of red onions and apples to protect against external pests, while curcumin is concentrated strictly within the root structure of the turmeric plant to deter soil-dwelling pathogens.

This evolutionary origin matters enormously, because it means these compounds have been shaped by hundreds of millions of years of plant-pathogen co-evolution. They are not general-purpose antimicrobials that happen to be broadly toxic. They are refined, targeted weapons – designed to recognise and act against specific types of pathogen while leaving the plant’s own cells, and the commensal organisms it depends on, largely unharmed.

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The selectivity the story doesn’t explain

This brings us to something the conventional story about natural compounds struggles to account for. If these compounds are general pharmacological disruptors – if their anti-cancer effect works by blocking pathways – then consuming them regularly should disrupt similar pathways in the gut microbiome. Many of the fungi that live commensally in the human gut use versions of the same biological machinery that cancer-associated pathways involve.

But that is not what happens. People who consume curcumin, quercetin, and resveratrol regularly do not experience systematic disruption of their gut microbiome. The commensal fungi that form part of a healthy gut ecology are not significantly affected. The compounds appear to be selective in a way that simple pathway disruption cannot fully explain.

The phytoalexin framing offers a more coherent account. These compounds are not broadly antifungal. They are specifically targeted – refined by evolution to recognise the structural features of pathogenic fungi, features that commensal organisms do not present. The selectivity is not pharmacological. It is evolutionary. The compound does not simply disrupt any cell that uses a particular pathway. It recognises a specific type of threat and responds to it.

Which raises a question that this series is building toward. If these compounds are evolved to target pathogenic fungi specifically – what are they recognising when they appear to concentrate their activity in cancer cells?

The same evidence, read differently

The conventional story reads the laboratory data and concludes: these compounds affect cancer cells because cancer cells depend on the pathways the compounds disrupt. It is a pharmacological explanation that fits within the broader framework of cancer as a disease of genetic malfunction.

But there is another reading of the same data. One that starts not with cancer pharmacology but with what these compounds actually are and what they were built to do from an evolutionary perspective.

What if the reason plant compounds appear to concentrate their activity in cancer cells is not primarily about which pathways those cells happen to rely on – but about what those cells contain? What if the selectivity is the phytoalexin doing what it was always built to do: recognising and acting against a fungal pathogen – one that, under this reading, is present within the cancer cell itself?

This is the possibility that the Cell Suppression Theory raises, and it is one that draws on a growing body of evidence showing that fungi are not merely present in tumours as bystanders – they appear to be active participants in the biology of those tumours. Through this lens these pathogens actively hijack and manipulate particular pathways that increase their chances of surviving and thriving within any given cell. The implications of that, if correct, extend well beyond which supplements might be worth considering. They go to the heart of what cancer actually is.

What changes if this reading has merit

If plant compounds are acting as phytoalexins – targeting a fungal pathogen within cancer cells rather than disrupting cancer pathways directly – then several things that currently seem puzzling start to make more sense. The breadth of their apparent effect across many different cancer types and many different pathways. The consistency of their selectivity for cancer cells. The fact that they do not disrupt the commensal gut microbiome.

It also changes the questions worth taking into a conversation with a medical team. Not “which supplement targets which cancer pathway?” but something deeper: what role might the microbial environment within a tumour play in its behaviour, and what approaches address that environment directly?

These are questions that mainstream oncology is only beginning to take seriously. The research on the tumour associated microbiome – the community of bacteria and fungi that appear to live within tumours – is among the most rapidly developing areas of cancer science. The phytoalexin reframing of natural compounds sits at the intersection of that research and the much older, well-established science of plant-pathogen co-evolution.

Next week, we move from the general to the specific. One of the most striking pieces of evidence in this area involves a property that some of these compounds share – a very precise kind of selectivity that targets not just a pathogen, but a particular form of it. The shape-shifter problem. Some fungal pathogens exist in two distinct forms – one relatively harmless, one invasive and destructive. The evidence that natural compounds can distinguish between them is more specific than anything a general pathway-disruption theory can account for.

The short disclaimer:
The Cancer Vigilante offers a research-led perspective on cancer science, built from independent, ongoing investigation – not medical advice. Nothing here should replace guidance from your oncologist or medical team; always consult a qualified healthcare professional about your individual diagnosis and treatment options. See T&C’s for full disclaimer.

What are we missing when it comes to beneficial plant compounds?

If you have cancer, or you love someone who does, there is a good chance you have encountered them. Curcumin. Quercetin. Resveratrol. EGCG from green tea. CBD. Sulforaphane from broccoli. The list of natural plant compounds associated with cancer research is long, and growing. So is the confusion surrounding them.

The confusion is understandable. The studies are real – these compounds do appear to affect cancer cells in laboratory settings, often quite dramatically. And yet the mainstream medical establishment largely regards them as unproven, their mechanisms poorly understood, their clinical relevance uncertain. So which is it? Are they doing something meaningful, or not? And if they are – how?

That last question is the one this series is built around. Not whether these compounds have any effect – the evidence that they do is substantial enough to take seriously. But why. Specifically, why do they appear to affect cancer cells while leaving healthy cells largely unharmed? That selectivity is the puzzle. And the mainstream explanation for it, it turns out, has some significant gaps.

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The explanation most people accept

The conventional answer to this question runs roughly as follows. Cancer cells are abnormal. They have accumulated genetic mutations that force them to rely on certain biological pathways more heavily than healthy cells do – pathways involved in growth, survival, inflammation, and energy production. Because cancer cells are so dependent on these pathways, compounds that interfere with them are more damaging to cancer cells than to healthy cells. The selectivity is pharmacological: the compounds hit targets that cancer cells need more urgently.

This explanation is coherent, and it is not wrong exactly. There is evidence that these compounds do interact with the pathways in question – NF-κB, mTOR, STAT3, and others. Researchers have documented these interactions extensively. The explanation has become the dominant framing for why natural compounds might have anti-cancer relevance, and it has the significant advantage of fitting neatly within the broader genetic theory of cancer that mainstream oncology is built on.

So far, so reasonable. But here is where it starts to become complicated.

The question the explanation struggles to answer

If cancer cells are selectively vulnerable to these compounds because they depend on specific pathways, then those cells need to be reliably stuck in those pathways. The selectivity only works if the target is consistent.

But the evidence suggests cancer cells are not stuck. Research over the past two decades has demonstrated that cancer cells exhibit remarkable metabolic flexibility. They can switch between different energy sources – glycolysis, fatty acid oxidation, oxidative phosphorylation, substrate level phosphorylation (glutamine fermentation) – depending on what is available and what the environment demands. They appear to adapt. A cell that can shift its energy strategy when one pathway is blocked cannot be reliably killed by targeting that pathway.

And yet these compounds consistently show selective activity against cancer cells across diverse cancer types and metabolic states. The selectivity holds even when the specific pathways it supposedly targets are not the dominant ones in a given cell. That is a puzzle the conventional explanation does not comfortably resolve. If cancer cells can adapt in similar ways to healthy cells to utilise the same fuels, then one wouldn’t expect such selectivity.

There is also a second problem, quieter but equally awkward. These compounds – curcumin, quercetin, resveratrol and the others – appear to affect many supposedly independent cancer pathways simultaneously. The conventional explanation treats each interaction as a separate pharmacological effect. But hitting so many different targets at once, reliably, across so many different cancer types, is a very unusual property for any compound to have, and for so many to hit the same targets. It invites a question that is rarely asked: what if the pathways are not the primary target at all? What if there is a simpler explanation – a consistency that has not yet been considered?

To be clear, the adaptability of cancer cells – whether or not they can and do adapt – is a fierce area of debate. The likes of Professor Thomas Seyfried claim that cancer can only use glycolysis (glucose fermentation) and Substrate Level Phosphorylation (SLP – glutamine fermentation) as fuel pathways because the others are broken. While a large portion of the medical literature challenges that, including influential pioneers such as Jane McLelland, who mapped this out in a recent article.

To give everyone their due, Professor Seyfried’s argument is not without validity – he claims that all of the studies concluding that cancer cells are creating ATP energy via OXPHOS are wrong, because they were measuring oxygen consumption with ATP output, but in those experiments they failed to consider the glutamine fermentation pathway (SLP) that allows mitochondria to create ATP without using oxygen (OXPHOS). And I largely agree with Seyfried here – most of those studies didn’t assess the potential contribution of SLP to energy creation, they just assumed oxygen in, ATP out, meant that OXPHOS was working. But a failure to assess SLP in those studies doesn’t automatically confirm that those cells were using this glutamine fermentation pathway either – nor that OXPHOS wasn’t operational – we simply cannot confirm either way from the data provided - both could potentially be right.

A number of cancers that Jane and others have outlined, such as prostate cancer, are confirmed to be OXPHOS driven, at least initially. Moreover, a ketogenic diet aimed at restricting glucose has mixed results in patients, while statins that inhibit fat have shown a benefit, as have OXPHOS inhibitors – which suggests OXPHOS is operational and may be required for cancer to progress – I’m referring to the study of oncocytomas in case you’re interested in that line of enquiry.

Forgive me I digress, while this level of detail is a subject for a different series – I wanted to highlight that the science isn’t settled, I think it’s important for us to remain open-minded when we come into contact with others who claim to know either way. Regardless of the pathways natural compounds are thought to affect, they have shown to be beneficial, and working out why that may be is just as important because it offers beneficial insight, not only to support the use of these compounds, but for the purpose of identifying the origin of the disease once and for all.

A different starting point

So what if the selectivity is not pharmacological – not about which pathways cancer cells happen to depend on – but something else entirely?

What if these compounds are selective because of what they were originally built to do, long before anyone thought to study them in a cancer context? Plant compounds like curcumin, quercetin, and resveratrol are not nutrients in the conventional sense. They are not produced by plants to nourish anything. They are produced in response to a threat – specifically, to attack from a micro-organism likely to cause harm or disease (pathogen). They are part of the plant’s defence system.

And one of the primary threats that plants have been defending against, across hundreds of millions of years of evolution, are these pathogens.

This is not a fringe observation. It is well established in plant biology. These compounds belong to a class called phytoalexins – antimicrobial agents synthesised on demand when a plant detects a pathogen. They are absent in healthy, unstressed plant tissue. They appear when the plant is under attack. And here’s the clever part, they are refined by evolutionary pressure to target the specific pathogens that threaten the plant – not the commensal organisms it coexists with. It turns out that pathogens that actively invade cells often take a different form and have distinctive identifiable features that can be exploited selectively.

That evolutionary origin raises an interesting question for cancer research. If these compounds are, at their core, anti-microbial agents – what exactly are they doing when they appear to affect cancer cells?

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Why this might matter

This series is going to explore a specific reinterpretation of the evidence. It is one that has not yet made it into mainstream oncology, but it draws on published, peer-reviewed science – across plant biology, microbial pathology, immunology, and cancer research – and it resolves some of the explanatory gaps that the conventional position leaves open.

The reinterpretation does not require dismissing what is already known about these compounds. The pathway interactions are real. The laboratory evidence is genuine. The question is whether those interactions are the primary mechanism – or whether they are downstream of something else. Something that would explain the selectivity, the breadth of effect, and the curious fact that compounds designed by evolution to fight pathogens appear to concentrate their activity in cancer cells.

If the reinterpretation has merit, it changes the questions worth asking. Not just in the laboratory – but in the conversations patients have with their medical teams about the full landscape of approaches worth exploring. That is why it deserves a serious examination rather than a dismissal.

We are going to give it one.

The short disclaimer:
The Cancer Vigilante offers a research-led perspective on cancer science, built from independent, ongoing investigation – not medical advice. Nothing here should replace guidance from your oncologist or medical team; always consult a qualified healthcare professional about your individual diagnosis and treatment options. See T&C’s for full disclaimer.

Welcome to The Cancer Vigilante. What follows isn’t a pitch – it’s a declaration: patients deserve a clearer understanding of cancer than the one we’ve settled for, and a genuine say in what gets investigated next, not a seat on the sidelines waiting for someone else to decide. This is what this publication stands for – honest, rigorous inquiry, followed wherever it leads, with patients invited to help shape its direction. This isn’t just a manifesto. It’s a movement staking its claim, and an invitation to stand here with me.

Background

Before discussing the elephant in the room, and for those who aren’t aware of my story, you may be wondering why a graphic designer is talking with so much confidence about cancer and is able to offer such valuable insight. In short – this wasn’t a direction of enquiry I had planned. At the age of 28 I developed cancer, my friend at the age of 30. In a bid to understand more, to help myself and support my friend, I delved into cancer research, interested to know the driving mechanism to both improve survival and prevent recurrence. My friend sadly passed away within a year of conventional treatment just as my research started to make in-roads. During that time my eyes were opened not just to the severe flaws in the current system, but of the abundant and beneficial information that most of us are rarely made aware of.

The loss of my friend drove me forward, and in some sense it provided therapy, a way of dealing with her loss. During my research I experienced everything most people with cancer do when attempting to gain clarity – overwhelm, confusion, contradictory information, misinformation (misplaced assertions) and even disinformation (intention to mislead). A sense of helplessness driven by an industry that on the one hand claims to know what cancer is, but hasn’t been able to develop a cure, and on the other hand a realisation that the established view of cancer that drives standard of care may indeed be incorrect – a chilling possibility that has far-reaching consequences if true.

Awareness of other cancer theories came as a revelation. This insight propelled my inquisitive mind forward intrigued to know more. Now acutely aware that the origin of cancer was still up for debate, my creative problem-solving instincts took hold. It became my mission (some would say obsession) to ensure Sam did not die in vain – to make sense of her loss. Eight years of independent research (now more than 11) led me to identify correlations that established theories had missed, correlations that point to a completely different mechanism behind cancer and an overlooked cause that most dismiss at their peril.

Eight years of meticulous research, self-education, and a desire to make sense of what’s missing, I single-handedly developed a new theory of cancer – The Cell Suppression Theory – the first to coherently explain all 10 of cancer’s recognised hallmarks. After debating the merit of my theory with a panel of 10 cancer experts in front of a live audience of 200 medical professionals, they collectively provided a confidence score of 7.9/10 – a remarkable response from a theory generated by someone outside the medical field, even if I do say so myself. I subsequently published the theory in the now multi-award-winning book The Cancer Resolution? – specifically targeted at empowering people with cancer by translating the science behind what cancer is thought to be in to patient friendly terms. It is through this new lens that I now provide you with new insight that illustrates the key features of cancer we have potentially been missing – features that offer additional clarity on what cancer may be and how we may better deal with it.

