Fungal infections are clearly associated with cancer. There's some research into its possible carcinogenic role in at least some cancers. There's a strong consensus that certain viruses can, but usually don't, cause cancer. Personally, it seems like a perfectly reasonable hypothesis that fungal infections can play an interactive causal role in driving some cancers. In general, the consensus is you typically need at least two breakdowns of the numerous mechanisms that regulate the cell cycle and cell death for cancer to occur.
I'm a PhD student in the cancer space, focusing on epigenetics and cancer. Basically, this is the field where we try to explain both normal cellular diversity (where DNA mutations are definitely not the cause except in very specialized contexts like V(D)J recombination) and cancers apparently not driven by somatic mutations in protein-coding genes.
Mutations not in protein-coding genes are not necessarily inert. RNA can be biologically active. Noncoding DNA serves as docking sites for proteins, which can then go on to affect transcription of genes into mRNA. The proteome can also be affected by alternative splicing of mRNA. Non-coding mutations can potentially affect any of these processes and thereby affect the RNA and protein landscape within a cell.
In 2024, our ability to detect mutations varies widely across the genome, due both to the way we obtain sequencing data in the first place and the way we attempt to make sense of it. NGS sequencing involves breaking the genome into short fragments and reading around 150 base pairs on either end of the fragments, then trying to map it back to a reference genome. Mapping quality will suffer or completely degrade both if the patient has substantial genetic difference from the reference genome or in regions that are highly repetitive within the genome, such as centromeres. When I work with genetic data, there are regions spanning multiple megabasis that are completely blank, and a large percentage of our reads have to be thrown out because we can't unambiguously map them to a particular location on the genome. This will be partially overcome in the future as we start to use more long-read sequencing, but this technology is still in its early stages and I'm not sure it will completely replace NGS for the foreseeable future.
In the epigenetics space, we focus on several aspects of cell biochemistry apart from DNA mutations. The classic example is DNA methylation, which is a methyl group (basically a carbon atom) present on about 60% of cytosines (C) that are immediately followed by guanine (G). The CpG dinucleotide is heavily underrepresented relative to what you'd expect by chance, and its heavily clustered in gene promoters. Methylated CpG islands in promoters are associated with "off genes". The methylation mark is preserved across mitosis. It's thought to be a key mechanism by which cell differentiation is controlled. We also study things like chromatin accessibility (whether DNA is tightly packaged up and relatively inaccessible to protein interactions or loose and open) and chromatin conformation (the 3D structure of DNA, which can control things like subregion localization into a particular biochemical gradient or adjacency of protein-docking DNA regions to gene promoters).
These epigenetic alterations are also thought to be potentially oncogenic. Epigenetic alterations could potentially occur entirely due to random events localized to the cell in which the alterations occur, or could be influenced by intercellular signaling, physical forces, or, yes, infection. If fungal infections control cells like puppets and somehow cause cancer, my guess is that it would be through some sort of epigenetic mechanism (I don't know if there are any known fungi that can transmit their DNA to human cells).
Epigenetics research is mainstream, but the technology and data analysis is comparatively immature. One of the reasons it's not more common is that it's much harder to gather data on and interpret than it is to study DNA mutations. Most of our epigenetics methods involve sequencing DNA that has undergone some extra-fancy processing of one kind or another, so it's bound to be strictly more expensive and difficult to execute than plain ol' DNA sequencing alone. Compounding this, the epigenetic effects we're interested in are typically different from cell to cell, meaning that not only do you have these extra-challenging assays, you also need to aim for single-cell resolution, which is also either extremely expensive (like $30/cell, isolating individual nuclei using a cell sorter and running reactions on each individually, leading to assays that can cost millions of dollars to produce) or difficult (like using a hyperactive transposase to insert DNA barcodes into intact nuclei that give a cell-specific label the genetic fragments originating from each cell, bringing assay costs down to a mere $50,000-$100,000 driven mainly by DNA sequencing rather than cell processing costs). This data is then very sparse (because there's a finite amount of genetic information in each cell), very large, and very difficult to interpret. We also have extremely limited technologies to cause specific epigenetic changes, whereas we have a wide variety of tools for precisely editing DNA.
