Revealing the Dark Matter of Cancer

By Jerome Burne

Part 1

According to a graphic designer with no medical or even scientific training, the conventional theory about what causes cancer is badly flawed, and as a result, the way we treat it is far less effective than it could be.

His name is Mark Lintern, but he is no lone oddball. When recently he was invited to present his theory and explain what, he claimed, was the real cause, the audience of over 200 cancer professionals and a panel of scientists, clinicians, and patient experts, agreed it was well-worth investigating further.  A book of around 600 pages plus over 800 scientific references is due to be published shortly,

Conventionally the cause is said to be damaging but random changes in a few genes that set a cell off on a path of uncontrolled growth. This was the explanation given to Mark when he developed skin cancer eight years ago. ‘The more I researched, however, the more unconvincing it became,’ he says. 

Installing Biological Apps

I couldn’t understand how changes to DNA, which were supposedly random  and so were just the result of bad luck, as one consultant put it, produced the remarkably sophisticated and varied modifications to a cell that are caused by cancer. The way the disease develops is as though a series of biological apps have been installed – damp down the immune system, stop damaged cells from destroying themselves, hook up to a nearby artery for nutrients, and so on. 

‘Maybe  there was a one-in-a-million chance that my random gene changes could produce such a combination of cell modifications.  But even more unbelievable was that  the changes taking place in  my cancer cell were exactly the same as those taking place in the cells of all other skin cancer patients, who inevitably would have different mutations to mine and to each other.

‘It didn’t make sense that randomness could cause such consistent modification. So, I started researching. I soon found that this was not the only serious flaw in the DNA theory of cancer, which had been driven by the sequencing of the human genome in 2000. At the time, the expectation had been that each mutated gene connected with cancer would be involved with one of the changes being made to the cell – damping down the immune system, preventing cell death (apoptosis) etc.

‘But that wasn’t the picture that emerged. There was no correlation between the changes in the genes and changes in the cell. Some cancers had lots of changes, while some had none.

Problems with cancer theory increase

‘Gradually, the problems for the DNA gene mutation theory multiplied. For instance, animal research showed that transplanting the nucleus of a tumour cell – where the DNA is held – into a healthy cell, doesn’t produce cancerous changes. However, transplanting the surrounding area, the cytoplasm of a cell, does.

‘And yet, despite the buildup of evidence, the cancer establishment has for decades refused to acknowledge there is a problem. Dogma continues to trump evidence.’

So, if there are serious flaws in the official theory about the cause of cancer, it seems very probable that treatment is being aimed at the wrong targets. This might explain why the results are so much poorer than in other medical specialties.

 Between 1955 and 2004, for example, the death rate from heart disease dropped by 64%, from influenza/ pneumonia by 58% but for cancer by just 5%. After treatment the life extension was an average of 4.1 weeks. 

Solution to problems was to ignore them

So how did Mark Lintern, a designer with little to no scientific knowledge, spot something that cancer experts, who have studied this complex and difficult disease for decades, missed?

In fact, it hadn’t been missed, just overlooked. In 2006 The Cancer Genome Atlas (TCGA) showed that the gene changes within the cells of individual tumours are far more complicated and chaotic than anyone had anticipated. As a result, the hope that it would soon be possible to identify the genes driving your particular cancer, knock them out and stop the tumour, should have evaporated.

‘If faulty genes were the problem’ says Mark ‘there should have been driver genes – ones that made it very likely you would develop cancer if you had them. But the number of driver genes is sporadic with some not present at all.

Faulty theory drives out beneficial treatments

‘One of the results of hanging onto the DNA theory,’ Mark continues: ‘is that we are presented with an extremely narrow view of cancer and health, which favours drug treatments almost exclusively. The result is that medical students and patients never get to hear of alternatives such as salvestrols (plant chemicals that can destroy tumours), the ketone diet (sharply reducing carbohydrate intake), the importance of the gut microbiome to health and the role of glucose, iron and glutamine in cancer.

‘Something more elusive must be driving cancer, ,’ commented Bert Vogelstein, Director of the Ludwig Center and Clayton Professor of Oncology and Pathology at Johns Hopkins, ‘There must be some dark matter in the genome that we can’t detect.’

Mark now believes he knows what that dark matter is. But before going into that, it’s helpful to mention a rival theory to DNA mutations.

‘This is the metabolic theory, which is currently the most plausible alternative,’ Mark says.’ It’s a theory of cancer that focuses on the abnormal energy use of cancer cells, something that is obviously crucial to its survival.’