The Cancer Vigilante publication is the ongoing investigation of cancer through this Cell Suppression lens, my ongoing thinking since the book was published and as my research and insight has deepened. Join the journey, share your insight and let me know what you think. Together I believe we can make a genuine difference. Now for the all important missing detail.

The elephant in the room

There’s an uncomfortable truth that everyone involved in cancer – from patients to clinicians – needs to hear, because not acknowledging it will likely affect a patient’s survival prospects.

While medical professionals on the whole have your best interests at heart, they’re working within a dysfunctional medical system – one that struggles to supply you with the full picture, and rarely tells you so. Patients often only discover this gap through experience, by which point it may have already cost them time they didn’t have. As a consequence, there’s a risk you’re not being made aware of the full spectrum of options available to you.

This should clarify my point: Conventional treatment for cancer is informed by the Somatic Mutation Theory (SMT) – the notion that cancer is a genetic disease caused by DNA mutations. The theory informs which treatments are created and used. Conventional treatments are therefore designed to target those mutations. This is currently the dominant view because a conventional medical education asserts that cancer is a genetic disease.

But here’s the deeper problem: not only does the SMT remain unproven, but as a direct result of that, there exist at least seven competing theories – and most importantly all propose a different mechanism is responsible for driving the disease. What does that mean?

If you are being advised on the options available to you through the lens of only one theory – namely the SMT – then loosely speaking, you are only being made aware of 14% of the information and options currently available to you. That is, 86% of the information surrounding what cancer might be, and the additional options this surfaces, are not being considered and presented to you. Does that sound like a good comprehensive strategy for combatting a disease we still don’t fully understand?

To compound the issue, sufficient evidence exists to suggest that the SMT on which Standard of Care treatments are based, might be incorrect or at least of minimal influence – cancer may not even be a predominantly genetic disease – yet here we are placing all of our eggs in that one basket, as if it is. Surely amidst so much uncertainty, both patient and clinician should be weighing up all of the information to utilise a more comprehensive treatment toolkit that naturally arises from a more complete understanding. To give you the lay of the land:

• The Somatic Mutation Theory (SMT): Cancer is thought to be a genetic disease. Mutations should be targeted.

• The Mitochondrial Metabolic Theory (MMT): Cancer is thought to be a metabolic disease. Metabolism should be targeted.

• The Tissue Organisation Field Theory (TOFT): Cancer is thought to be a disease of disrupted tissue signalling. Healing the chronically inflamed tissue should re-establish signalling and reverse wayward tumour growth.

• The Cancer Stem Cell Theory (CSCT): Cancer is thought to arise in corrupted stem cells, not somatic cells. Cancer stem cells should therefore be targeted.

• The Atavistic Theory: Cancer arises in cells that revert to an old evolutionary survival programme that’s triggered by excess damage. Inhibit the pathways and genes the cancer uses, force it to reverse its evolutionary programming.

• The Aneuploid Theory: Cancer is thought to be driven by an abnormal number of chromosomes. Target specific genetic and chromosome abnormalities to exploit the instability of the cell.

• The Cell Suppression Theory (CST): Cancer’s metabolic shift and proliferative state arises in response to intracellular infection, primarily caused by fungi. Under this theory, the pathogen, its mycotoxins and its biofilm would be the relevant targets, with restoring tissue health and microbiome balance the goal.

And you could add another five theories or hypotheses into the mix if you have the time to delve in to that rabbit hole: The Viral Theory, The Trophoblast Theory, The Toxin Sequestration Theory, The Parasite Theory, and Dr Jack Kruse’s biophysics light theory of cancer.

To illustrate the oversight of focusing on one theory, and to close the point: under the SMT, chemotherapy is offered as standard treatment on the rationale that it targets the DNA of fast-dividing cells – which is what cancer is understood to be. But there’s more nuance to the disease than any one theory can account for alone. The Cancer Stem Cell Theory proposes that around 2% of a tumour is made up of cancer stem cells – and because these cells aren’t fast-dividing, they often don’t absorb enough chemotherapy to be eliminated by it. Since stem cells have unlimited growth potential, any that remain could, in principle, regenerate the entire tumour – a pattern that is too often seen in patients and is referred to as chemotherapy resistance. That’s not a minor detail. Yet it’s rarely considered, simply because one theory has been favoured above the rest. Details like this – the ones that fall through the cracks between theories – are exactly what get missed when only one lens is used. It’s the starting point for what I set out to do with the Cell Suppression Theory (CST).

I just want to be clear: this is not to say you should avoid chemotherapy altogether. On the contrary, it can be beneficial under certain circumstances, even at lower doses – see the work of Dr Robert Gatenby for a deeper understanding. As ever, the recommendation is to always consult a medical professional with any concerns you may have.

The coherence gap nobody’s addressed – until now

The Cancer Vigilante is where I share my insight through the lens of the CST – a framework for explaining cancer that I’ve spent more than a decade building. This isn’t guesswork. It’s over a decade of research, already tested in front of international cancer experts, with the work continuing in collaboration with scientists and clinicians right now.

But this is where the CST and this publication offer something distinct from any person attempting to help you make sense of cancer. It exists because over a decade ago I set out to make sense of cancer in its entirety – objectively analysing every one of those theories, and then asking what they were all missing. The CST isn’t just another entry on that list above, offering nothing more than the same 14% slice of the picture. The Cell Suppression Theory is a meta-theory that not only proposes how all other theories of cancer fit together, but also offers a paradigm shift in what cancer actually is: not a malfunction-based disease, as all other established theories propose, but a suppression-based one. And this distinction makes all the difference.

Under the malfunction paradigm that underpins the first six theories listed above, the proposal is that cancer cells are cells that have gained autonomy. They are something foreign, an enemy to be inhibited, starved and attacked, often with toxic substances.

The suppression-based paradigm I’m proposing through the CST suggests the opposite – that we should treat the body holistically and encourage the healing process, because cancer cells are our own cells, and they’re attempting to help us – they are not the enemy we’ve demonised them as being.

The problem is that their supporting functions have been hijacked and their defensive capabilities suppressed by an external parasitic threat that has invaded the tissue and the cell – namely bacterial and fungal pathogens. While small in number, I propose that the fungal pathogens are the generals that largely orchestrate and control the process – aided by bacteria, viruses and parasites. These fungal pathogens are, as the medical literature puts it, ‘immunologically potent’ – you only need a small number to elicit a significant response to their presence.

That response is the proliferative state we see occurring and have termed ‘cancer’ – the runaway growth of the tissue. The CST suggests that the metabolic shift described by the Metabolic Theory is the defensive response to the infection – a key interaction that has been overlooked and misinterpreted. The proliferation of cells is the secondary feature of this defensive response, which the CST interprets as the body’s attempt to contain the infection and limit the spread of its toxic byproducts. The runaway proliferation (tumour growth) and subsequent hallmarks of the disease that are generated, are the pathological consequence of the tissue’s and immune system’s failing attempts to eliminate the pathogens present at the core of the tumour.

Through the lens of the CST, the TOFT explains the inflammatory conditions required for these pathogens to take hold and lock that proliferative pathological state in place.

The CSCT would explain the unlimited growth potential of a tumour, metastasis and the chemotherapy resistance angle through the corruption of stem cells by these pathogens.

The random genetic instability that the SMT and the Aneuploid Theory point to as driving the disease is explained as a symptom of the chronically inflamed tissue, largely generated by the toxins and Reactive Oxygen Species (ROS) produced by both the pathogens and cells themselves during this extended battle for supremacy.

The Atavistic Theory, meanwhile, describes this entire process through the genetic and metabolic pathway changes we see occurring. Through the CST lens, this perceived Atavism – the notion that a cancer cell is reverting to using old evolutionary pathways – isn’t the cell trying to return to its microbial roots from over a billion years ago. Rather, these pathways and genes are upregulated as part of the machinery used to defend the cell against these pathogens: ancient pathways that evolved a billion years ago to combat the pathogens present at the time, and that have been conserved ever since to fight those same pathogens as they continue to evolve alongside us. It’s the same defence mechanism from long ago, doing exactly what it evolved to do, the problem being that it’s extended use becomes pathological - all because the pathogens remain.

What I believe

Interpretation over open questions. Whether you’re a patient, a caregiver, or a clinician, here’s the situation, plainly. There’s more cancer research out there than anyone could read in a lifetime. And it’s entirely possible to make sense of that information as it currently stands – careful communicators can take each existing theory, distil it, and explain it clearly. That’s a real skill, and it’s genuinely useful.

But here’s what that clarity can’t do. It can only make sense of what’s already known. And what’s already known has pieces missing.

So the sense-making you’ll find elsewhere is sense-making of an incomplete picture. However well it’s explained, it’s still incomplete underneath. That’s not a criticism of the people doing the explaining – it’s simply the limit of working only with what already exists.

What’s actually missing is something different: a new interpretation of cancer – one that identifies missing pieces themselves, not just organises the pieces we already have. That takes original thinking. Thinking that can join dots nobody else has joined, and bring back pieces that render a more coherent picture.

That’s what I’ve spent more than a decade doing. Not collecting more information, and not simply re-explaining what’s already known more clearly – but thinking the problem through from first principles, until new pieces started to emerge. Those pieces became the Cell Suppression Theory.

And here’s the part that matters most: that thinking hasn’t stopped.

The theory as it appears in my book is a snapshot – a picture of where my thinking had reached at the time I wrote it. Since then, my understanding has kept moving forward. The same original thinking that found the first missing pieces is still at work today, still testing the evidence, still building a clearer picture of what cancer actually is.

So when you read this publication, you’re not just getting a clear explanation of what’s already known. You’re getting the missing pieces themselves that fill in the gaps, articulated by the originator of that new perspective – and the ongoing thinking that keeps finding more missing pieces that generates fresh insight.

An investigation, not a verdict

The CST isn’t a finished theory sitting still on a shelf – it’s an active investigation, being tested and refined in real time, in collaboration with the scientists and clinicians willing to look closely. I’m sharing that work as it happens, not just the tidy conclusions at the end of it. Which means the story isn’t over. There’s more coming, and I’d like you to be part of watching it unfold – maybe even part of shaping where it goes next.

Right now, that means two things moving at once. A second, expanded edition of my book is in the pipeline, built on research that’s developed since the first was published. And a growing group of scientists and clinicians are coming together as the CST Science Consortium, testing the theory more rigorously than one person working alone ever could. This publication is the middle layer – presenting new insight and stress-testing old interpretations in the interim, before the second edition and the wider testing of the theory are complete – both of which are going to take time. So I invite you to come along for the ride, and influence where it goes.

The ultimate goal – to improve survival outcomes

I wrote the Cell Suppression Theory in the hope that it might one day help improve survival outcomes for people with cancer, nudging Standard of Care in to a more complementary arena that encompasses more than just one interpretation of the disease. A desire to reduce suffering and improve the lives of others is why I’ve continued to work tirelessly to advance the theory and gain scientific recognition for the three years since I published it in The Cancer Resolution? back in May 2023. Since then it’s been a roller-coaster ride – I often feel like I’m living a movie. I’ve been to America three times, then Colombia and invited to Algeria and Hungary to speak. The book has been translated into French and published. It features as part of a Mycology Masters degree course at Exeter University, while professional endorsements have been coming thick and fast. Dr Peter Rogers, a Stanford and Harvard trained medical doctor recently reviewed my book on his YouTube channel, stating:

So far I’ve spoken at three cancer conferences in the last five months – the last one in London and to a medical professional only audience. I’ve also been in touch with some of the leading scientists and clinicians of our time who have praised my work and offered guidance, such as Professor Angus Dalgleish, Professor Neil Gow, Professor Michael Lisanti, Professor Brigitte Konig, Dr Robert Naviaux and Dr Ravid Straussman to name a few.

But while the book and theory offers hope for so many by already providing crucial insight in to an overlooked factor influencing the disease, that’s not the end of this story. And neither should it be. While I’ve made great strides in medical circles without a credible challenge to the theory in three years, change that can benefit cancer patients directly, and recognition of my work outside of these medical circles, isn’t happening anywhere near as fast as I’d have hoped. Admittedly I’ve focused more on gaining acceptance within the medical profession and stress-testing the theory through them to ensure it is robust, than on pushing the theory into the public domain.

I naively thought that if I put this work in front of scientists and institutions, they would run with it and it would take on a life of its own. That hasn’t happened, that’s not to say nothing has come of this, myself and Robin Daly MBE from the cancer charity Yes to Life, have formed a consortium consisting of independent scientists, clinicians and a biotech company called Ultra Botanica – all of whom are volunteering their time and skills to establish a non-intervention observational pilot study to test the validity of my theory. If you are a Founders Circle member you will receive behind the scenes quarterly updates on the progress being made.

My experience so far has taught me something I already knew and mention in my book, most professionals are busy doing whatever it is they currently do and either don’t have the interest or capacity to take on board a different perspective, especially one from a citizen scientist – not to mention there are strict guidelines for them to follow which means they might not be able to adopt this information even if they wanted to.

These last few years have reinforced the notion that beneficial change will primarily come from the grass-roots up, from you the public, people with cancer who are living the disease every day, and are crying out for guidance and new insight. It is the informed patient who’ll usher in the change – by asking sharper questions, bringing new options into the conversation, and advocating for a more integrative approach alongside their medical team, not around them. My work aims to help make that possible.

It’s going to take time but with your help we can reach the following lofty goals:

1. Publish the Cell Suppression Theory in a credible medical journal and have it peer-reviewed. While I received a 7.9/10 confidence score for my theory during the Cancer Through Another Lens event that saw me present it to, and debate, a panel of 10 cancer experts, that confidence score does not represent a full peer-review.

2. Test the theory in pre-clinical and clinical trials to both determine its validity and identify potential solutions based on the new targets identified by the theory.

3. Disseminate the theory within medical circles to provide clinicians with additional insight that can better inform treatment decisions for patients.

4. Disseminate the theory to patients in a patient-friendly manner translating cancer, and the wider cancer landscape, into plain, accessible language at a moment when a diagnosis can already feel overwhelming. Understanding that landscape gives you the foundation to better advocate for yourself, ask sharper questions that allow you to explore the additional options it may surface – options worth discussing with your medical team, options that offer renewed hope that a different path may be possible.