For potentially oncogenic infections, fungal or otherwise, you'd want to show things like:
All of this seems like a perfectly respectable research project, just difficult. I can't imagine anybody I work with having a problem with it. Where they probably would have a problem would be if the argument was that "fungal infections are the sole cause of cancer, and DNA mutations or epigenetic alterations are completely irrelevant to oncogenesis."
There's an angle I've neglected in this post until now, which is the perspective from evolutionary theory. it's more common to refer to this in explaining how cancer evolves within an individual. But it's also relevant to consider how it bears on the Peto paradox. Loosely, species tend to evolve such that causes of reproductive unfitness (including death) tend to balance out in terms of when they occur in the life cycle. Imagine a species under evolutionary pressure to grow larger, perhaps because it will allow it to escape predation or access a new food source. If the larger number of cells put it at increased risk of cancer, then at some point there would be an equilibrium where the benefit of increased size was cancelled by the cost of increased oncogenesis risk. This also increases adaptive pressure to stabilize new oncopreventative mechanisms in the population that weren't present before. This may facilitate additional growth to a new equilibrium.
This helps explain why cancer isn't associated with larger size: adaptive pressure to develop new oncopreventative mechanisms increases in proportion to the risk to reproductive fitness posed by cancer.
Thanks. You've convinced me that Lintern overstates the evidence of mutation-free cancer cells.
My first significant thought (which came up a bit in the AIs' output) is that it would seem that, if fungi cause cancer, then the fungi would at least sometimes be transmitted from one person to another, and if you weren't aware of the fungi, then this would look like cancer being transmitted from one to the other. Yet I think this has basically never been observed.[1]
One could try supposing that each fungus is only rarely able to infect people—only the few individuals that are unusually vulnerable to it. But, well. I imagine that would generally include anyone whose immune system is crippled. Surely there have been enough cases of people with cancer next to old, immunocompromised people in a hospital, with sufficient mistakes in hygiene that the one would have infected the other. Maybe there are additional requirements for an individual to be infected (the fungus has a favorite temperature? Acidity? Salt level?)... but even taking that into account, I think there should have been enough cases that we would have noticed. (If the chance of an individual being infectable by a given fungus is so low that we never see transmission, then how is it that, er, 1/6th of all deaths are caused by cancer? There would have to be zillions of different fungi, each of which is able to infect only a tiny number of people... which surely would have led to natural selection for much better infectivity by now?)
Incidentally, I think it is known that there are some viruses (like HPV) that cause (or greatly heighten the risk of) cancer. It's plausible that fungi play a significantly larger role of this type than people realize. But for it to be the primary cause seems implausible.
The strongest evidence is that they found cancers that seem to have no mutations.
This seems worth digging into.
There are a few cases of cancers where it's known that the actual cancer cells themselves go from organism to organism: https://en.wikipedia.org/wiki/Clonally_transmissible_cancer
How would transmission be detected? It probably takes years before a tumor grows big enough for normal methods to detect it.
I assume that transmission is common, mild infections are common, and they rarely become harmful tumors.
It probably takes years before a tumor grows big enough for normal methods to detect it.
There exist fast-growing cancers. I figure that if the fungi theory is correct, then probably a good amount of this is caused by the specific fungus (and perhaps what part of the body that fungus targets), and most of the rest comes from the target's immune system (not sure what else would contribute significantly). If transmission and mild infections are common, and if, say, 1% of cancers are fast-growing, I feel like there should be lots of cases where an immunocompromised person picks up a fast-growing cancer fungus at a hospital or something and, within a few years, gets diagnosable cancer. Enough that it should have been noticed. I don't have numbers for this, but that's my suspicion.
