Pathogenic Cancer: A New Theory
Podcast interview and notes of Mark Lintern's synopsis of his cell suppression theory of cancer
Mark Lintern posits a new theory for the understanding of the origins of cancer. He rejects what he calls the “Cell Malfunction Theory,” which encompasses the traditional DNA Theory along with the newer (more accurate, but still not fully explained) Metabolic Theory and others. He claims that none of these theories fully explain the 10 hallmarks of cancer. He instead proposes an alternative theory: the “Cell Suppression Theory.”
Highlights of Cell Suppression Theory
Download the Mark’s free synopsis document.
Current theories evaluated
Cell Malfunction Theory: Nearly all mainstream theories suffer from the same flaw, in that they all view the disease through the same lens – the collective notion that cancer arises from a malfunction within the cell. It is this breakdown in cell functionality that allegedly drives the disease, providing the cell with autonomy to such an extent that cancer may be referred to as a separate species.
Metabolic Theory, which he calls a subtheory to Cell Malfunction Theory, stands as the most accurate mainstream cancer theory currently available when evaluated against the Hanahan and Weinberg hallmarks. However, not even the Metabolic Theory can explain the “Warburg Effect,” a phenomenon where cancer cells predominantly produce energy by glycolysis (which is their backup cellular energy pathway), even in the presence of sufficient oxygen (when the primary patheway should be available).
There is a strong case for offering metabolic treatments as standard of care for cancer patients, as opposed to the genetic treatments currently offered by mainstream oncologists, which are developed from the inferior DNA Theory. Despite all of the promising new drugs that have been developed, life expectancy for metastatic disease has only been improved by around 8 weeks on average. Moreover, when the studies that form the backbone of the DNA Theory were re-assessed, up to 80% of these foundational studies could not be replicated, meaning, they are incorrect.
The new “Cell Supression Theory” encompasses all the very same treatments advocated for by the Metabolic Theory, but it also highlights the need to consciously target an additional factor that many metabolic treatments are often inadvertently targeting. All that may be needed to improve treatment efficacy is to make minor adjustments to the metabolic approach.
Cell Supression Theory explained
Cancer resulting from infection is not new. Mainstream medicine recognizes that at least 20% of cancers are pathogenic in origin. But in 20% of cancer cases, the pathogens damage the cell, which fits into the Cell Malfunction Theory paradigm.
The author proposes that it’s the ongoing suppressive actions of a pathogen, and the pathogen’s control over specific cell functions, such as cell death and cell growth mechanisms, that triggers and mediates the disease, not the random damage inflicted by infection or carcinogens. The pathogen is an active participant while the random cell damage witnessed in cancer is the result of this prolonged pathogen interaction.
Within this captured, suppressive state, cell damage is magnified and sustained, resulting in excessive damage to mitochondria and the DNA present within the nucleus – the damage thought to be driving the disease. Ultimately excessive damage to mitochondria over time triggers retrograde-signalling and an epithelial-mesenchymal transition, where a regular cancer cell is transformed into a cancer stem cell, accounting for cancer’s unlimited growth and resistance to treatment.
The Warburg effect is instigated as part of an anti-infection strategy. Under these circumstances our cells intentionally switch to glycolysis, even in the presence of oxygen.01 – 08 I later discovered Dr Robert Naviaux’s work that explains in detail, how, and why cells trigger the Warburg effect in response to infection. Through his Cell Danger Response model (CDR), he explains that upon detection of a pathogen, mitochondria intentionally suppress OXPHOS in favour of re-purposing oxygen for energy, to combat the pathogen. As a result, a switch to aerobic fermentation (glycolysis) occurs to account for the ATP energy shortfall and to trigger an inflammatory response leading to a proliferative state of being, if sustained for long periods.
Tumours – previously thought to be sterile – harbour intracellular pathogens and a tumour-specific microbiome that interfere with cell functionality and drug effectiveness. A pan-cancer analysis of 35 different cancers in 2017 found intracellular pathogens to be present in all samples. In fact, scientists were able to distinguish a healthy person from someone with cancer through the dysbiosis of their tumour-associated-microbiome, and predict outcomes.
The increased absorption of glucose due to a reliance upon the Warburg effect, feeds the pathogen while depleting glucose within the surrounding tissue – glucose is the pathogen’s primary fuel. This further suppresses the immune response at the tumour site because immune cells require glucose to operate. This provides an alternative explanation for why glucose feeds the disease – in sustaining the voracious demand of the pathogen, the monopolising of available glucose simultaneously depletes and weakens the immune response, all while the proliferative state of aerobic glycolysis continues to stimulate cell proliferation.
The cancer also utilizes metabolic fuels to fuel its own growth.
Viewing cancer through the lens of cell suppression enables us to re-interpret why certain treatments appear effective, and why the survival rate is so low with current standard of care. For instance: it turns out that all four drugs (Metformin, Atorvastatin, Doxycycline and Mebendazole) used by the Care Oncology Clinic to combat cancer’s metabolic pathways, are also highly antimicrobial. Hyperbaric oxygen therapy, 3BP (3-Bromopyruvate), Tamoxifen, Arimidex, Lovastatin and many more off-label drugs that appear to have efficacy, are also effective at killing specific pathogens in question.
Regarding chemotherapy, while the free radicals generated by initial chemotherapy treatment can eradicate a large portion of the infection and reduce initial tumour size, chemotherapy often fails because it generates the same inflammatory conditions that go on to feed the infection – namely, immune weakness, chronic inflammation, overproduction of lactic acid and iron overload. Not to mention that the free radical production capacity generated by chemotherapy reduces with subsequent treatments, because its toxicity incapacitates the mitochondria that generate these defensive free radicals.
Regarding treatment: evidence supports a metabolic approach, detoxification of the cellular terrain, and re-balancing of the microbiome in conjunction with the addition of a targeted and powerful anti-microbial solution. Theoretically, once control over the cell has been relinquished through the death of the pathogen, mitochondria are free to once again instigate apoptosis in severely damaged cells, resulting in tumour regression.