I’ve pursued Stage 3 to great success in terms of acceptance and recognition of my work. But in terms of helping move the needle on cancer survival, not so much, simply because so few people are aware of my work. Don’t get me wrong, I’ve had many a cancer patient express their gratitude at how my book has helped them in their journey. But these cases need to be document, and as of yet they are few and far between simply because so few are aware my work exists.

Stage 2 – testing the theory – is already well underway. Our consortium of scientists and clinicians meet every month, actively volunteering their time to action the first pilot study, something genuinely useful that has arisen from my previous commitment to Stage 3.

Stage 1 – publishing my work in a medical journal – is not yet underway. As I’m sure you’ll agree, making significant progress in any field requires money and time, and I’m a little short of both. There’s only so much a one-man-band can get done at this stage. I’ve focused for too long on gaining acceptance in medical circles, to the detriment of bringing awareness to the people who need it most – people living with cancer. This is why I’m now dedicating significant time to building something powerful here on Substack. This platform lets me offer you new insight and meaningful value you won’t find anywhere else as and when I develop it. In return for your support – just the cost of one coffee a month – I’ll be able to spend less time at the graphic design day job and more time doing the research, creating the resources, writing and doing the relationship-building with key influencers who can help disseminate the work more widely. That’s the trade I’m hoping you’ll help me make.

Because here’s the truth of it: every hour spent on me doing freelance design work, is an hour not spent moving Stage 1 forward, feeding the consortium’s evidence base, creating resources to benefit patients, or making the case to the next clinician who might join this movement. Your subscription doesn’t just support this publication. It buys back that time and moves the theory closer to a place where it can benefit more people sooner rather than later.

If you’ve read this far, it’s probably already starting to make sense why that matters: a genuinely different lens on a disease that hasn’t yielded to the old ones, however hard we’ve tried, needs time to be tested properly. Whether you become a paid subscriber, or step further in as one of the Founders Circle members watching the pilot study and consortium work unfold from the inside, you’re helping fund exactly that – the time and independence this research needs to keep joining up the missing pieces.

I won’t pretend a coffee a month solves everything on that list above. Peer review, clinical trials, a consortium of volunteers doing this alongside their own day jobs – none of that happens quickly, whatever the funding. But it moves the work from something I do around the edges of a working week, to something that can become the working week itself. That’s the difference your support makes. And with enough money I can build a team to move this forward at pace.

So thank you for reading this far, and for considering standing here with me. Every subscriber, free or paid, is part of what this publication is building. If you’re able to become a paid supporter, you’ll be helping turn Stage 1 and Stage 2 from a list of intentions into a body of finished, tested, peer-reviewed work – the lever that opens doors and helps to make real change happen. And if you’re not able to right now, sharing this with someone who might find it useful does something just as real.

This is a movement, not a mailing list. I’m glad you’re here for it.

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The short disclaimer:

The Cancer Vigilante offers a research-led perspective on cancer science, built from independent, ongoing investigation – not medical advice. Nothing here should replace guidance from your oncologist or medical team; always consult a qualified healthcare professional about your individual diagnosis and treatment options. See T&C’s for full disclaimer.

Prostate cancer is an enigma, it doesn’t appear to follow the normal pattern of cancer. No established framework has been able to explain it’s seemingly odd characteristics. On the one hand, this is unsettling because it raises uncomfortable questions about how complete our current understanding really is – indicating that established frameworks maybe wrong, which in turn may feel like a resolution to the disease is slipping further from our grasp. On the other hand, such outliers offer great potential for resolution, because if they can be understood, they may open up invaluable insight that could expose a different origin story – one that could lead us to better survival outcomes.

This is why I love science – the barriers seemingly put before us can be seen as such, and ignored – and often they are when they don’t fit the prescribed narrative. But they can also be seen as stepping stones capable of leading us to greater insight if we so choose. It is with the latter inquisitive mindset that I move forward, and hope that you will join me so that we may uncover something of value. So, where should we start?

Prostate cells are metabolically different from the outset

Beginning from first principles, and before we even start looking at prostate cancer, what do we know about healthy prostate cells? Is there anything different that sets them apart from regular cells that may help shed light on their cancerous behaviour?

Yes. A key feature often overlooked in discussions of prostate cancer is that normal prostate epithelial cells are metabolically unique, even before any disease process begins.

N.B – epithelial cells represent a certain type of cell within the body. They primarily encase organs and act as the first protective barrier against infection and first contact with the world around us. Skin, the lining of the gut, and the lining of most organs such as the lining of the lungs, are made up of epithelial cells. Incidentally, up to 85% of all cancers are of epithelial cell origin.

Unlike most epithelial cells, healthy prostate epithelial cells intentionally truncate the tricarboxylic acid (TCA) cycle at citrate. Rather than oxidising citrate for energy, these cells accumulate and secrete it as part of normal prostate function. This is a pivotal difference that sets prostate cells apart from all other epithelial cells.

The TCA cycle within mitochondria enables the conversion of macronutrients such as glucose, fat and protein, into different substrates that our body’s need for everyday function. The conversion of substrates within this cycle also drives energy creation through the Electron Transport Chain – an energy pathway known as OXPHOS that also exists within mitochondria. In simple terms, when the TCA cycle is operational the OXPHOS pathway can and does create ATP energy. This is the primary energy pathway of most cells.

But prostate cells do not use the full TCA cycle, highlighted in the graphic below.

Instead, the cycle is blocked (truncated) at citrate. Rather than citrate being converted into Isocitrate - the next step in the cycle, and so on and so forth, it is expelled out of the cell. This is normal for a prostate cell because citrate is used to create the seminal fluid for reproduction. This means that the OXPHOS pathway, which includes the Electron Transport Chain (ETC) that generates energy within mitochondria, isn’t operational. This is because the electrons required to run the ETC are only transferred to it further along in the TCA Cycle after Citrate – as prostate cells stop the TCA cycle at Citrate to expel it, electrons are not transferred to the ETC to allow the OXPHOS pathway to generate energy. As a backup option, glucose is fermented in the cytosol (the gel-like cell area that mitochondria swim within) to lactic acid, in order to create energy. This supports the energy requirement of prostate cells allowing them to create citrate and export it, a process that wouldn’t happen if OXPHOS was the primary energy state. Of note, this is the Warburg effect we see described in cancer (a cell relying on the backup energy state of glycolysis even in the presence of oxygen), and yet it forms the base metabolic state of a healthy prostate cell. This suggests that a reliance on, or a preference for, glycolysis doesn’t necessarily result in cancer - something other than an energy shift may be needed for malignancy to occur.

Not shown in this graphic, is the use of fat. Fat is converted in the TCA cycle of prostate cells to produce citrate, so the fat oxidation pathway is prominent and active. Fatty Acid Oxidation can also be used to generate ATP energy and serves as another backup energy pathway - but in this instance, fat is being used to create citrate.

Zinc is the key

Crucial to this conundrum is zinc. It is the abnormally high levels of zinc imported into prostate cells that inhibits the Aconitase enzyme that would otherwise convert citrate into Isocitrate – the next step in the TCA cycle. High zinc levels ensure that citrate is exported rather than converted. Zinc specifically truncates the TCA cycle so that it doesn’t progress, as highlighted in the graphic above.

What changes in prostate cancer – and why it is so puzzling?

In early stage prostate cancer, several well-documented metabolic changes occur:

Read more

This week I’ve opted to provide an explanation for prostate cancer. Why? Because prostate cancer is an anomaly. It is one of the most difficult cancers to explain – and at present its profile doesn’t fit neatly into any established paradigm. The benefit of wrestling with such an anomaly is that it separates the wheat from the chaff. It highlights which theories of cancer are more likely to be correct, and that matters, because it is from cancer theory that treatments are developed. A theory capable of explaining an anomaly as stubborn as prostate cancer is far more likely to be pointing toward cancer’s true origin – which means the treatments associated with that theory are likely to be more effective due to the greater probability of targeting a pivotal mechanism.

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If you’ve been following my work for a while, or have read my book The Cancer Resolution?, you’ll be aware of the shortcomings of the established theory of cancer – the notion that genetic mutations drive the disease. For those yet to pick up a copy, there are at least seven credible theories of cancer currently on the table. So many exist because the dominant interpretation of what cancer is, has struggled to provide a coherent explanation for carcinogenesis and generate an effective treatment.

That dominant interpretation – the Somatic Mutation Theory – struggles to explain more than two of the ten hallmarks of cancer that any viable theory is expected to account for. These 10 shared hallmarks are the metric by which a theory’s validity and accuracy are judged. The more of these fundamental cancer traits a theory can explain, the more robust that theory is considered to be.

To put this simply: imagine two scientists proposing two different mechanisms for what causes cancer. If the mechanism behind hypothesis A cannot explain most of the hallmarks, then it is unlikely to be responsible for the disease. Conversely, if hypothesis B can account for all 10, then it is likely that the mechanism proposed in B is either responsible, or at the very least central to disease development.

This matters because once the correct mechanism is identified, effective treatment becomes possible. Targeting mechanism A – when A is wrong – will lead to weak or inconsistent treatment outcomes, because you’re effectively targeting a red herring. You could argue this is precisely where we currently stand with mainstream cancer treatment and its fixation on DNA mutations, because the dominant theory also struggles to explain more than two of these hallmarks, a point I document extensively in my book.

On the other hand, targeting the mechanism outlined in hypothesis B would likely produce far better outcomes, because you’re addressing a mechanism closer to the root cause. This is why understanding the validity of each cancer theory is so important for patients and clinicians to understand – their accuracy varies greatly, and so too does the efficacy of the treatments developed from them. In essence, cancer theory can be used as a practical tool to help one determine which therapeutic approach is likely to be the most effective.

It is therefore essential to recognise and understand the implications of the current zeitgeist. While DNA mutations are still said to “drive” cancer, the origin of the disease is very much unresolved. Scientists do not actually know what initiates or sustains tumour growth because no established theory has ever been proven. This is why so many alternative theories exist, why we still have no cure, and why the scientific community continues to debate cancer’s origin – we are still searching for the answers.

When the literature is examined objectively, we find it contains a wealth of conflicting evidence that challenges the genetic model. More importantly, much of this same evidence strongly suggests that intracellular fungal pathogens are at the heart of tumour development. This is why the Cell Suppression Theory – which proposes that intracellular fungal infection is the origin of cancer – is so significant. It is the first theory capable of comprehensively explaining all 10 hallmarks, strongly suggesting the mechanism it proposes is correct. And crucially, it provides the first coherent, biologically plausible explanation for prostate cancer.

Before we explore that explanation, a little more context is helpful. In the absence of the genetic theory’s ability to explain the hallmarks, the Metabolic Theory has stepped into the void. With DNA mutations increasingly out of favour in progressive circles of oncology, proponents of the Metabolic Theory – such as Professor Thomas Seyfried – argue that cancer arises from defective mitochondria, the bacteria-like organelles that act as the cell’s energy factories.

According to this view, a defect in mitochondrial energy production forces the cell to switch to the Warburg effect – characterised by the unusual reliance of cancer cells on glycolysis, which is the backup energy system that ferments glucose without using oxygen. Most healthy cells generate energy through OXPHOS, where oxygen and glucose are converted into ATP – this happens within mitochondria. But cancer cells revert to glycolysis even when oxygen is available. This is unusual because glycolysis is inefficient and inflammatory, and mitochondria are the preferred energy pathway when oxygen is present.

This reliance on glycolysis even in the presence of oxygen suggests that mitochondria are dysfunctional. Because Otto Warburg first observed this metabolic switch in the 1920s, the phenomenon became known as the Warburg effect. From this perspective, defective OXPHOS > Warburg effect > cancer.

As the Warburg effect is a core feature of cancer, proponents of the Metabolic Theory claim that it can explain all 10 hallmarks. And while most cancers do exhibit the Warburg effect – there is a major problem: prostate cancer the most prevalent cancer in men by a large margin, is not driven by the Warburg effect. At least not initially. Only in late-stage disease does the Warburg shift appear. This is the elephant in the room.

In early prostate cancer, OXPHOS appears to function normally. This is why early prostate cancer cannot be reliably detected by PET scans, which measure glucose uptake. Cancer cells typically absorb at least 18 times more glucose than healthy cells because glycolysis is glucose-intensive. But if prostate cancer cells are not reliant on glucose to the same degree as most cancers – because they aren’t driven by the Warburg effect – the tumour won’t “light up” on a PET scan.

This has obvious implications for patients considering metabolic therapies such as a ketogenic diet. If early-stage prostate cancer isn’t driven by glucose in the same way, then restricting glucose will have little to no effect in the early stages of the disease.

So we must ask: How could the Warburg effect – defective OXPHOS – be the origin of cancer if it doesn’t occur in the most common cancer found in men? Much like the issue facing the Somatic Mutation Theory (some cancers develop without the alleged DNA mutations claimed to drive the disease), prostate cancer exposes a gap in the Metabolic Theory. If neither DNA mutations nor the Warburg effect are responsible, what is?

It could be that prostate cancer is an outlier, that is simply driven by something completely different. But the moment we allow that possibility, we also allow the possibility that this same mechanism could be driving all other cancers too – opening the door to a completely new understanding of what cancer is and how to treat it. Conveniently, the Cell Suppression Theory provides a comprehensive explanation for all other cancers using a single mechanism: the same mechanism that I will shortly use to explain the nuance associated with prostate cancer.

Now, those familiar with my work might point out a potential contradiction as it leans heavily on the involvement of the Warburg effect. Under the Cell Suppression Theory (CST), infection triggers the Warburg shift seen in cancer because this metabolic transition forms part of the cell’s defensive response to infection. When a fungal pathogen is detected, the cell shifts to the Warburg effect to create a hostile environment for the invader, freeing up mitochondria to use oxygen to combat the pathogen, instead of using that oxygen to produce energy.

If some sort of infection is responsible for prostate cancer, surely we would expect to see the Warburg effect initiated too – but it isn’t. So, does this undermine the CST?

No. In fact it reinforces it.

Varying tissues can respond to infection differently – in the case of prostate cells this is due to the unique baseline metabolism that differs from other epithelial cells. Once this nuance is understood, the unusual behaviour of prostate cancer makes complete sense. The “anomaly” dissolves and the potential origin of cancer is revealed. The devil, as always, is in the detail – and that detail points consistently toward an infection-driven origin.

To explore that detail, join me for part two – coming soon…

If this work resonates with you, and if you would like to be part of a community that is helping redefine how we understand and treat cancer, I’d love to welcome you as a paid subscriber. Your support doesn’t just keep this research going — it helps ensure my unique insight and progressive interpretation of health and cancer remain available, accessible, and continually evolving for all to benefit.