Or, for example... How often do couples get the same type of cancer? I found this:
METHODS
The authors identified 25,670 cancer-free married couples in northern California who were followed for up to 31 years for the development of cancer. In Cox proportional hazards analysis, the development of cancer in a spouse was treated as a time-dependent, independent variable, and spouse-with/spouse-without risk ratios were determined, controlling for age and gender. For selected concordant espoused pairs, additional explanatory information was sought in their medical records.
RESULTS
There was no excess concordance for all cancers combined; the spouse-with/spouse-without risk ratio was 0.97 (95% confidence interval, 0.90–1.05). Statistically significant husband-wife associations were found only for cancer of the tongue and stomach and for non-Hodgkin lymphoma. Except for cancer of the penis/endometrium and testis/vulva, based on one couple with each combination, gender specific cancers did not aggregate within married couples. Established and suspected risk factors, not necessarily related to the marriage, were found for some individuals who had concordance with their spouses.
CONCLUSIONS
Little spousal concordance for cancer occurrence was found. The study of spousal aggregation does not appear useful in identifying unsuspected environmental causes of cancer in heterogeneous populations in urban areas of affluent Western countries. A cohort study would have to be much larger than this one to detect weak spousal concordance reliably..
Also, for whatever Claude's opinion is worth:
Q: How often do couples get the same type of cancer?
While it's not extremely common for couples to get the same type of cancer, it does happen occasionally. This phenomenon has been studied, and there are several factors to consider:
- Shared environmental factors: Couples often share the same living environment, diet, and lifestyle habits, which can expose them to similar cancer risk factors.
- Similar behaviors: Shared behaviors like smoking, alcohol consumption, or sun exposure can increase risk for certain cancers in both partners.
- Infectious agents: Some cancers are caused by infectious agents (like HPV for cervical cancer), which can be transmitted between partners.
- Age-related risks: As couples age together, they may face similar age-related cancer risks.
- Genetic factors: While not directly shared between couples, people might choose partners with similar genetic backgrounds, potentially influencing cancer risk.
- Coincidence: Given the prevalence of cancer, some couples will develop the same cancer by chance.
- Screening effect: When one partner is diagnosed, the other may be more likely to get screened, potentially leading to a diagnosis of a cancer that might have otherwise gone undetected.
Studies on this topic have shown:
- A slight increase in cancer risk for partners of cancer patients, but this varies by cancer type.
- Higher correlations for smoking-related cancers, suggesting shared lifestyle factors play a role.
- Increased risk for cancers with infectious causes, like stomach cancer (H. pylori) or liver cancer (hepatitis viruses).
It's important to note that while interesting, these occurrences are not common enough to be considered a significant public health concern.
Enough that it should have been noticed.
My guess is that almost nobody looks for this kind of connection.
Even if they do notice it, they likely conclude that pathogens are just another small influence on cancer risk.
Genes vs environment seems like an obvious thing to track. Most people in most places don't move around that much (unlike many members of our community) so if cancers are contagious for many cancers, especially rarer ones, you'd expect to see strong regional correlations (likely stronger than genetic correlations).
Maybe? It doesn't seem very common for infectious diseases to remain in one area. It depends a lot on how they are transmitted. It's also not unusual for a non-infectious disease to have significant geographical patterns. There are cancers which are concentrated in particular areas, but there seem to be guesses for those patterns that don't depend on fungal infections.
If you're willing to take my rude and unfiltered response (and not complain about it) here it is:
This is very fucking stupid.
Otherwise (written in about half an hour):
I think the fungal theory is basically completely wrong. Perhaps some obscure couple of percent of cancers are caused by fungi. I cannot disprove this, though I think it's very unlikely.
My response, written in about half an hour, from the top of my head:
I think the fungal theory is very likely something that oncology has missed.
+1000
It’s certainly possible that a small subset of cancers are caused/initiated by a fungal infection, but it’s extremely unlikely that our basic understanding of what causes most cancer is wrong at this point.