The mystery of switching energy suppliers

The role of metabolism in cancer was first noticed by the German researcher Otto Warburg in the 1920s. He spotted that when a tumour starts growing, the way the cell makes energy changes. Many cells make energy in the form of ATP in organelles called mitochondria, using a process known as ‘oxidative phosphorylation’ (OXPHOS), which involves oxygen and glucose.

The arrival of cancer in a cell turns off this very efficient mitochondrial production line, replacing it with a much less efficient one that requires much more glucose, known as glycolysis. This switch to glycolysis, even when oxygen is available, is known as the ‘Warburg effect’.

‘Why this happens,’ says Mark ‘is controversial. Warburg thought it was because the mitochondria had been damaged, but there is still disagreement over whether such damage can account for it. 

More recently, Professor Thomas Seyfried of Boston College and one of the leading researchers into metabolic disorders, came out in support of Warburg suggesting that the change was due to what he called, rather more technically, ‘defective Oxidative Phosphorylation’ (OXPHOS)’ which refers to the way mitochondria create energy.

But, as Mark points out, many cells that share a similar energy metabolism with cancer do not become cancerous, and even cancer cells can re-activate the OXPHOS pathway within mitochondria.

What links nearly all theories of cancer is that they all view cancer through the same lens – the notion that it begins as the result of damage to some aspect of the cell – such as disabling genes, the mitochondria, or surrounding tissue.

But for Mark, these all suffer from the logical problem that damage to a cell is very unlikely to make it able to do more complicated and organized things, especially as that damage appears to be random.

It was the recognition that cancer followed a consistent pattern and that randomness cannot generate consistency that lead him to his radical and original big idea. That by the time cancer was starting to develop, the control of the cell by the DNA had already been lost. It was my ignorance about cancer theory that allowed me to entertain such heretical ideas.’

Part 2

The dark matter is revealed

Something else was in charge, something else that was able to make all those changes, such as turning off the cell death mechanism, damping down the immune response, and ramping up cell growth. Something that sounded very much like Bert Vogelstein’s ‘dark matter’. 

A plausible candidate for this tiny controller are micro-organisms – a pathogen, a virus or fungus. Once Mark started searching for evidence of pathogen activity in cells linked to cancer, he found there was plenty. 

‘Researchers used to think that tumours used in laboratory experiments were sterile,’ he says.‘But in fact, they harbour intracellular micro-organisms and have their own microbiome that can interfere with cell functionality and drug effectiveness.

‘What’s more, studies analyzing the microbiome of oral cancer patients have found that a particular type of micro-organism dominates, which can instigate most of the signs of cancer such as hooking up to a nearby blood supply or preventing defective cells ‘committing suicide’ known as apoptosis.

Cancer – a sign of cell refurbishment 

This provides more evidence for the superiority of what might be called the pathogen theory. One of the ways of assessing new theories about cancer is how many of the so-called hallmarks of cancer – the changes a cancer makes to a cell – the theory can explain. ‘On that yardstick,’ Mark says, ‘the pathogen theory comes out top. It can account for 9 out of the ten, more than any other.’

These changes being made in a cell look quite different when seen as the work of a controlling pathogen, keen to improve its own chances of survival. It suggests, for example, a neat solution to the puzzle of what triggers the Warburg effect. 

From the point of view of a pathogen, there are several immediate benefits to switching from efficient OXPHOS energy production to one that uses a lot of glucose.

Firstly, because OXPHOS produces a lot of ‘free radicals ‘which can damage micro-organisms, so closing it down is a survival mechanism,’ says Mark. ‘But secondly, a switch to glycolysis increases glucose consumption by the cell, which is the pathogen’s primary food source. What’s more, this allows the cell to grow faster and increase the production of  lactate, both of which can help protect pathogens living within the damaged tissue of the tumour mass.’

Carcinogens don’t cause cancer 

The pathogen perspective also provides a new way of thinking about carcinogenesis – cancer-causing agents such as tobacco smoke, pollutants, or asbestos. The conventional view is that they are just something else that damages a cell, causing cancer.

 But when you look at what they actually do in a cell, they turn out to be pathogen enablers. They set up conditions that make a cell attractive to infection – increasing lactate production and making iron more available, dialing down the immune response and increasing inflammation.