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Additionally, there are some more resources for you to investigate below including my award-winning book.

FREE THEORY SYNOPSIS DOWNLOAD:
A simple summary of the Cell Suppression Theory and how it can benefit you, provided for free as a PDF download – feel free to share this with your oncologist.

MULTI-AWARD-WINNING BOOK – ‘The Cancer Resolution?’:
An evidence-based survival guide for cancer patients and their oncologists

WEBSITE:
Official home of the Cell Suppression Theory – browse resources, podcasts and learn more about why and how I developed this revolutionary view of the disease

PODCASTS:
Check out some of my leading podcasts to gain instant insight into key concepts of my theory and book, and how both are challenging conventional thinking and redefining how we treat the disease.

DISCLAIMER
The information presented here and within the book ‘The Cancer Resolution?’ is not intended to be used as personal medical advice, instruction, or for treatment, it is purely for information purposes. This information is not an advertisement to sell treatment products, nor does the author guarantee that such information will lead to a cure or successful resolution. Any decision to implement treatment based upon the information presented is made at your own risk. The author and publisher are not liable for any harm you may incur that results from acting upon the information and evidence presented. It is not advisable to undertake any action affecting your health without consulting a qualified health professional. The author and publisher are not doctors, medically qualified or health care providers. As all current cancer theories – including the Somatic Mutation Theory that forms the basis of mainstream treatments – are currently unproven, it is imperative that any cancer patient consult a qualified medical practitioner, and acquire as much information as possible from multiple sources to ensure treatment decisions are as objective and informed as possible.

It’s been a while since my last article, where I pondered on the exciting months ahead, the awards, my upcoming visit to Colombia, America and my first speaker appointment at a major cancer conference. And now I’m back, fresh from my recent escapades, if not still a little jet-lagged, and what a whirlwind experience it has been.

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Professor Seyfried

First off, I had the privilege of meeting Professor Thomas Seyfried at the Public Health Collaboration conference earlier this year. I’ve admired Prof Seyfried and his work for a while, his research has provided an understanding that has enabled me to generate the unique insight I have.

The talk he gave was very inspiring and was worthy of the standing ovation he received, but I will admit, our meeting wasn’t as pleasant as I would have hoped, maybe I was expecting too much. I’d been in contact with Prof Seyfried for a while over the years during the period I was developing my theory. During this time he’d offered advice and kindly provided his latest research papers for me to read.

Upon introducing myself to him at the conference, he admitted he’d read half of my book - I was chuffed he’d read any at all - but his response stumped me, when I asked what he thought about the relevance of fungi being present in all cancers with the capability of triggering and sustained the Warburg effect, he replied “I think you should re-consider your hypothesis”. It wasn’t quite the response I was hoping for from someone I had admired for so long, and still do. Needless to say, when asked to, he didn’t offer any reasoning for his statement and then abruptly excused himself to check out the books on an exhibition stall behind us - with that we parted ways.

I felt a tad deflated to say the least, especially considering that, in a previous podcast he acknowledged not only that micro-organisms are present in all cancers, but that they “facilitate glucose fermentation (Warburg metabolism)”, his words not mine. This prompted the interviewer to suggest an insightful strategy, that cancer patients would surely benefit from targeting the pathogen as well as cancer’s metabolic pathways - as I advocate for, but Professor Seyfried dismissed that suggestion. Here’s the link to the Finding Genius Podcast. His comments start around the 16 minute mark. I’m sure we’ll meet again and hope he’ll be in a more receptive frame of mind. He’s still a legend in my book.

Yes To Life conference

In September, I had a book stall at the Yes to Life conference. It was a fantastic conference full of great insight. For me, I love connecting with people directly, it inspires me when I hear patient stories and to listen to their concerns.

On this occasion a very kind lady came to my stand who I shall refer to as my angel investor. This wonderful person gifted me a generous donation to help with facilitating the pilot study we are designing, and for setting up a private community and creation of a course that can help people more easily understand my theory and how it can help them. Let’s face it, while my book is a patient-friendly read, it is nonetheless a daunting looking book - any 600 page offering would be, and first impressions are not helped by the seriousness of the content discussed, cancer theory isn’t exactly bed-time reading. This community and video course will be coming soon. And the need for it couldn’t be more timely.

Cancelled by Facebook

Prior to my escapades abroad I had a telling shot across my bow. Without any warning I woke to my personal Facebook account being disabled! Not suspended, completely shut down without any explanation or any means to appeal against it. Normally an email is sent with a link to appeal, no such email was received and the help section was not very helpful. This meant that I couldn’t access my cancer theory Facebook group. I couldn’t approve posts, engage in conversations with patients or even let them know my account had been disabled. The censorship apparatus had reached my shores and was relentlessly unforgiving, didn’t we used to live in a democracy?

I tried to setup another account with a different email address, but that was disabled too. I can only assume this had something to do with the cookies on my browser that meant Facebook identified any activity as being from the same person. This new account though did allow me to appeal, so I did. Possibly because of this, two weeks later my original Facebook account was fortunately, and quite unexpectedly, restored. To this day I have no explanation for why this happened. A very scary prospect. That by practicing good scientific investigation, I can be cancelled for simply challenging the consensus, is a sad reflection of the political state we now find ourselves in, and the dangerous erosion of science itself. If we continue down this path, science will cease to exist as a valid discipline, only to be used to serve the desires of those in power. This threatens my work and my ability to help cancer patients.

This scare has prompted me to consider creating a private membership community, to safeguard the much-needed conversations that patients want to have that can advance our understanding and improve survival outcomes. Watch this space, a community will be coming soon.

COLOMBIA - and MOUNTAINS of HOPE

On to a more positive note. We’re now moving into the manic period of the last two months. Mike Murphy, the owner of the health sanctuary Mountains of Hope, which is based in the picturesque mountains surrounding Medellin in Colombia, reached out to me after reading my book. Mike created Mountains of Hope after the loss of his dear wife Margot to cancer. He’s created an incredible health retreat, I can say that because Mike flew me out to meet him at MOH where I spent 3 days soaking up the healing energy, tasting the delicious organic food they grow onsite, and sampling the treatments - spiritual, mind and body, as well as the spar/health facilities that are available.

Along with genetic testing, hyperbaric oxygen therapy, spiritual ceremonies and the option of immunotherapy treatments at an additional charge, Mountains of Hope is an incredible destination for healing. It’s not just a spar or clinic that offers a range of therapies, it’s a community that focuses on wellness at its core, from the soil, to the plate, the body and the mind. First and foremost it sets the body on a path for optimum functioning with the nutrients it needs to enhance the immune system and the body’s innate healing ability, while fostering peace and mental well-being, all before offering any type of treatment.

I was particularly impressed with the genetic testing and how the food is prepared with your specific nutritional needs in mind; with the shamanic spiritual ceremonies that can help you reconnect with the inner you, and the attention to detail regarding the organic food that is grown onsite. Emmanuel is in charge of cultivating the organic food grown, he has a PhD in an agricultural discipline. Not only is he acutely aware of the need to monitor the natural compost to encourage a healthy microbiome in the soil, but he monitors and protects the soil nutrient and microbial diversity to the extent of supplying different plants with the type of soil microbiome that benefits those plants the most. This ensures a very high level of nutrient density within your food that you are not likely to find anywhere else in the world - this is a game-changer when it comes to healing.

Effectively Mike has created the perfect environment to detox and heal the terrain of the body providing it with the best chance of fighting cancer. MOH then provides the spiritual support and a number of key additional treatments to target cancer cells. The beauty of a stay at MOH? All of this is done for you, you don’t have to lift a finger - you are provided with a schedule for testing, relaxing, exploring and above all your nutritional needs are catered for, all you need to do is turn up, giving you all the time you need to focus on you, and your well-being, no stress, no organising, just being.

During my stay, myself and Mike discussed a potential collaboration where I could offer consultations to cancer patients at the sanctuary to help them gain the insight I have acquired and gain awareness of additional options available to them - this would be a welcome change on my part from having to work as a graphic designer to pay the bills. In this regard, my research provides extra hope for patients through the unique insight I can offer, and will be a nice addition to the fantastic foundation that Mike has cultivated at his magical sanctuary in Colombia. I will keep you updated on progress.

Healing for the AGES - Texas

From here, Mike generously flew me on to my next destination, such is his conviction in my theory - the Healing for the AGES conference in Texas. The plan from here was for me to connect with the doctors behind the conference, and for me to advocate for Mountains of Hope on their exhibition stand while promoting my theory and book as an independent advisor. This was a fantastic opportunity to help raise the profile of Mountains of Hope and the Cell Suppression Theory. I made some good connections and learnt a great deal - taking home more books I don’t have the time to read, but read them I will.

While it was fantastic to meet Dr Ardis, Group, Ealy and Shmidt, I was super chuffed to meet Dr Judy Mikovits and astounded to hear her say “she believes me” as I was explaining my theory to her. I loved how she was able to explain in detail the pathways, proteins, and genes affected by different compounds. That detail matters, because it provides the logical rationale for why a natural compound or drug may work - helping patients make informed treatment decisions. For too long cancer patients have been operating on faith, faith that this product or that compound will work, without knowing why or how. That’s been one of my motivations, to provide an explanation for why natural compounds or drugs have anti-cancer properties. In this regard my work offers the ability for patients and clinicians to make better informed treatment choices and maximise health outcomes. Judy speaks my language - and what a lovely down to earth person she is too.

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Wichita State University - Cancer Care Reimagined

I flew back home from Texas with just a week to finalise my presentation for the up and coming Cancer Care Reimagined Conference I was due to speak at on November 8th. This was my first keynote speaker appointment, and I was the last speaker at the conference, so it was a huge deal for me and my theory, would I come across well, would the scientists and public understand and accept my reasoning? Would I be able to read my notes to give the presentation!!!!? This and many more concerns were interfering with my focus on completing my presentation in time, not helped by the accompanying Jet lag. I know, everyone experiences it, but this just side-swiped me for two days, at a time when I needed to focus on an incredibly important talk.

I would later be humbled when speaking to Dr Nasha Winters, who was also speaking at the same conference, just before me. This conference was her 38th this year, and here I am moaning about a little jet lag from a flight back from America. I don’t know how Nasha does it, she must be super human is all I can say. Well, she’s certainly doing super human things in the cancer space - reflected in the ‘Pearl Maker Award’ she was presented with at the conference. Congratulations Nasha.

I also had the pleasure of flying out to Kansas with Robin Daly MBE, the founder of the UK cancer charity Yes to Life, he was speaking too, and deservedly picked up another award, the ‘Ripple award’, aptly named for his tireless work and the benefit he has brought to so many. Congratulations Robin.

So how did my first speaking appointment go? Very well would be an understatement. To start with Robin introduced me at the end of his talk, which set me up nicely. Thank you Robin.

Although I recoiled, as I’m sure everyone did, at the overblown picture of my face on the big screen (I would never have given Robin that image if I’d known he was planning such a frontal assault on the audience, or at least I would have photoshopped it), but every cloud has a silver lining, and that gave me a chance to joke about it, lightening the mood at the start of my presentation. You set them up Robin, I’ll knock’em down, as they say. That settled the nerves, and off I went.

I must admit, it’s difficult to judge the audience when you’re focused on presenting, but I needn’t of worried, not only was my presentation very well received, I made many more influential connections, so much so that I am thrilled to announce that a wealthy investor, who attended the conference, has offered to facilitate the pilot study that I am in the process of organising, to test my theory. I have scheduled a meeting next week with the investor and my science group to discuss the details of the study and secure funding. This is just one of many priorities I’ve been working towards for the last two years.

All this, and I haven’t even mentioned my discussion with the scientific legend that is Dr Robert Naviaux that I had 5 days ago - those of you who’ve read my book will know who he is and what he represents. But that’s for another post. If this is the kind of reaction I continue to get from public appearances, then who knows what we can achieve. I’m already booked to talk at the Annie Appleseed Conference in America next February, bring it on I say - look out cancer, we’re coming for you.

“Connect enthusiastically, give relentlessly, and lead bravely” - Professor Paul Cadman:

Under the banner of those wise words, I move forward with pushing the boundaries on cancer, challenging established norms and committing myself to this cause - at this stage I’m not even sure if the story of David and Goliath compares to what I feel like I’m up against.

Next week this journey takes me to the final of the Life Sciences Innovator of the Year award, where, on the 11th September, I will be standing in front of judges answering questions that can help them determine if my theory is worthy of such an accolade, let alone worthy of outcompeting the other finalists and their incredible innovations.

It is thanks to you and your votes that I have made it this far. Just one more hurdle to go - wish me luck.

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Speaker appointment:

Following the award interview, on the 18th September I’ve been asked to speak during Life Sciences week at the University of Birmingham (UOB) no less - a great honour indeed. Life Sciences week is a major, multi-day event taking place in the West Midlands region, including Birmingham, from September 15-19, 2025, that brings together life sciences professionals, researchers, businesses, and investors to discuss innovations, foster collaboration, and showcase the region's strengths in medical research, biotechnology, and healthcare. The event features keynotes, panels, and workshops led by experts, along with networking opportunities, to explore emerging trends and drive advancements in the global life sciences sector.

It’s a real privilege to be part of such an event, and has the potential to help propel the Cell Suppression Theory to a new level. I’ve been reliably informed that some very influential people will be in the audience during my talk - does anyone have any tips on how to prevent knees from knocking that doesn’t involve whiskey?!

This is particularly significant because UOB is the research home of Cancer Research UK in the midlands. Of course, Cancer Research UK do some fantastic work, but I can’t help but think of David and Goliath when I picture myself presenting my theory on their patch, so to speak. Am I about to head into the lions den…is this where I and the CST hit resistance? Who knows, but I’m game. This meeting has been inevitable and a long time in coming - I feel like I’m ready, I’ll give it my best shot. Again, wish me luck.

Moulding the minds of medical students:

Two days ago I was thrilled to speak with Professor Neil Gow at Exeter University. This truly was a dream come true and a tad surreal - I had to pinch myself a number of times. I have to this life seems a far cry from the graphic design days of old - but a welcome change - even if sometimes I feal like I’m living within a movie.

Neil is Professor of Microbiology and, until 2023, was the Deputy Vice Chancellor for Research and Impact at the University of Exeter. His research focuses on life-threatening fungal diseases, addressing critical challenges such as diagnosis difficulties, the lack of vaccines, and limited treatment options.