Also an interesting recent paper showing the potential for cancer to be driven by epigenetically (rather than through direct DNA mutations).
Epigenetic cancers are super interesting, thanks for adding this! I vaguely remember hearing that there were some incredibly promising treatments for them, though I've not heard anything for the past five or ten years on that. Importantly for this post, they also fill out the (rare!) examples of mutation-free cancers that we've seen, while fitting comfortably within the DNA paradigm.
Very interesting. Thank you for sharing this theory.
I had two thoughts. The first is: "Doesn't radiation cause cancer? Isn't this effect well established with evidence?". Because if radiation does cause cancer then that is strong evidence that the DNA theory is true of at least some cancers. (Because radiation cannot spread a fungus).
My second thought (which I agree is in some tension with the radiation one), is that, even if I subscribe to a DNA theory of cancer, I don't have to imagine that every tumour has a mutation (relative to the rest of the organism), or that tumour cells are unable to produce healthy embryos without a cancer. To use a software analogy, lets imagine we have a piece of software with a bug. We have all played a computer game where things are basically fine but there is that one time you ended up halfway inside a wall because of some collision error thing. You never worked out quite what did it that time, but the game was usually fine.
When a piece of software shows that collision bug, we don't need to assume that a cosmic ray has flipped a bit in the software. We can check that the code is the same before and after we saw the collision error. This doesn't mean we are going to see collision errors every single time we play that computer game, it just means that the game has a bug that can appear in some limited situations. Similarly, I can imagine that many organisms contain "bugs" in their DNA (the DNA they were born with, undamaged) and that some of these bugs only express themselves rarely, when specific circumstances arise, and sometimes the result of the "glitch" is cancer. In this model the tumours are not mutated. This model is consistent with the idea that radiation and so on can make cancer more likely, as flipping a bunch of bits in a piece of software is much more likely to introduce more bugs than to reduce the number. But it also seems consistent with some tumours being genetically identical to the rest of the organism. The main prediction of this sort of model would be a strong inherited tendency for certain cancers, especially for identical twins.
As a final thought. If the fungus theory is correct, it doesn't seem like it would be impossibly hard for someone to find some of the fungus cells in mouse A. Look at them under a microscope, "Yes, fungus all right." and then use them to give cancer to a bunch of other mice. So the fungus theory (unlike my speculations above) has the great advantage of seeming to be very testable.
Because radiation cannot spread a fungus
Anything that causes cell damage and inflammation has effects that sometimes make cells more vulnerable to pathogens.
The tenet that radiation cannot spread a fungus is incorrect. Fungi radiotrophic effects in the literature is exactly aligned with radiation making cancer worse. See cryptococcus neoformans and ionizing radiation triggering a melanin synthesis virulence loop. See the lichen that grew on the international space station. Other fungi including sacchyromyces are also included here. You can match this phenomenon to reports of mammogram induced cancers of which there are studies available.
You are correct, the fungus theory is testable.
I want to take a look at the epistemics of this post, or rather, whether this post should have been written at all.
In 95% of cases someone tearing down the orthodoxy of a well established field is a crank. In another 4% of cases they raise some important points, but are largely wrong. In 1% of cases they are right and the orthodoxy has to be rewritten from scratch.
Now these 1% of cases are extremely important! It's understandable why the rationalist community, which has a healthy skepticism of orthodoxy would be interested in finding them. And this is probably a good thing.
But you have to have the expertise with which to do so. If you do not have an extremely solid grasp of cancer research, and you highlight a book like this, 95% of the time you are highlighting a crank, and that doesn't do anyone any good. From what I can make out from this post (and correct me if I'm wrong) you do not have any such expertise.
Now there are people on LessWrong who do have the necessary expertise, and I would value it if they were to either spend 10 seconds looking at the synopsis and saying "total nonsense, not even worth investigating" Vs "I'll delve into that when I get the time". But for anyone who doesn't have the expertise, your best bet is just to go with the orthodoxy. There's an infinite amount of bullshit to get through before you find the truth, and a book review of probable bullshit doesn't actually help anyone.