‘Once you start looking, there are several clues that pathogens and cancer inhabit the same territory,’ says Mark. ‘The Warburg effect is not only triggered by early signs of cancer but also by the onset of an infection.’

The part played by pathogens can also explain the puzzle of why certain treatments are effective when, according to the conventional idea of cancer, they should have no effect. Both silver and honey have been found to be effective – honey can restore apoptosis to a cancer cell – but why? The possible link is that both have anti-microbial properties. 

How treatments look through this new lens

‘Those kinds of connections are rarely noticed by the establishment because medical expertise is organized in silos,’ Mark continues. ‘Cancer geneticists are unlikely to share views with infection specialists.’ 

Fortunately, this new perspective does not change treatment advice if you are taking a metabolic approach, such as following the ketogenic diet, intermittent fasting or using a hyperbaric oxygen chamber – it turns out that metabolic approaches tend also to be antimicrobial. But it does increase your range of options. 

‘It makes absolute sense to pay more attention to the health of your system or ‘terrain’ as it is sometimes called,’ says Mark ‘making it harder for pathogens to mount an invasion. These include clearing out toxins, a diet that doesn’t push up your blood sugar, and eating foods that provide the fibre your gut bacteria need as they provide the lion’s share of your immunity.’

It’s time for a change

Mark’s theory needs a lot of testing before it gets even close to acceptance, but if he’s right, the implication is that cancer researchers and clinicians are trying to understand and treat cancer using a model that seems very likely to be wrong.

The Expert Panels at the meeting generally agreed that Mark’s theory was plausible and made valuable points.

Professor Lisanti – Chair in Translational Medicine at Salford University – welcomed Mark’s doubts about the gene theory, adding that ‘most of the mainstream ideas on cancer are wrong.’

Professor König – senior cancer researcher at the Institut für Medizinische Mikrobiologie und Infektionsepidemiologie, University of Leipzig – commented that: ‘Doubts about the theory of cancer have been around for a long time, and this is a good opportunity to challenge them and offer an alternative.’

Dr Rob Verkerk -Scientific Director of the Alliance for Natural Health – made a similar point. ‘Now is the time to re-evaluate our idea of oncogenes (ones thought to cause cancer). Concentrating on them has not led to clinical success. 

‘However, I struggle with the idea of a single origin for cancer. I love the logic of it, but my understanding is that there are multiple factors that lead to its development.’

Science thrives on challenges. Dogma Kills it

Mark responded by suggesting a distinction between ‘triggers’ such as carcinogens and the ‘cause’. Under the new paradigm, he argues, multiple factors can trigger the infectious process of opportunistic pathogens, but the cause is the outcome of the battle between the pathogen, the cell and the immune system. A victorious immune system can remove the tumour.  

One question raised by the Expert Panels was whether widespread adoption of the pathogen theory could cause an over-use of antibiotics, with harmful and  unintended effects on humans, and so drive micro-organism resistance.

 Mark agreed: ‘Some antibiotics, such as anti-fungal drugs, are extremely toxic to humans, and if not taken under the supervision of a medical professional, could do more harm than good.’

It will take time for the new theory to be assessed and tested. Some claims will inevitably be found to be wrong, but a new perspective with new and plausible approaches to treatment has to be welcomed. The flaws in the very limited number of official treatments have been ignored for too long, 

The conference where Mark presented his theory was organized by the integrated medicine cancer charity Yes To Life. The delegates were impressed by the format, which allowed an objective and rational scientific debate to be held. Something that is all too often lacking in responses to officially sanctioned  ‘scientific facts’ such as doubts about the DNA theory of cancer.

_________________________________

If you are interested in diving more deeply into Mark Lintern’s theory, there are several options at https://yestolife.org.uk/.

His book, ‘Cancer through another lens’ is out shortly. It drills down into the science and is packed with references. 

A pre-release version, aimed at professionals, is available to buy on in the website bookstore. 

You can also find 6 interviews with Mark by Robin Daly (founder of the charity) on his radio show.

https://yestolife.org.uk/radio-shows/

 

Jerome Burne

Jerome Burne

Jerome Burne is the editor of HealthInsightUK. He is an award-winning journalist who has been specialising in medicine and health for the last 10 years and now works mainly for the Daily Mail. His most recent book “The Hybrid Diet” was written with nutritionist Patrick Holford, published 2018. Award: 2015: Finalist for 'Blogger of the Year' Medical Journalists' Association.