We had a very deep discussion about my research and the potential role of fungi in cancer. But what I didn’t expect was to have the honour of my research being used as an example of critical thinking within a module in one of the Masters degree courses offered to students. It’s quite surreal to see my work being taken seriously in such a prestigious scientific setting.

Here’s Professor Gow taking me through part of the course with my book on one of his slides. The whole point of this module is to encourage students to question established science, and there’s no better way of doing that than by having them re-address the origin of cancer through the lens of fungal infection. This was already part of the module as there is so much evidence linking fungi to the disease. It’s only recently that Professor Gow has included my research as part of the course - what an honour.

Yes to Life conference:

At the end of the month I will be frequenting the Yes to Life conference in London where I have a book stand, and will be available to speak to the public, so please do come along and show your support. There are many great speakers at the event offering some extremely useful guidance on cancer. A must for any cancer patient.

Flying the nest - Riordan clinic conference key note speaker appointment

In early November I have been invited to speak at the Riordan clinic conference in America, all expenses paid - thank your to Dr Ron Hunninghake and all involved. This will be my first major conference speaking event, and one I am very much looking forward to. I will be accompanied by Robin Daly MBE from the cancer charity Yes to Life who will also be speaking. This provides a great opportunity to raise the profile of the Cell Suppression Theory and that of Yes to Life, a fantastic charity that not only supports cancer patients, but is one of the leading charities helping to push for meaningful change and support innovation.

Accelerating the CST

And last but not least, I’ve been accepted into the NatWest business accelerator program, which provides access to mentors and support that can enable me to disseminate the theory to a greater audience, and help to raise the funding needed to test the theory. This is a fantastic supportive network that can also provide me with the tools to create meaningful assets, such as courses explaining my theory in layman’s terms, professional courses for medical practitioners to grow the pool of health professionals who can advise patients on treating the disease based on my research, and hopefully an App that can help patients and oncologists track their progress as well the treatments they are using to see what’s working. There are many other projects I would like to pursue.

This month is already off to a whirlwind start, and it promises to only get more…well, windy. As things inevitably progress, at some point I will be looking to grow this movement. The accelerator is part of this process, but you are the real movers and shakers. So if you believe in my research, like where I’m going and would like to be part of something different, I would love to hear from you.

For now, thank you for your interest in my work. I will keep you updated on progress and how you can help if you want to. Here’s to connecting enthusiastically, giving relentlessly, and leading bravely…

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DISCLAIMER
The information presented here and within the book 'The Cancer Resolution?' is not intended to be used as personal medical advice, instruction, or for treatment, it is purely for information purposes. This information is not an advertisement to sell treatment products, nor does the author guarantee that such information will lead to a cure or successful resolution. Any decision to implement treatment based upon the information presented is made at your own risk. The author and publisher are not liable for any harm you may incur that results from acting upon the information and evidence presented. It is not advisable to undertake any action affecting your health without consulting a qualified health professional. The author and publisher are not doctors, medically qualified or health care providers. As all current cancer theories – including the Somatic Mutation Theory that forms the basis of mainstream treatments – are currently unproven, it is imperative that any cancer patient consult a qualified medical practitioner, and acquire as much information as possible from multiple sources to ensure treatment decisions are as objective and informed as possible.

When faced with cancer, the biggest challenge isn’t just the diagnosis itself – it’s the overwhelming question of what to do next. Which treatment should you take? When should you start? How do you know if it will work? For most people, the need is simple and urgent: you want a solution, and alongside that, you want emotional support.

But finding that solution is far from straightforward.

Standard of Care:

Understandably, many place responsibility for their recovery on Standard of Care (SOC) treatments – surgery, chemotherapy, radiotherapy. A cancer diagnosis can be overwhelming for a very good reason, it’s not everyday we are forced to contemplate our own mortality so it’s only natural to place these important health decisions in the hands of the experts. The problem: most people aren’t aware that SOC treatments are based on a limited understanding of cancer – the notion that cancer is driven by genetic mutations. This can be problematic because the Somatic Mutation Theory (the formal name for the genetic theory of cancer) remains unproven and could very well be wrong – as the bulk of evidence seems to indicate. Moreover, these treatments are toxic and can work against the body’s own healing abilities. This is fine if the tumour can be eliminated and the body is strong enough to heal from the damage inflicted.

For patients who would rather take a less toxic path, one that uses treatments to compliment SOC or alternatives instead of SOC, this task is incredibly daunting because there is no clear direction or framework for supporting such a decision. In fact the depth and breadth of information can be extremely confusing, contradictory and can risk further overwhelm.

To provide some context:

A 2023 survey in America found that more than 60% of cancer patients strongly believe in complementary therapies with 71% wanting their health systems to offer them.

Among oncologists, 57% believe complementary therapies are effective at managing side-effects with 33% indicating they improve overall survival [source]. While just over 50% of patients the UK admit using complementary options.

Alternative offerings:

Delving into the alternative realm we find examples such as the Metabolic Theory of cancer, which suggests you should restrict glucose and glutamine, the two main fuels that appear to fuel cancer. Others branch off from that idea, using repurposed drugs or targeted metabolic strategies. For example:

• Dr Ben Williams, who survived terminal brain cancer using a concoction of off-label drugs

• Pablo Kelly, who outlived his prognosis by approximately 10 years on a ketogenic diet

• Dr Nasha Winters, who teaches a “terrain”-based metabolic approach

• Jane McLelland, who focuses on off-label drugs and metabolism

• Mark Sean Taylor, who is looking at a range of modalities including metabolism but focusing on immunotherapy with SOC

• Dr Paul Marik, who has recently proposed a protocol similar to McLelland’s

There are many more. Beyond these, many individuals share personal protocols they believe saved them, such as:

• Rick Simpson Oil

• Joe Tippens’ fenbendazole protocol

• Chris Wark’s organic, plant-based terrain approach

• Shane Clark’s use of mebendazole, cimetidine, and glutamine supplementation

• The Budwig protocol

• Gerson therapy

• Ann Cameron’s “carrot cure”

And then there are inspiring stories like Dale Atkinson’s, who became NED (no evidence of disease) using an extensive mix of complementary and conventional approaches, supported by a strong team – though at a cost most people may not be able to afford.

There are also “blueprints” and “evidence-based roadmaps” offered by others claiming to know the best path forward for patients.

Yet here lies the dilemma: all of these approaches rest on assumptions about what cancer actually is. And the truth is, despite decades of research, the origin of cancer remains uncertain. If the root cause is misunderstood, then treatment advice – however well-intentioned – can overlook key features of the disease. This is one of the main reasons there is still no universal cure, at the most individuals and commentators are making a ‘best guess’ based on incomplete evidence and an incomplete understanding of what cancer actually is. But as demonstrated by Dale, and many others, they’ve done something right – determining what that was, is the difficult task.

The other factor to consider, is that people will react differently to treatments that may have worked for someone else for a number of well-documented reasons. This may be why so many are looking to supplement SOC with complementary approaches with only limited success – the standard approach doesn’t work for everyone, and neither does the addition of complimentary approaches.

So, how can patients make decisions in the face of this uncertainty?

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Making informed decisions

In my view, there are two paths. One is to rely on treatments with the greatest evidence behind them. The other is to work from the origin of the disease itself – because if you can understand what drives cancer, you have a far clearer chance of targeting it effectively.

On paper, “evidence-based medicine” should be the gold standard. But there’s a catch: the system is biased. Natural compounds and off-label drugs that hold promise and are the mainstay of many alternative protocols, are rarely profitable, which means they seldom make it to expensive clinical trials that could prove them effective. As a result, the clinical evidence you’re told to rely on often favours drugs based on the Somatic Mutation Theory (the idea cancer is a purely genetic disease) – a model that may be incorrect.

That leaves patients in a difficult position. Pre-clinical studies on plant compounds and repurposed drugs look promising, but the translation from lab to clinic is notoriously poor. While approximately 95% of drugs that succeed in pre-clinical testing fail in human trials – we don’t know if that failure rate applies equally to natural or repurposed medicines because they haven’t been tested to the same degree under the same clinical conditions. This bias has left a void in the evidence base, we can neither confirm or deny that natural compounds have efficacy in humans, because they simply haven’t been tested, this uncertainty creates a gamble.

And so the dilemma becomes this:

• SOC is where the evidence lies, but the evidence itself shows these treatments are not cures – just a “best guess,” often accompanied by 5-year survival odds instead of genuine cure rates.

• Alternatives are out there, but the evidence is anecdotal, inconsistent, or limited to pre-clinical studies.

So, where does that leave patients?

In my view, the most logical way forward is not to chase what worked for someone else in the hope it will work for you because your physiology is likely different, but to first understand what you’re truly targeting. If genetic mutations aren’t driving cancer, why base your choices on treatments designed to target them? Why choose approaches that damage the microbiome, impair metabolism, weaken the immune system, or even stimulate cancer stem cells – if those are the very features said to promote cancer?

A science-based framework emerges
After 8 years of meticulous research I became familiar with a number of established cancer theories and developed my own, the Cell Suppression Theory – the view that cancer arises from a failed metabolic adaption to intracellular fungal pathogens. Through this process I realised that a science-based framework for choosing the most beneficial solution already existed, its just that no one had articulated it. While complex, the premise behind it is very simple.

In lieu of sufficient clinical evidence, we can best determine which treatments to use by understanding and assessing the validity of each cancer theory because it is from cancer theory that cancer treatments are developed – theory informs treatment creation and clinical practice. For instance, almost the entirety of SOC treatments offered by oncologists are developed from the Somatic Mutation Theory, metabolic treatments are based on the Metabolic Theory, treatments that target cancer stem cells are developed from the Cancer Stem Cell Theory and so on and so forth. Most science-based treatments are born from a theory. The more accurate the theory, the more effective the treatments derived from it are likely to be.

By comparing and understanding different theories – seeing which ones best explain the disease – you can create a framework that helps guide treatment decisions. And with the addition of my Cell Suppression Theory seemingly the most accurate (when measured against cancers 10 hallmarks), new options surface that can enable better conversations worth having with your medical team.

This is the approach I’ve worked to simplify and make accessible. My goal has been to provide a clear, science-based framework to help cancer patients gain a more rounded understanding of what might actually be driving the disease, so that we know what to actually target. One that doesn’t exclude SOC, but helps you see where metabolic, off-label, and natural therapies might fit in and why they should be considered - this helps to reduce the guess-work in the decision-making process.

My book The Cancer Resolution? doesn’t just discuss my own theory. It’s a holistic guide that weaves together the most important cancer theories, showing how they connect and where they differ – while also pointing to overlooked mechanisms that may hold the key to better outcomes if targeted. The exciting feature of this new understanding is that it helps patients cut through the noise to identify a therapeutic path worth discussing with their oncology team, one that’s based on sound scientific reasoning.

It’s my hope that this framework empowers you to step away from guesswork and towards a clearer, more informed path in your treatment journey.

If you would like to know more about my work and how it is challenging established paradigms to offer patients new treatment avenues and renewed hope for the future, visit:
www.cellsuppression.com

You can access my multi-award-winning book here:
https://shorturl.at/e44KT

And some interesting podcasts discussing my work can be found here:

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DISCLAIMER
The information presented here and within the book 'The Cancer Resolution?' is not intended to be used as personal medical advice, instruction, or for treatment, it is purely for information purposes. This information is not an advertisement to sell treatment products, nor does the author guarantee that such information will lead to a cure or successful resolution. Any decision to implement treatment based upon the information presented is made at your own risk. The author and publisher are not liable for any harm you may incur that results from acting upon the information and evidence presented. It is not advisable to undertake any action affecting your health without consulting a qualified health professional. The author and publisher are not doctors, medically qualified or health care providers. As all current cancer theories – including the Somatic Mutation Theory that forms the basis of mainstream treatments – are currently unproven, it is imperative that any cancer patient consult a qualified medical practitioner, and acquire as much information as possible from multiple sources to ensure treatment decisions are as objective and informed as possible.

This rare phenomenon is known as the abscopal effect – derived from Latin, meaning ‘away from the target.’ It has fascinated researchers and clinicians alike for decades. How is it possible that targeting the primary tumour could trigger the regression of distant metastatic tumours?

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In the past, such cases were chalked up as mysterious flukes. But with the advent of immunotherapy, the abscopal effect has been observed more frequently, albeit still unpredictably. This has reinvigorated efforts to understand this process. And more importantly, discussions around whether we can trigger the abscopal effect with greater consistency.

A 2020 article published by the National Cancer Institute titled ‘Cracking the Abscopal Code’ (source) highlights this renewed interest. According to the piece, the prevailing idea is that radiation damages tumour cells in a way that makes them more visible to the immune system. Pieces of dying cells (neo-antigens) are thought to be picked up by antigen-presenting cells, which then prime T cells to recognise and attack similar cancer cells throughout the body. This immune activation may also be boosted when immunotherapy is used in tandem with radiotherapy.

But here’s the catch: it doesn’t always work, and when it does, we still don’t really understand why. This sentiment is captured in a 2018 paper titled “Using immunotherapy to boost the abscopal effect” (source)

“The rarity of the abscopal effect suggests that even primed anti-tumour CD8+ T cells are unable to overcome the suppressive effect of the tumour microenvironment.”

Why conventional explanations fall short

If the immune system is truly being alerted to cancer due to tumour damage, why doesn’t the abscopal effect happen more often? Why do so many tumours continue to evade detection?

There are a combination of issues at play. The micro-environment is hostile to immune cells due to the nutrient depletion that occurs, for instance, a deficiency in glucose and glutamine within the vicinity of the tumour hinders immune cell activity because these compounds are essential for effective immune function. Another is iron overload and accumulation of lactic acid (a result of cell damage and sustained Warburg metabolism). Both further interfere with and suppress immune activity.

It doesn’t help that cancer cells are able to ‘hide’ from immune cells by expressing immune evasive molecules such as PD-L1, CD47 and by suppressing receptors that alert immune cells into action, such as Macrophage Activation Factor (MAF). Moreover, cancer cells appear to suppress the immune response by encouraging immune cells to adopt a more passive pro-cancer Th2 or M2 phenotype, as opposed to an aggressive anti-cancer Th1 or M1 phenotype making it near impossible for immune cells to recognise cancer cells to eliminate them.