Now it can be very frustrating to hear "you can't have an opinion on this because you're not an expert", and it sounds very similar to credentialism.
But it's not. If you'd demonstrated a mastery of the material, and came up with a convincing description of current evidence for the DNA theory and why you believe it's incorrect, evidence which is not pulled straight out of the book you're reviewing, I wouldn't care what your credentials are.
But you seem to have missed really obvious consequences of the fungi theory, like, "wouldn't it be infectious then", and all the stuff in J Bostock's excellent comment. At that point it seems like you've read a book by a probable crank, haven't even thought through the basic counterarguments, and are spreading it around despite it containing some potentially pretty dangerous advice like "don't do chemotherapy". This is not the sort of content I find valuable on LessWrong, so I heavily downvoted.
I replied to J Bostock. To address the "wouldn't it be infectious", that mental model has the assumption of being able to actually detect transmission. That type of thinking seems inherited from acute infectious models rather than chronic disease modelling. In the chronic pathogenic model, progression of disease can be slower and causal attribution can be unassigned. To understand this point, see link below re: latency in cryptococcus neoformans, where the fungi can go dormant in white blood cells for years or decades.
https://pmc.ncbi.nlm.nih.gov/articles/PMC7324190/
For what it's worth I found OP extremely valuable.
But you seem to have missed really obvious consequences of the fungi theory, like, "wouldn't it be infectious then",
I very much did not miss that.
containing some potentially pretty dangerous advice like "don't do chemotherapy".
Where did I say that?
I very much did not miss that.
I would consider this one of the most central points to clarify, yet the OP doesn't discuss it at all, and your response to it being pointed out was 3 sentences, despite there being ample research on the topic which points strongly in the opposite direction.
Where did I say that?
I never said you said it, I said the book contains such advice:
Lintern suggests that chemotherapy is generally a bad idea.
This comment describes some relevant research.
From Somatic Mutation Theory - Why it's Wrong for Most Cancers:
It should come as no surprise, therefore, that somatic mutations are questioned as representing "the" cause for the majority of cancers [10,11] and it should be noted that some cancers are not associated with any mutations whatsoever.
Importantly, a detailed analysis of 31,717 cancer cases and 26,136 cancer-free controls from 13 genome-wide association studies [48] revealed that "the vast majority, if not all, of aberrations that were observed in the cancer-affected cohort were also seen in cancer-free subjects, although at lower frequency" [47]. Thus, the notion that somatic mutations are necessarily harmful and can lead to cancer is not borne out by this study and further affirms the hypothesis that mutations observed in cancers are not the triggering event but more likely a means for the clonal replication of already transformed cancer cells.
From Speciation Theory of Carcinogenesis Explains Karyotypic Individuality and Long Latencies of Cancers:
However, despite 65 years of research on the mutation theory, there is still no proof for even one set of mutations that is able to convert a normal cell to a cancer cell.
Because the prevailing mutation theory has dominated the search for the genetic causes of cancer since the discovery of gene mutation in 1927 [111], consistent mutations or consistent karyotypic abnormalities with specific mutations were expected [15,21,22]. Instead, individual mutations [43,44] and individual karyotypes [2,9,112,113] were found, of which over 68,000 are listed in the NCI-Mitelman database of cancers [6].
From Cancer Treatment: A Systems Approach
When the first results of The Cancer Genome Project were reported, many scientists were shocked to learn that most patients, including those with the same type of cancer, did not share the same cancer-related mutations.
The DNA Theory predicts that cancer will be more common in cells that replicate more frequently and/or in organs that have more cells. Lintern's theory suggests more cancer in organs that have more surface area that are accessible by fungi. I think the evidence favors Lintern here, but probably not very strongly.
Itraconazole therapy in a pancreatic adenocarcinoma patient: A case report: an example of a patient with a terminal cancer diagnosis recovering in apparent response to getting an anti-fungal drug.