21 Comments

  • IMO, probably the most important paragraphs are:

    quote: Fortunately, this new perspective does not change treatment advice if you are taking a metabolic approach, such as following the ketogenic diet, intermittent fasting or using a hyperbaric oxygen chamber – it turns out that metabolic approaches tend also to be antimicrobial. But it does increase your range of options.

    ‘It makes absolute sense to pay more attention to the health of your system or ‘terrain’ as it is sometimes called,’ says Mark ‘making it harder for pathogens to mount an invasion. These include clearing out toxins, a diet that doesn’t push up your blood sugar, and eating foods that provide the fibre your gut bacteria need as they provide the lion’s share of your immunity.’ End quote.

    IMO; The Pathogen Theory drives closer to the ultimate root cause of cancer. That can only be good (though somehow trials will test this; Ethics?).

    IMO; The treatment for both (Metabolic and Pathogen Theories) follow similar paths which focus on improving the Immune system. That can only be good – for many reasons.

    So besides improved Gut Biome (Keto diet and IF etc.) and salvestrols I add: garlic, onions, vitamin C, quercetin, ivermectin and perhaps zinc to the mix in order to not only improve immune system but actively attack whatever is the root cause of the disease.

    NOTE: Ivermectin is currently in trials as a treatment for cancer.
    Why?
    Why does it apparently work. Oh! perhaps it is because it kills pathogens?

    • The obvious observation of the Metabolic / Pathogen theories is that it costs little in money terms.

      The current genetic dysfunction theory as the root cause of this disease has been, IMO, debunked as it has been around far too long with no clear root cause identification.

      So, why does it persist? Perhaps, follow the money applies.

      • Some great points Robert. I think that’s the beauty of this new way of looking at the disease, I’m not looking to completely change how the disease is treated, additional anti-microbial treatments can be applied with any current treatment regime, provided there are no contraindications.

        It makes sense to me, to include the targeting of the pathogens found to be present and influencing the disease, especially as doing so has been shown to provide a benefit, even if one doesn’t beleive these pathogens are the underlying cause, regardless, they have a direct influence.

        • The thoroughness and devotion you have given, and continue to give, to tracking down the underlying cause of such conditions as cancer is truly great. “The Cancer Re-solution? Cancer Reinterpreted thorugh another Lens” is a must-read book. Thank you Mark!

        • In describing the fungal pathogens that exist inside the cells and at some point become the cause of the growth of tumours, I notice you have described the pathogen as ‘opportunist’. We tend to think of life forms that cause infection as ‘malicious’, and imbue them with the characteristics of an anti-social personality or a villain with destructive intentions.

          Equally we know that there are countless micro-organisms essential to our own life-form, in which case these instead are described as having the characteristics of social personalities or friends.

          What differs in these two descriptions is intention, or ability to reason.

          Is it correct however in our understanding of how diseases are caused to consider there is this difference in types, or indeed that there is a decision-making strategist at the wheel of these critters, changing their minds about whether they be friend or foe?

          All life forms are composed of matter that is animated, and there is a constant process of life and death (life taking up matter and life leaving matter). From a human way of looking, where we are five foot tall or so, we form our judgements from what our senses, our eyes and our ears, tell us. We are biassed, you might say, and seemingly cannot help imbuing matter and animated matter with goodness or badness, or good and bad intentions.

          The fungal micro-organisms just do their thing. They act according to the conditions round them. How and why they became created is a tough one to answer. But is it not an error to label them as having ‘good’ or ‘bad’ intentions? The work of dealing with infection is essentially the work of altering or influencing the conditions. However I just wished to highlight this tendency to view life as a fight more than a flow. Not as a criticism, just as an observation.

  • Thanks for that fascinating new insight, Jerome!

    Somehow the way modern research is organised seems to end up obsessing on one approach – then there is Big Pharma of course.

    It has been argued that Big Pharma doesn’t want a good treatment for cancer, even if it were to invent it, because it makes a huge amount of money out of lingering disease.

  • As I wrote the above comment a further idea was tickling the back of my mind.

    Merlin Sheldrake wrote an extremely readable book about fungi – “Entangled Life”, and at one point he describes the remarkable ability of a fungus called Ophiocordyceps to take over a particular species of ant and change its behaviour profoundly so that it climbs tall stalks and then grips hard and dies (normally the ants stay low to avoid predation). The spores from the fungi within its body are then released and disperse. This fungus is also referred to as the zombie fungus for obvious reasons.