There is something else that very few have contemplated, but is brought to our attention by the Cell Suppression Theory – the concept that the vast majority of cancer cells are seen as normal to the immune system, because that’s exactly what they potentially are, normal cells responding in the correct manner. This revolutionary insight challenges established thinking, and is touched upon shortly.

All of this raises further questions: if these cloaking signals are still active in the distant tumours (PD-L1, CD47, MAF), or if cells labelled as cancerous are in fact just cells playing out their normal defensive roles to the extent the immune system doesn’t recognise their behaviour as abnormal, how is the immune system able to trigger the abscopal effect in the manner suggested by established thinking? How would damage to the primary tumour convince the immune system to overcome these cloaking signals in distant tumours, or view otherwise normal cells as foreign? And does the rarity of the abscopal effect – despite the regular use of cytotoxic chemo- and radio-therapy – indicate another mechanism is at play?

A new lens: the Cell Suppression Theory

My own research into cancer over the past 10 years has led me to a different way of understanding the disease. The Cell Suppression Theory (CST) that I developed over 8 years of meticulous research, proposes that cancer isn’t a result of cellular malfunction, but of a failed metabolic adaption to intracellular fungal infection where cell pathways have been hijacked and suppressed. Looking at cancer through another lens is essential for patient survival because correctly identifying the root cause of the disease is the key to identifying effective treatment solutions. This is why questioning established dogma is important.

Under this model, infected cells enter a metabolic emergency mode – what Dr. Robert Naviaux calls the Cell Danger Response – shifting from oxygen-based energy production (OXPHOS) to energy produced via fermentation (Warburg effect). Where apoptosis (programmed cell death) is suppressed, and where surface markers are altered to evade immune detection.

This is not a sign of rogue behaviour, the CST argues – but a sign of a coordinated, tissue-level response to microbial invasion. The Warburg Effect, described by the Metabolic Theory and proposed as the cause of cancer, can also be understood as an anti-infection response. This potentially changes everything – how we view and treat the disease.

Cell to cell communication:

Under the CST framework a tumour forms precisely because an infected cell communicates to the cells around it – the message: instigate the Warburg Effect.

To prevent the spread of infection, these surrounding cells, although not infected themselves, work together to implement Warburg-like metabolism. This is where the oxygen-based energy system is ‘intentionally’ suppressed by mitochondria to favour the fermentation energy pathway – switching the cell into an anti-infection phenotype. Such a coordinated response from the mass of cells surrounding an infected cell, generates a tumour if the infection is chronic.

Failure to eliminate the pathogen results in prolonged use of Warburg-like metabolism, couple this with excess cell damage, and the ability of the intracellular pathogen to prevent cell death from occurring, and the result is a proliferative state of excessive cell growth - a tumour if you will.

In fact Dr Vikram MD from the Mayo Clinic in America, highlights the correlation between the ‘palpable mass’ that can be generated by fungal infection and the mass of a cancerous tumour, in that, both appear to be the same thing. When making a diagnosis, the infectious mass and cancer are impossible to tell apart (source). While Dr Vikram isn’t confirming that fungal infection is cancer, or indeed that it causes cancer, what is clear is that fungal infection can generate a palpable mass that looks and operates just like cancer. For me, the difference is the interpretation of the data - under the established view of cancer being a genetic disease, a tumour mass cannot be classed as cancer if fungi are identified and the source of the tissue growth, because cancer can only be caused by DNA mutation.

Interestingly the case studies that Dr Vikram discusses were initially diagnosed as cancer, but were downgraded to a novel fungal infection with anti-fungal drugs used to treat and reduce the tumour…sorry, I meant palpable mass. It’s interesting to note, that according to the medical literature, the anti-fungal drug Itraconazole appears to be one of the best performing off-label drugs in pre-clinical trials against a broad range of cancers. One can’t help but contemplate the possibility that fungi are an integral component of the cancer story…

Forgive me, I digress…getting back to the anti-infection process discussed above regarding cell communication, cells become stuck between phase 1 (pathogen elimination) and phase 2 (cell repair/regeneration) of the Cell Danger Response; that is, they are attempting to both eliminate the pathogen and repair cell damage that accumulates over an extended period. If both are not resolved, as we see with cancer and in persistent infections – a proliferative metabolic state is sustained, potentially explaining why a tumour forms.

A key point of note: is that most of the cells that are classed as cancerous, and form the bulk of a tumour, are not infected – according to the CST. They are by and large normal cells responding collectively to a fungal infection by intentionally instigating and sustaining the Warburg Effect, because this is a normal tissue response. Under this paradigm cells utilising the Warburg Effect for longer than normal is clearly not the result of cell malfunction, but from a choice made by cells to collectively instigate this metabolic adaption for the purpose of working together to combat the infection.

This would explain why immune cells fail to recognise and attack tumours – these cells are viewed as normal ‘self’ cells, not as being foreign, because they are technically doing nothing out of the ordinary. While the actual cells that are infected and dictating events, are protected and hidden within the center of the tumour mass, due to the immune suppressive factors already highlighted.

Incidentally, is it just a coincidence that intracellular fungal pathogens upregulate PD-L1, suppress MAF to evade detection, and manipulate the immune system to favour a Th2 response, just as we see occurring in cancer? To clarify, fungi actively suppress the Th1 immune response during infection because Th1 primed immune cells specifically target intracellular pathogens. This allows the infection to evade immune detection and elimination – a clever strategy that highlights how novel fungal infections can generate a mass that mimics the conditions of cancer. Again I have to wonder, could the two be related?

Based on this new perspective, can the CST provide the first coherent explanation for the abscopal effect, and why it is so rare?

Breaking the silence: EVs, hive-mind signalling, and immune awakening

One of the most overlooked yet powerful mechanisms in this model is extracellular vesicle (EV) communication. These are tiny lipid-bound packets released by cells, carrying cargo such as RNA, proteins, and lipids – they form part of a signaling and communication network between distant cells. Evidence confirms that the primary tumour uses EVs to communicate with distant tumours, in this sense, and from the perspective of the CST, these EVs are communicating with distant tumour cells to sustain Warburg metabolism, because the intracellular fungal infection has not yet been eliminated within the primary tumour – remember, the distant tumour is just an extension of the primary tumour tissue, so it is still functioning and responding as if it is still part of that original tissue/tumour.

EVs ensure the proliferative state of the Warburg effect persists even at a distance. This is a ‘hive mind’ of sorts, where the primary infected cells dictate the behaviour of the cells around them, and by extension the distant cells that have broken away from the original tissue, all based upon the infection status of the initially infected cell(s) in the primary tumour.

The explanation for the abscopal effect through the CST framework works in a similar ‘hive-mind’ fashion.

While evidence shows that infection can travel with the metastatic cancer cells, most cells within a tumour are likely not infected. Some metastatic tumours therefore, may contain no, or extremely low abundance of fungi. In this instance the abscopal effect is explained through this ‘hive mind’ signaling process.

Killing the fungi present within the primary tumour has a cascading effect on all non-infected cells. The proliferative Warburg-like metabolism that was induced by the initial infection, is no longer required. The primary tumour stops producing EVs to that effect, halting the communication to distant tumours to sustain the Warburg effect. Distant tumours subside because they are able to complete the Cell Danger Response cycle as they are no longer required to sustain this Warburg metabolic state. Returning back to normal, these distant cells commit apoptosis (programmed cell death) because they recognise they exist within the wrong tissue – thus offering a plausible explanation for the abscopal effect.

For distant tumours that are also harbouring sufficient fungi, when the primary tumour is damaged through radiotherapy, this signaling network is disrupted. These damaged cells may suddenly release fungal antigens that had previously been hidden inside them, or their EV profile may change. This disruption may break the silence that was shielding the fungal threat, prompting the immune system to finally take notice – not of the cancer cells per se, but of the underlying pathogen, thus triggering a much-needed shift from a Th2 to a Th1 immune response that targets intracellular pathogens.

As this immunological attention is redirected, the immune system may begin targeting other infected sites, identifying not mutated cells, but consistent microbial signatures across tissues. The shrinkage of distant tumours could then be explained not as the immune system ‘recognising cancer’, but finally identifying fungal signals previously masked by immunosuppressive tactics.

Radio- and chemo-therapies are not generally anti-fungal, but they can damage the tumour enough to expose the pathogen, or induce sufficient Reactive Oxygen Species to kill the pathogen. The double-edged sword here, and likely the reason for why the abscopal effect is so rare, is that the immune system is required to eliminate the fungal pathogen to enable the abscopal effect to occur. The toxic nature of these therapies may weaken the immune response to the extent it cannot deliver the fatal blow to the infection that is required to trigger this abscopal cascade.

This interpretation would help to explain why immunotherapy appears to work in only about 20% of patients – and why, in a similar proportion, it triggers hyperprogressive disease. If the immune system is being artificially pushed to attack, but the target is unclear, the response may lead to increased inflammation, tissue damage, and ultimately worsen the infection by favouring an immunosuppressive, exhausted state where the immune system is primed to attack our own tissue rather than the pathogen driving the disease, handing the advantage to the fungal infection.

In this context, identifying an effective treatment approach all comes down to correctly identifying cancer’s root cause. Immunotherapy will never be as effective as it could be if we are stimulating immune cells to target the wrong thing – our cells, as opposed to the fungal cells that I propose are driving the disease. Is this why the promising approach of immunotherapy has not produced the results we were hoping it would - and can result in detrimental autoimmune responses?

An invitation to reconsider what we’re seeing

The abscopal effect is often presented as a mystery. But perhaps it’s a clue – an opportunity to rethink what cancer is, and what our therapies are really doing.

Could it be that cancer cells aren’t enemies, but messengers? That by addressing the underlying infectious cause, we could shift the entire trajectory of the disease?

This is what the Cell Suppression Theory invites us to explore. Humbly, openly, and with fresh eyes.

Want to learn more?

My book The Cancer Resolution? presents the Cell Suppression Theory in a patient-friendly way. You can also explore articles and interviews on www.cellsuppression.com, or join our growing community of patients, researchers and clinicians.

Together, we’re reimagining what’s possible.

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DISCLAIMER
The information presented here and within the book 'The Cancer Resolution?' is not intended to be used as personal medical advice, instruction, or for treatment, it is purely for information purposes. This information is not an advertisement to sell treatment products, nor does the author guarantee that such information will lead to a cure or successful resolution. Any decision to implement treatment based upon the information presented is made at your own risk. The author and publisher are not liable for any harm you may incur that results from acting upon the information and evidence presented. It is not advisable to undertake any action affecting your health without consulting a qualified health professional. The author and publisher are not doctors, medically qualified or health care providers. As all current cancer theories – including the Somatic Mutation Theory that forms the basis of mainstream treatments – are currently unproven, it is imperative that any cancer patient consult a qualified medical practitioner, and acquire as much information as possible from multiple sources to ensure treatment decisions are as objective and informed as possible.

What they found was surprising: fungi were detected in every single cancer type studied. In one of the largest cohorts (TCGA) fungi were found in around 97% of all tumour samples. Not only that, but the fungi detected varied depending on the type of cancer. This suggests we may be looking not at random contaminants, but specific fungal ecosystems associated with different tumour environments. This is specifically interesting considering my previous article discussing the micro-organisms present in ovarian cancer and how they are specific to the tumour tissue.

For those of us exploring whether microbes might play a deeper role in the origin of cancer, this is a big deal. But the most intriguing finding wasn’t just in what they found, it was in what they couldn’t identify.

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The unknown DNA no one’s talking about

Buried in the technical data was a quiet revelation: 6–7% of all DNA reads extracted from tumours could not be matched to any known organism – not bacteria, not fungi, not viruses, and not human.

In today’s world of high-resolution genomics, that’s a staggering number. What could this mean?

It suggests there are entire groups of micro-organisms we haven’t yet discovered. While some of that could be contamination, there is an argument that holds that these represent micro-organisms/pathogens that we have yet to discover. Organisms whose genetic fingerprints don’t appear in any of our reference libraries. At you first you might think this could be a stretch, but not so much when it’s disclosed that scientists estimate less than 1% of the planet’s microbial life has been formally identified – that is we haven’t yet identified, much less able to detect, 99% of the micro-organisms that potentially exist. In other words, the majority of what’s out there – especially rare, slow-growing, or intracellular species – remains invisible to our current tools.

So while this study confirmed that fungi were present in the vast majority of tumours, it also hints that even more fungi, or unknown microbes, might be there too, just beyond the edge of what we can currently detect.

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Why this supports a new way of thinking about cancer

In my own work on the Cell Suppression Theory, I explore the idea that cancer may begin not because a cell “goes wrong,” but because it becomes suppressed from within – perhaps by an intracellular pathogen like a fungal organism. These pathogens can hijack the cell’s normal energy systems – triggering the Warburg effect, shutting down apoptosis (cell suicide) – preventing the cell from dying, suppressing the immune response – ensuring cell survival, and send the cell into a hyperactive survival mode – an unbridled state of cell growth that we commonly refer to as “cancer.”

To be clear: I fully understand that correlation doesn’t equal causation. Just because fungi are found in cancer tissue doesn’t necessarily mean they are a cause or the origin – robust evidence would be needed to confirm such claims. But when you start combining multiple lines of evidence – detection studies like this one, the metabolic shifts we see in tumours, the suppression of immune signals, the ability to explain all 10 hallmarks of cancer through this fungal lens, and more – it becomes difficult to ignore the pattern, and effective problem-solving is all about the consistency of the pattern.

That’s what I lay out in my book The Cancer Resolution? – a step-by-step look at the mounting case for the influence of fungi in cancer, and why they might play a significant role in your survival outcome, if targeted.

What about the 3%?

Some might ask: what about the 3% of tumours where no fungal DNA was identified? Doesn’t that challenge the Cell Suppression Theory?

It’s a good question, but it needs to be viewed in context – the devil is always in the detail.

Detecting fungal DNA in general, not just cancer, is extremely difficult. Fungi exist in very low amounts in most tumours. The tissue samples used in this study were also heavily filtered to avoid contamination – which is good science, but it also means that some real fungi may have been removed from the data if they were below the detection threshold.