Case studies with salvestrol treatment: a class of natural anti-fungals helped cure some "terminal" cancer patients. 6 more case studies. New clinical study with phytonutrients (phytoalexins) a randomized controlled trial.
Fungal diseases mimicking primary lung cancer: radiologic--pathologic correlation: cancer and fungal infections look similar. Somehow, this is rarely taken as evidence that they're the same thing.
How a plant's anti-fungal defence may protect against cancer.
From Finding the "Missing 50%" of Invasive Candidiasis:
Blood cultures are limited for diagnosing invasive candidiasis by poor sensitivity and slow turn-around time.
Importantly, a detailed analysis of 31,717 cancer cases and 26,136 cancer-free controls from 13 genome-wide association studies [48] revealed that "the vast majority, if not all, of aberrations that were observed in the cancer-affected cohort were also seen in cancer-free subjects, although at lower frequency" [47]. Thus, the notion that somatic mutations are necessarily harmful and can lead to cancer is not borne out by this study and further affirms the hypothesis that mutations observed in cancers are not the triggering event but more likely a means for the clonal replication of already transformed cancer cells.
Isn't case-control GWAS the wrong tool for the job since it's blind to rare mutations? I'd compare a person's cancerous cells to their normal cells instead, though I'm not an expert so maybe there's a problem with this.
Almost as important is that the mutations that are found seem more randomly distributed than would be expected if they caused consistent types of malfunctions.
Can you expand on this? I can't help but think of performance problems caused by software extensions as an analogy; these are often quite randomly distributed, with there being many different kinds of extensions that can cause program activity to expand uncontrolledly. Shouldn't we expect the same with mutations?
The beginning of this comment is how Lintern expands on that claim. But it sounds like you have an objection that isn't well addressed there.
If cancer merely involved one bad feature, I could imagine software analogies that involved a large variety of mistakes producing that one bad feature.
The hallmarks of cancer indicate that all cancers have a number of bad features in common that look sufficiently unrelated to each other that it seems hard to imagine large sets of unrelated mutations all producing those same hallmarks. Lintern lists many other features that could be considered additional hallmarks.
When I try to imagine software problems that seem analogous to cancer, I come up with problems such as spam where there's an optimizer that's generating the problems.
I'm unclear whether you're imagining software problems that I haven't thought of, or whether you're modeling cancer differently from me.
Book review: The Cancer Resolution?: Cancer reinterpreted through another lens, by Mark Lintern.
In the grand tradition of outsiders overturning scientific paradigms, this book proposes a bold new theory: cancer isn't a cellular malfunction, but a fungal invasion.
Lintern spends too many pages railing against the medical establishment, which feels more like ax-grinding than science. I mostly agreed with his conclusions here, but mostly for somewhat different reasons than the ones he provides.
If you can push through this preamble, you'll find a treasure trove of scientific intrigue.
Lintern's central claim is that fungal infections, not genetic mutations, are the primary cause of cancer. He dubs this the "Cell Suppression theory," painting a picture of fungi as cellular puppet masters, manipulating our cells for their own nefarious ends. This part sounds much more like classical science, backed by hundreds of quotes from peer-reviewed literature.
Those quotes provide extensive evidence that Lintern's theory predicts dozens of cancer features better than do the established theories.
Older Theories
The DNA Theory (aka Somatic Mutation Theory): The reigning heavyweight, this theory posits that cancer results from an accumulation of genetic mutations in critical genes that control cell growth, division, and death.
Another old theory that still has advocates is the Metabolic Theory. This theory suggests that cancer is primarily a metabolic disease, characterized by impaired cellular energy production (the Warburg effect). It proposes that damage to mitochondria is a key factor in cancer development. I wrote a mixed review of a book about it.
Lintern points out evidence that mitochondria are turned off by signals, not damaged. He also notes that tumors with malfunctioning mitochondria are relatively benign.