    The amazing thing is that this fungus can apply such detailed control of another species to make this possible. I think this makes Mark Lintern’s idea seem much more plausible, assuming the pathogen in question is a fungus.

    • Interesting indeed, thanks

    • Hi David, yes opportunistic fungal pathogens are the antagonist according to my research. It’s interesting, because when viewed through this suppressive fungal lens cancer starts to make sense. I think we’ve been stuck in a rutt in terms of our assumption that cancer is due to cell malfunction, and that it has developed a mind of its own turning over to the dark side. We’ve been trying to make the data align with this paradigm. I think it’s telling that no one has been able to identify the specific damage that allegedly leads to this rogue behaviour.

      It seems more logical, given millions of years of evolution where our cells have learnt to work in a commensal manner, that our cells are still attempting to protect us, but have fallen prey to a parasitic organism that has the capacity to control key cellular mechanisms related to survival. And that it is this loss of control, combined with a sustained infection, that makes the cancer cell appear to have developed a mind of its own.

  • There is a great similarity between the way a plant cell when ‘infected’ by a particular insect or fungus will effectively mutate and produce a growth or gall.

    The plant will grow a gall to house and support a mite, wasp larva or fungus spore in place of a bud or a fruit, just as a cell mutates into a ‘cancer’ cell. The gall does not sit on the plant, it is actually produced by the plant.

    https://treesforlife.org.uk/into-the-forest/habitats-and-ecology/ecology/plant-galls/

  • Some excellent comments and thank you Jerome for the great article. For anyone interested to know more, my book and theory is now available on Amazon at the following link: https://www.amazon.co.uk/dp/B0C5BMKJV1/?coliid=I2ECOKAO2DLRH3&colid=32GOYUL7X5E3H&psc=1&ref_=list_c_wl_lv_ov_lig_dp_it

  • https://www.nature.com/articles/s41392-023-01334-6#Bib1

    The fungal mycobiome: a new hallmark of cancer revealed by pan-cancer analyses.

    Zhi Zong, Fangfang Zhou & Long Zhang / China.

  • https://www.nature.com/articles/s41392-023-01334-6#Bib1

    The fungal mycobiome: a new hallmark of cancer revealed by pan-cancer analyses.

    (Zhi Zong, Fangfang Zhou & Long Zhang / China)

    …While these studies provide an explicit link between cancer and fungi, more research is needed to understand the underlying mechanisms by which fungi induce inflammation and promote cancer progression. To answer these questions, researchers need to study one type of cancer at a time and use cells and animal models to examine whether fungi drive healthy cells to become cancerous. Once researchers gain a more comprehensive picture of how fungi function in cancer, they may be able to develop antimicrobial therapies or targeted pre- or probiotic therapies that benefit patients with cancer.
    … “

    • Great study, thanks for sharing Philbh.

      When determining the cause of the Warburg effect, we might do well to consider the influence of intracellular pathogens, that their sheer presence triggers this response, which can then be hijacked by the pathogen to sustain it:

      ‘Many intracellular pathogens have evolved to either hijack the
      Warburg metabolism of activated host cells to their own
      advantage, or to infect and “push’” host cells into a state of
      increased glycolysis.’
      Immunometabolism 2021 > https://ij.hapres.com/htmls/IJ_1341_Detail.html

      ‘…these data confirm that glycolysis plays a central role in the
      induction of an effective anti-C. albicans host response both in
      vitro and in vivo:
      …glycolysis-mediated mechanisms were demonstrated to be crucial
      for the defence against the pathogen.
      Inhibition of glycolysis led to hosts that were significantly more
      susceptible to the infection.’
      PLOS Pathogens 2017 > https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1006632

      • https://www.sciencedirect.com/topics/neuroscience/candida-albicans

        Yeast-like fungi are certainly ‘implicated’.

        I do think it important also to recognise that all life-forms basically ‘do their thing’, influenced solely by the conditions around them. It is perhaps misleading to assign false personalities to them. The term pathogen can be taken to mean the organism has a malicious intent.
        The world, the natural world, is not a them it is an us. We are part of it, though man is inclined to think he can think his way out of trouble. And that thinking can, by it’s inaccuracy and arrogance, result in the current resort of attacking infections with heavy artillery. To blast them out of the water along with all other life and tissue round it as in some current so-called therapies becomes criminal when viewed in the light of this knowledge that you have highlighted in your discussions and book etc.! Softly softly and stay strictly empirical has to be our way forward.

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