More importantly, fungi that we haven’t yet identified, or whose DNA isn’t in the databases, wouldn’t be detected at all. This is where those 6–7% of unidentified DNA reads become relevant. While that could represent contamination of other non-human cells, it’s entirely possible that a number of these reads represent novel fungi that are present in all tumours, but simply not yet visible to our current diagnostic tools, or identifiable. This also plays into and offers a highly relevant explanation for the ‘Abscopal effect’ - where treating the primary tumour results in metastatic tumours also regressing. Even a small number of tumours without fungi present can be explained through the Cell Suppression Model – I wrote the article Re-thinking the Abscopal Effect to show how this evidence supports the theory. Moreover there’s also the possibility that past a certain level of damage, fungi lock cancer cells into a metabolic feedback loop that ensures runaway proliferation continues to occur despite them no longer being detectable within the tissue – runaway proliferation caused by runaway inflammation that has outpaced the bodies ability to get it under control – all caused initially by the presence of the pathogen.

In other words, the absence of ‘known’ fungi in 3% of tumours from one of the 4 cohorts, doesn’t prove fungi aren’t present, or that they aren’t responsible – it just adds further nuance. It just means the fungi we can identify didn’t appear to be present using the limited technology and techniques we currently have at our disposal, not that all potential fungi, known and unknown, are confirmed absent – a subtle but critical difference. Absence of evidence is not evidence of absence.

Staying curious, not conclusive

What this study reminds us is that science is a moving target. Our ability to detect and identify microbes is limited by the tools we have, the databases we’ve built, and the assumptions we make along the way. While these tools are incredibly sophisticated and can help move us towards the right conclusions if interpreted correctly, we cannot make definitive statements when we don’t have all the data available.

Rather than close the door on the fungal-cancer link, this research opens it wider – not only confirming fungi in most tumours, but revealing just how much remains unknown. And when nearly ~6% of tumour DNA can’t even be matched to any known lifeform, it’s worth asking: what else are we missing?

For those of us exploring alternative ideas to do with cancer’s origin and how this can influence patient survival, this isn’t about disproving one idea or proving another. It’s about keeping the door open to new data, new hypotheses, and new ways of thinking about one of the world’s most complex diseases.

After all, isn’t that what science is supposed to do?

So, how may this affect how we treat the disease?

If fungi are found to be causative, the implications are huge. It would mean that instead of viewing cancer solely as a genetic malfunction or a random error in cell replication, we might begin to understand it as a suppressive, infectious-like process where the body’s own cells are responding to an intracellular threat. This could shift our entire approach to prevention, diagnosis, and management.

While no treatment recommendations can be made here – and nothing in this article is intended to replace medical advice – this perspective opens up new lines of scientific inquiry, and treatment avenues. For instance:

• Could anti-fungal therapies play a supporting role in managing the tumour micro-environment?

• Might some metabolic interventions already in use be working, in part, by disrupting microbial fuel sources?

• Should we be rethinking immune modulation in a way that accounts for intracellular pathogens, not just rogue cells?

The Cell Suppression Theory proposes a unifying framework: that intracellular fungal pathogens may be driving many of the core features of cancer by hijacking the cell’s metabolism, blocking apoptosis, and manipulating immune signaling. It is a theory pushing the boundaries of our understanding, asking important questions to help us reframe how we understand its origin, progression, and treatment.

If this paradigm proves even partly correct, it could help explain why some patients respond unexpectedly well to certain off-label or metabolic therapies, and why immune responses are often skewed in the same direction across many cancers. It may explain why immunotherapies have not lived up to expectations, and why standard of care often misfires when it comes to efficacy.

But much more research is needed, and we must remain humble in what we claim to know. The goal is not to make definitive statements or claim that a silver bullet for treatment exists, there are too many nuances. It is to widen the lens. To ask new questions. To follow the data, even when it challenges long-held assumptions.

And, perhaps most importantly, to remain open to the possibility that cancer is not what we’ve long believed it to be.

More information:

If you’re curious to explore this perspective further, I invite you to read my multi-award-winning book The Cancer Resolution? – a patient-friendly guide that lays out a new theory of cancer known as the Cell Suppression Theory (CST). It offers a new framework for identifying additional therapeutic approaches to cancer.

You can also explore supporting research, tools, and community resources at www.cellsuppression.com - such as my free theory synopsis, which summarises the CST in layman’s terms, allowing you to gain further insight before investing in the book.

Together, we can question assumptions, stay curious, and search for better answers.

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DISCLAIMER
The information presented here and within the book 'The Cancer Resolution?' is not intended to be used as personal medical advice, instruction, or for treatment, it is purely for information purposes. This information is not an advertisement to sell treatment products, nor does the author guarantee that such information will lead to a cure or successful resolution. Any decision to implement treatment based upon the information presented is made at your own risk. The author and publisher are not liable for any harm you may incur that results from acting upon the information and evidence presented. It is not advisable to undertake any action affecting your health without consulting a qualified health professional. The author and publisher are not doctors, medically qualified or health care providers. As all current cancer theories – including the Somatic Mutation Theory that forms the basis of mainstream treatments – are currently unproven, it is imperative that any cancer patient consult a qualified medical practitioner, and acquire as much information as possible from multiple sources to ensure treatment decisions are as objective and informed as possible.

Reference:
Narunsky-Haziza L, Tolomeo P, Borcherding N, et al. Pan-cancer analyses reveal cancer-type-specific fungal ecologies and bacteriome interactions. Cell. 2022;185(20):3789–3806.e17. Available open access at PubMed.

I’ve just read a fascinating paper, one of those studies that “rides a coach and horses through the middle of what we think we know about cancer” — to borrow a turn of phrase from Dr Robert Verkerk. It’s not the first paper to present findings that question our very understanding of the disease, but it is a recent paper that took a detailed look at features of cancer that have been long overlooked and largely misunderstood. The study analysed ovarian cancer, and asked a simple but powerful question:

Do tumours have their own microbial ecosystem?

Up until recently the consensus in oncology was that tumours were sterile, that is, free of micro-organisms. Many still make this claim. And not for the first time the consensus has been shown to be wrong, as the results from this study show, the answer, is a yes. A resounding, data-rich yes.

And what stood out to me – more than the viruses, more than the bacteria, more than even the parasites – was something we rarely talk about in cancer: Fungi.

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What the study found

The study I’m referring to is by Banerjee et al., 2017 (you can read it free here). The researchers analysed 99 ovarian tumour samples, along with adjacent healthy tissues and benign ovarian tissue. But instead of only looking for bacteria or viruses, they cast a much wider net using a microarray called PathoChip, which can detect:

• Viruses

• Bacteria

• Parasites

• Fungi

The idea was to see whether the microbial “fingerprint” of cancer tissue differs from that of non-cancerous tissue. And it absolutely does. Tumour tissue wasn’t just teeming with a few random microbes – it had a distinct, reproducible microbial signature that simply didn’t show up in healthy samples. Not even in the tissue right next to the tumour. That’s remarkable, right?

The fungi were hard to ignore

Among all the microbial classes, what grabbed my attention was the fungal profile. Eighteen fungal species showed up only in the tumour tissue. Gone from the controls. Entirely absent.

And we’re not just talking trace amounts. Some of these fungi were present in every single cancer sample, and with incredibly strong signals. The main culprits?

• Cladosporium (the most dominant—detected in 100% of tumours)

• Malassezia

• Acremonium

• Pneumocystis

• Rhodotorula

• Microsporidia

• Alternaria

And a handful more. Even Geotrichum, the one fungus that showed up in both cancerous and non-cancerous samples, was far more abundant in the tumours.

This finding is significant, it suggests a distinct fungal signature associated with ovarian cancer tissue. The presence of fungi in tumour samples, but not in healthy ones, may point to a specific relationship between certain fungal species and the cancerous micro-environment.

So I found myself wondering: why aren’t we talking about this? Why are we continuing to focus on genetic mutations when it’s clear — in the medical literature — that not only are these microbes present throughout the body in far greater numbers than previously thought, but that they can manipulate and influence cell behaviour, as well as control the immune response?

Viruses, bacteria, parasites… and fungi?

To be clear, the study also found other pathogens – and I think it’s important to mention those.

There were viral signatures (including retroviruses and herpesviruses), and a number of bacterial species like Chlamydia, Fusobacterium, and Mycoplasma. Interestingly, several parasites popped up too – Toxoplasma gondii, Cryptosporidium, and even Plasmodium.

And yes, I know there’s growing interest in using ivermectin and mebendazole (anti-parasitic drugs) in cancer care. This study might help explain why. If parasites really are present in the tumour environment, even occasionally, then perhaps these drugs are doing more than we realise.

But again, what makes this study so powerful is that it doesn’t pin cancer on one pathogen. It shows a synergistic microbial environment inside the tumour. Multiple organisms, multiple classes, all potentially working together.

Yet it’s the fungi, for me, that remain the most overlooked, and the most intriguing, they are barely mentioned in oncology circles. One of the many reasons for my focus on fungi — which I highlight in my book ‘The Cancer Resolution?’ — is that most off-label drugs being used for cancer that show efficacy, including the anti-parasitic drugs mentioned, also have the secondary property of being anti-fungal. Given my extensive research, I would argue that anti-parasitic drugs may have efficacy for three reasons: they target the same metabolic pathways found in parasites that cancer uses, they target the parasites that work in synergy with fungi, and they also target the fungal pathogens I propose mediate the disease.

How does this fit with the Cell Suppression Theory?

If you’re new here, let me give you a very quick overview of the theory I’ve developed and published, called the Cell Suppression Theory (CST).

CST proposes that cancer doesn’t start because cells randomly mutate and go haywire. Instead, it asks: what if cancer is a compromised survival response? A metabolic adaption initiated by the cell in response to a threat, and that the symptoms of cancer arise because this response has failed to rectify the problem? That threat might be intracellular fungal infection.

Here’s how the CST sees it:

1. A fungal pathogen invades/attempts to invade a cell.

2. The cell detects the intrusion and activates what’s known as the Cell Danger Response — a coordinated suppression of the primary energy pathway (OXPHOS) that uses oxygen, switching to the backup fermentation (glycolysis) energy pathway instead. This enables mitochondria (the powerhouse in the cell) to utilise oxygen for other purposes such as, cell signaling to alert immune cells for help and to directly combat the pathogen.

3. This shift, known as the Warburg effect in cancer circles, is usually temporary. It’s a way to survive stress, conserve resources, signal for help and enable tissue repair — it is associated with a proliferative (cell growth) response.

4. But fungi are clever. They suppress apoptosis (cell death mechanisms), manipulate immune signalling (e.g. through PD-L1 or nagalase), and block the cell’s return to normal function.

5. The cell gets stuck in this fermentative, proliferative Warburg-like state, with the ability of the cell to commit cell death blocked.

6. And that, over time explains tumour growth, and looks exactly like cancer.

This theory doesn’t require random mutations. It doesn’t rely on the idea of “rogue” cells. It sees cancer as suppressed cells behaving abnormally due to a failed response to eliminate microbial interference. So when I read that Cladosporium, Malassezia, Microsporidia and others were found only in ovarian tumours — and in all of them — I couldn’t help but see the overlap.

Are fungi the missing link?

Of course, this study doesn’t prove that fungi cause ovarian cancer. It doesn’t even say whether the microbes found are alive, active, or just debris. But it does show one thing, undeniably:

Cancerous tissue has a fundamentally different microbial signature than healthy tissue.

And in ovarian cancer specifically, that signature includes a fungal profile we’ve barely begun to study. So the question becomes: are these fungi passive passengers, taking advantage of a compromised system? Or are they early instigators, helping to trigger the metabolic shifts that define cancer? Could they be suppressing the cell’s normal function in a way that causes it to lock down, ferment, and eventually proliferate?

And if so… could anti-fungal or microbiome-based therapies hold some of the answers we’ve been missing? In an interview on the ‘Finding Genius Podcast’, Professor Thomas Seyfried — a key proponent of the Metabolic Theory of cancer who claims the cause of cancer is the Warburg effect — admits not only that micro-organisms exist inside tumour cells, but that they facilitate the Warburg effect – they can force the cell to switch to the very energy state that is claimed to cause the disease [his comments arise16 minutes in to the conversation]. If that’s the case, as the medical literature confirms, even if cell malfunction is to blame for cancer, even if the our cells are at fault and fungi aren’t directly driving the disease, surely we would still benefit from targeting and eliminating the micro-organisms that are “facilitating” this process?

What might change if we took this seriously?

I don’t have all the answers. But I do think we need to ask better questions.

What if the origin of cancer isn’t in the nucleus… but in the microbiome?

What if fungi aren’t just moulds in the background, but drivers of cellular dysfunction?

What if the Warburg effect isn’t a mistake, but a desperate cry for help?

And what if we’ve spent a century fighting mutations, when we should have been listening to what the microbes were trying to tell us?

If this resonates with you, or if you’d like to read more about the Cell Suppression Theory, you can learn more on my website:

👉 www.cellsuppression.com

Or if you value my insight and would like me to continue writing this content, I would humbly accept a pledge or a donation to my gofundme page. Alternatively my book is available on Amazon: The Cancer Resolution? and explains the Cell Suppression Theory in layman’s terms empowering cancer patients with cancer science that is easy to understand and accessible to all.

Let’s keep exploring, together.

With curiosity,
Mark Lintern

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When you think of mistletoe you might imagine holiday traditions, but for cancer patients in Europe, this humble plant is a beacon of hope. As someone who’s spent years exploring new ways to understand cancer, I’m excited to share how mistletoe therapy (Viscum album extracts) could empower you in your fight against this disease. Backed by decades of clinical use and solid evidence, mistletoe offers direct anti-cancer effects – like boosting your immune system and triggering cancer cell death – that can improve your quality of life. Through the lens of my Cell Suppression Theory (CST), mistletoe’s benefits take on an even deeper meaning, suggesting a potential link to fighting fungal pathogens.

Mistletoe: a trusted therapy in Europe

In countries like Germany, Switzerland, and Austria, mistletoe therapy is mainstream, prescribed by oncologists in leading clinics alongside chemotherapy and radiation. It’s so widely accepted that some health insurance plans even cover it. For decades, patients have turned to mistletoe injections to ease treatment side effects, boost energy, and support their body’s fight against cancer.

Mistletoe therapy has been studied in over 150 clinical trials, including randomized controlled trials (RCTs) and meta-analyses. These studies have focused largely on quality of life, immune function, and, to a lesser extent, tumour response and survival. A 2013 study in European Journal of Cancer found that breast cancer patients using mistletoe alongside chemotherapy had less fatigue, nausea, and better quality of life. A 2019 review showed mistletoe could improve survival rates and strengthen the body’s defenses. Mistletoe’s widespread use in Europe proves it’s a trusted option for cancer patients.