Evidence Discrediting the DNA Theory
The standard version of the DNA Theory predicts that all cancer cells will have mutations that affect replication, apoptosis, etc.
Around 2008 to 2013, substantial genetic data became available for cancer cells. Lintern wants us to believe that this evidence fully discredits the DNA Theory.
The actual evidence seems more complex than Lintern indicates.
The strongest evidence is that they found cancers that seem to have no mutations. [Updated 2024-07-25: DirectedEvolution suggests that this evidence isn't very strong.]
Almost as important is that the mutations that are found seem more randomly distributed than would be expected if they caused consistent types of malfunctions.
Lintern's theory seems to explain all of the Hallmarks of Cancer, as well as a few dozen other features that seem to occur in all cancers.
He argues that the DNA Theory does a poor job of explaining the hallmarks. DNA Theorists likely reject that characterization. They appear to have thought their theory explained the hallmarks back before the genetic data became available (mostly just positing mutations for each hallmark?). My guess is that they are busy adding epicycles to their theory, but the situation is complex enough that I'm having trouble evaluating it.
He also points out that the DNA Theory struggles with Peto's Paradox (why don't larger animals get more cancer?), while his theory neatly sidesteps this issue.
Additionally, mouse embryos formed from cancer cells showed no signs of cancer.
Evidence of Fungi
A key game-changer is the growing evidence of fungi in tumors. Until 2017, tumors were thought to be microbe-free. Now? We're finding fungi in all types of cancer, with tumor-specific fungal profiles.
There's even talk of using fungal DNA signatures to distinguish cancer patients from healthy individuals.
It's not a slam dunk for Lintern's theory, but it shifts the odds significantly.
Medical Establishment Inertia
It looks like people in the medical mainstream respond respectfully to the ideas in the book, when they react at all. Yet the DNA Theory seems to remain the prevailing dogma. The shortage of reactions to Lintern is disappointing.
My impression is that researchers are hedging their bets when they can conveniently do so, but many of them have built careers that depend on the DNA Theory.
It's possible that some important parts of the establishment are pivoting their research in the directions that Lintern suggests, and are being quiet until they have something worth publishing.
It seems likely that some parts of the establishment are treating the DNA Theory as a religion rather than a theory. I can't tell how widespread that problem is.
Possibly some apathy toward fungal infections is because solutions are somewhat less likely to involve patentable treatments. But there's still some room for patenting new anti-fungals, so I doubt that this is the primary obstacle to accepting Lintern's theory.
Paul Ewald's book Plague Time anticipated some of Lintern's claims, arguing that pathogens are the root cause of many chronic diseases. It was published in 2000, and overlooks fungi (little of Lintern's evidence was available then). Ewald's reasoning is more theoretical than Lintern's.
My limited attempt to spread Ewald's theory stopped when someone pointed to evidence that mice raised in a sterile environment developed most of the same chronic diseases. Lintern counters that there are many microbes that aren't detected by the tests that supposedly confirmed that the mice were microbe-free, so we should wonder whether the experiments demonstrated much. I feel foolish for not wondering about that 20+ years ago.
This reminds me of how long it took to refute the theory of spontaneous generation, due to mistaken beliefs about what it took to create a sterile environment.
Lintern reports that fungal infections have also been implicated in Parkinson's disease and multiple sclerosis, yet many sources still say we don't know the causes of those diseases. Is there a pattern here?
I often say to myself that much of the medical establishment acts as if they believe our bodies are the result of semi-intelligent design rather than evolution. E.g. their disinterest in a paleo diet. This book reinforced that impression.
Experimental History has some relevant comments about the state of cancer research.
Many Cancers?
Maybe parts of the medical establishment have rejected the whole idea of a theory of cancer.
Researchers who try to take the DNA Theory seriously end up confused by the variety of different mutations that they end up studying. This focus makes it hard to see the similarities between tumors.