Mistletoe’s anti-cancer properties:

What makes mistletoe such a promising adjunctive (supplementary) therapy? Its number one attribute against cancer is it’s ability to modulate the immune response to one that is able to better target cancer cells.

Cancer and its treatments can tilt your immune system toward a Th2 (T-helper 2) and M2 (macrophage 2) profile, this is a more passive immune response that is inflammation suppressive and tissue regenerative. This is a problem because it means these immune cells are not focused on attacking the cancer itself. Mistletoe changes this by promoting a Th1 and M1 immune response. This Th1 response activates immune cells like T-cells, natural killer (NK) cells and macrophages that can target cancer cells. A 2020 study in Integrative Cancer Therapies found that mistletoe significantly increases NK cell activity, helping your body fight tumours more effectively.

Second, mistletoe can trigger apoptosis, the process where cancer cells are programmed to self-destruct. Its compounds, like lectins and viscotoxins, signal cancer cells to shut down, reducing tumor growth without the harsh side effects of some treatments. A 2010 review in Integrative Cancer Therapies highlighted how mistletoe’s ability to induce apoptosis and boost immunity makes it a powerful supportive therapy. For patients, this means a therapy that not only helps your body fight cancer but also improves your energy and resilience, making the journey feel less daunting.

A Deeper Perspective: Mistletoe and the Cell Suppression Theory

While mistletoe’s anti-cancer effects are exciting on their own, my Cell Suppression Theory (CST) offers a deeper, more nuanced explanation for why it might work so well. I propose that cancer may not be just random cellular chaos (as the mainstream Somatic Mutation Theory suggests) but a coordinated response to intracellular fungal pathogens. These pathogens, I hypothesize, invade cells, hijack their metabolism (triggering the Warburg effect, where cells rely on the backup energy pathway of glycolysis), and block apoptosis, locking cells into a tumour-growth state. Intriguingly, in order to survive within cells fungi need to modulate the immune response to evade detection, they do this by tilting the immune system toward Th2/M2 dominance, the same transition we see occurring in cancer. This pushes immune cells away from targeting intracellular pathogens – it is the Th1/M1 type immune cells that target intracellular pathogens – a very clever survival strategy that highlights how manipulative fungi can be.

Mistletoe’s properties align intriguingly with this idea. Beyond its immune-boosting and apoptosis-inducing effects, mistletoe has fungistatic properties, meaning it can slow or stop fungal growth. This is how a number of anti-fungal drugs work. The important aspect of note, is that as fungistatic compounds just inhibit fungi rather than kill them, the immune system needs to be fully functioning to finish the job. This is where mistletoe’s ability to shift the immune system to a Th1/M1 response could help your body zero in on these intracellular invaders. Th1-driven NK cells and M1 macrophages are uniquely equipped to detect and destroy cells harbouring pathogens, potentially addressing the root cause of cancer as the Cell Suppression Theory envisions. A 2022 study in Nature supports the idea that microbes, including fungi, may play a role in cancer metabolism, lending weight to this perspective.

I’m careful not to claim this as fact – my theory is unproven, open to scrutiny and testing as all current theories are. But the way mistletoe’s immune-modulating and fungistatic effects dovetail with the CST is exciting. It suggests mistletoe could be doing more than easing symptoms – it might be tackling an underlying driver of cancer, offering a hopeful new angle for patients.

Why This Matters for You

If you’re facing cancer or supporting someone who is, mistletoe therapy offers an extra weapon in our arsenal against the disease. Its ability to boost NK cells, trigger apoptosis, and rebalance your immune system toward a Th1/M1 response can improve your quality of life, reduce side effects, and strengthen your body’s fight against cancer. Backed by years of European clinical practice and research, it’s a practical, evidence-based option. Through the lens of my Cell Suppression Theory, mistletoe’s potential to target fungal pathogens adds a compelling layer, inviting you to explore a new way of understanding cancer.

Cancer can feel like a maze, but you have the power to navigate it. My book, ‘The Cancer Resolution?’ – in which the Cell Suppression Theory is published – dives deeper into this fresh perspective, offering a clear, evidence-based framework to evaluate treatments like mistletoe. Written in plain English, it’s relatable, hopeful, and designed to help you take charge of your health.

Mistletoe therapy, in conjunction with the insight provided by the Cell Suppression Theory, is a window into a hopeful new approach to cancer. I invite you to learn more – grab ‘The Cancer Resolution?’ on Amazon, or visit www.cellsuppression.com to connect with others and explore this transformative paradigm. Together, we can reframe cancer and unlock a brighter, healthier future.

DISCLAIMER
The information presented here and within the book 'The Cancer Resolution?' is not intended to be used as personal medical advice, instruction, or for treatment, it is purely for information purposes. This information is not an advertisement to sell treatment products, nor does the author guarantee that such information will lead to a cure or successful resolution. Any decision to implement treatment based upon the information presented is made at your own risk. The author and publisher are not liable for any harm you may incur that results from acting upon the information and evidence presented. It is not advisable to undertake any action affecting your health without consulting a qualified health professional. The author and publisher are not doctors, medically qualified or health care providers. As all current cancer theories – including the Somatic Mutation Theory that forms the basis of mainstream treatments – are currently unproven, it is imperative that any cancer patient consult a qualified medical practitioner, and acquire as much information as possible from multiple sources to ensure treatment decisions are as objective and informed as possible.

References

1. Kienle GS, Kiene H. (2010). Review article: Influence of Viscum album L (European mistletoe) extracts on quality of life in cancer patients: A systematic review of controlled clinical studies. Integrative Cancer Therapies, 9(2), 142–157. [Open Access: https://doi.org/10.1177/1534735410369673]

2. Tröger W, et al. (2013). Viscum album [L.] extract therapy in patients with locally advanced or metastatic pancreatic cancer: A randomised clinical trial on overall survival. European Journal of Cancer, 49(18), 3788–3797. [Open Access: https://doi.org/10.1016/j.ejca.2013.06.043]

3. Loef M, Walach H. (2020). Quality of life in cancer patients treated with mistletoe: A systematic review and meta-analysis. Integrative Cancer Therapies, 19, 1534735420947744. [Open Access: https://doi.org/10.1177/1534735420947744]

4. Straussman R, et al. (2022). Intratumoral bacteria and fungi as potential drivers of cancer metabolism. Nature, 608(7923), 344–352. [Open Access: https://doi.org/10.1038/s41586-022-05013-8]

5. Naviaux RK. (2014). Metabolic features of the cell danger response. Mitochondrion, 16, 7–17. [Open Access: https://doi.org/10.1016/j.mito.2013.08.006]

More specifically, let’s talk about the compounds they produce – mycotoxins – and the alarming blind spot in modern medicine when it comes to their potential role in chronic disease, including cancer.

For decades, the dominant view within mainstream oncology has clung tightly to the Somatic Mutation Theory (SMT) – the belief that cancer is the result of accumulated random mutations in our DNA. Anything outside that paradigm is often dismissed or ignored, no matter how compelling the evidence. Fungal involvement? Not even a footnote in the conversation for most oncologists.

But what if we’ve been looking at cancer through the wrong lens? And what if, in doing so, we’ve not only misunderstood the true origins of the disease but also overlooked a very real and measurable threat – mycotoxins, the toxic metabolic by-products of fungi that are known to suppress the immune system, damage DNA, and trigger chronic inflammation?

Even if you don’t accept the full implications of the Cell Suppression Theory that I propose – where intracellular fungal pathogens hijack cellular machinery to create cancer – there’s still an undeniable truth: mycotoxins are toxic, immunosuppressive, and inflammatory agents. And they may be a major missing piece in the cancer puzzle.

The Mycotoxin Problem: Hiding in Plain Sight

Fungi are everywhere. They exist in our environment, in our food, and even in our bodies. Under normal conditions, many of them are harmless. But certain species produce mycotoxins – secondary metabolites that can wreak havoc in the body.

These mycotoxins include, but are not limited to:

• Aflatoxins: Found in contaminated grains and nuts, aflatoxins are potent carcinogens and are classified by the WHO as Group 1 carcinogens, meaning there's clear evidence they cause cancer in humans.

• Ochratoxin A (OTA): Found in water-damaged buildings, coffee, and cereals, OTA has been linked to kidney toxicity, immune suppression, and DNA damage.

• Trichothecenes (e.g., T-2 toxin): Produced by Fusarium species, these interfere with protein synthesis, leading to immune dysregulation and tissue damage.

• Zearalenone (ZEA): An estrogenic mycotoxin that can disrupt hormonal balance, potentially playing a role in hormone-driven cancers.

• Gliotoxin: Produced by Aspergillus fumigatus, this toxin is particularly dangerous due to its immune-suppressing capabilities.

And those are just the best-known culprits.

Why the Medical Establishment Still Shrugs

Despite the fact that many of these mycotoxins are scientifically validated to cause oxidative stress, DNA damage, mitochondrial dysfunction, and immune exhaustion, the topic is often dismissed as fringe in cancer circles. Why?

Because acknowledging fungal involvement in disease – especially a disease as complex as cancer – would require rethinking foundational assumptions. It would challenge the mutation-centric dogma that underpins most drug development and clinical protocols. And that is something few institutions are prepared to do.

But here’s the reality:

You don’t have to accept fungal infection as the cause of cancer to acknowledge that mycotoxins – whether from environmental exposure or internal fungal colonisation – may play a central role in creating the inflammatory terrain that cancer thrives in.

The Chronic Inflammation Connection

Chronic inflammation is now recognised as one of the key drivers of nearly every modern disease, cancer included. It’s the fire that keeps the disease engine running. And mycotoxins are known accelerants.

Consider this: exposure to certain mycotoxins has been shown to upregulate NF-κB, a key inflammatory pathway associated with tumor progression. Others inhibit mitochondrial function, and trigger the oxidative stress that damages cellular machinery. Some are even designed to suppress the immune response enabling fungi and the cells they invade, to evade immune detection – sound familiar?

This is no small influence. It’s not merely a trigger – it’s a perpetual feed-forward cycle where inflammation begets immune dysfunction, which begets more inflammation, DNA damage, and cellular mutation, all while placing incredible stress upon the immune system that ultimately reduces it’s capacity to function optimally.

Environmental + Internal Exposure: The Double Hit

There’s a common assumption that mycotoxin exposure is primarily environmental – mouldy buildings, contaminated food, or water-damaged homes. While this is certainly one source, few acknowledge the second, more insidious pathway: internal fungal overgrowth.

Fungal infections can persist quietly within the human body – often undiagnosed and untreated. Candida, Aspergillus, and other fungi are part of our microbiome, but under the right conditions (e.g., over-exposure to antibiotics, immune suppression, poor diet), they can overgrow and begin to release mycotoxins directly within the host. Candida fungal species, for instance, can produce ‘Acetaldehyde’ which slowly chokes cells ability to respire – generate energy using oxygen.

This means that even individuals who don’t feel they experience mycotoxin exposure from the environment could still be under chronic internal assault from mycotoxins. These internal producers are even harder to detect – and rarely are they tested for in oncology clinics.

So ask yourself: how many cancer patients are struggling against invisible internal infections that are flooding their systems with immune-disabling and inflammation-causing mycotoxins? And how many of these patients are failing to respond to treatment because their immune system is already too depleted to fight?

Missing the Fungal Factor: A Dangerous Oversight

If practitioners aren’t testing cancer patients for fungal overgrowth or measuring their mycotoxin load, then we are fighting cancer with one eye closed.

This is not conjecture. Evidence such as that provided by Ravid Straussman and colleagues, has shown that fungal pathogens exist within all cancerous tissue, that is, those we have the ability to detect.

So even if you set aside the idea that fungi are actively driving cancer from within – as explained by the Cell Suppression Theory, you cannot ignore the physiological chaos they create through their toxins.

Let’s say it plainly: a patient filled with mycotoxins is a patient under siege. Their immune system is distracted, their inflammatory markers are elevated, and their cellular machinery is under oxidative assault. That is not the state you want a patient to be in when you’re trying to initiate remission, reduce inflammation and help the body return to an optimum level of healing.

Beyond the relevance of Mycotoxins:

The Cell Suppression Theory goes one step further than the discussion above.

It proposes that fungal pathogens don’t merely contribute to cancer through their toxins – they may actually cause cancer by hijacking cellular metabolism. In this model, the fungal pathogen enters the cell, triggers the Warburg effect as part of a coordinated Cell Danger Response locking it in place. It suppresses apoptosis, and manipulates the immune landscape to ensure its survival – all of which happen to mirror cancer's defining traits.

This theory not only accounts for the presence of mycotoxins but explains the deeper biological rationale for why fungal elements are so consistently present in cancer biology. It ties together metabolism, immune evasion, apoptosis suppression, and more into a unified model that the Somatic Mutation Theory (established genetic theory of cancer) has continually failed to offer.

Conclusion: It’s Time to Pay Attention

If you take nothing else from this article, take this:

You don’t need to believe that fungi cause cancer to understand that mycotoxins can significantly contribute to the conditions that allow it to take hold – and facilitate its progression.

While a positive mycotoxin test doesn’t confirm fungal infection – mycotoxins can come from food and the environment (a mouldy house) – those mycotoxins need to be removed from your body and prevented from re-entering, because they are potent toxins. Not only are they capable of damaging DNA, cellular respiration and weakening the immune system – but they can significantly inhibit healing - and that’s not good for anyone, least of all cancer patients, looking to recover from chemotherapy and ultimately heal.

Nearly every patient or clinician I have spoken to on this subject have expressed that they, or their patients, had mycotoxins present within their blood, often at significant levels capable of inhibiting healing and exacerbating their disease.

There’s no ambiguity here. Overwhelming evidence confirms that mycotoxins are toxic, immunosuppressive, and pro-inflammatory – Aflatoxin B1, for instance (created by Aspergillus fungal species that we are commonly exposed to) is categorised as the most naturally occurring carcinogen known to exist. We have increasing evidence that fungi are found within cancer tissue, and can influence disease outcomes. We have decades of patient cases, overlooked biomarkers, and failed treatments that all whisper the same truth: We are missing something.

And maybe that something isn’t genetic. Maybe it’s fungal.

At the very least, fungal involvement in cancer should be at the forefront of any strategy to combat the disease – if not because of their possible role in its origin, then because of their toxic, inflammatory, and immune-disabling by-products that could be quietly sabotaging treatment outcomes.

And in light of the growing evidence supporting the Cell Suppression Theory, perhaps it's time we gave the fungal connection the serious attention it deserves.