I've seen many denials that cancer is a single disease. I see a good deal of tension between those denials and the DNA Theory. And don't the Hallmarks of Cancer point to it being a single disease?
Ironically, Lintern advocates a single-disease model, even though his theory implies that a wide range of different fungi are responsible. Presumably many different anti-fungals are needed for the different types of fungi. So in some sense the many-cancers view is likely to be partly correct.
Implications for Treatment
Lintern doesn't offer much hope for reliable cures. He offers many somewhat new ideas for treatments that will sometimes work. The most obvious ones are anti-fungal drugs.
Progress at treating diseases that are known to be fungal infections may be a bit better than progress at curing cancer, but deaths from fungal infections have still been increasing.
Much of Lintern's advice for people who have cancer now consists of standard recommendations to adopt a healthy lifestyle. That shouldn't be surprising: if most chronic diseases are due to pathogens, there will be plenty of overlap in strategies for fighting them.
That includes a long section on the benefits of organic food. I was unimpressed by how it started, with a correlational study that likely had confounders that couldn't reasonably be controlled for. But he made up for that by explaining several causal models that I hadn't previously considered.
E.g. fungicides. Indiscriminate use of fungicides on non-organic crops means that there are fewer beneficial fungi which provide nutrients to the plant, leading the plant to have less nutritional value. More importantly, plants defend themselves against fungi, similar to the fungi that endanger us, by generating anti-fungal compounds that are well targeted against those fungi. Organic foods have more of those anti-fungals, because they're produced in reaction to fungal attacks. Those anti-fungals sometimes work in our bodies when we eat them.
I ended up deciding to give slightly higher priority to buying organic food.
Lintern suggests that chemotherapy is generally a bad idea. One clear reason is that it damages the immune system, and the immune system is the main defense against additional cancers. But he still supports it in cases where it shrinks the tumor enough to enable surgery. I continue to be concerned about how hard it would be to evaluate a doctor's recommendation to get chemotherapy.
What does Lintern's theory mean for Aubrey de Grey's proposed cure for cancer (WILT)? That looks much less promising now. WILT no longer looks like it addresses the root cause of cancer. Even if Lintern's theory is somewhat wrong, cancer stem cells now seem much more important than regular cancer cells as a source of excessive cell replication. Cancer stem cells don't depend on telomerase in the way that other cells do. It looks like Aubrey has a new version WILT 2.0 which does something to address cancer stem cells. What little I understand of it leaves me skeptical.
The good news is that cancer rates can likely be reduced to roughly the rates seen in young adults if other parts of Aubrey's plan work, particularly the parts that affect the immune system.
Concluding Thoughts
There's actually an important similarity between the DNA Theory and Lintern's theory. In both, eukaryotic cells have evolved to serve their own interests, in ways that conflict with the host's interests. The key difference is when that evolution started: years before the cancer was detected, or millions of years?
Evolutionary theory should create a moderate presumption that hostile organisms do more harm to our bodies than do mistakes.
Lintern's theory seems to have more explanatory power than any other theory.
Whether or not Lintern is entirely correct, his work highlights two crucial points:
We shouldn't demand that all proposed cancer treatments conform to the DNA Theory.
We need to rethink how we evaluate the effectiveness of cancer treatments. There's large room for improvement in the choice of criteria without adopting a strong opinion on which theory of cancer is correct. The evidence concerning cancer stem cells seems like a strong argument against relying on tumor shrinkage as evidence of success.
At one level, scientists have failed badly at explaining cancer, and it seems like only an outsider was able to point out that the emperor has no clothes.
But that's at the level of broad theory. At the level of small experiments, the medical establishment has been diligently uncovering plenty of evidence to reject the DNA Theory and to focus some attention on pathogens.
The book isn't as professionally written as I'd like. E.g. he sometimes cites news stories instead of the peer-reviewed papers on which the stories are based.
Parts of the book are difficult to read. Most people should feel free to skip parts of the book, mainly after page 250.
H/T Dave Asprey.