Smaller and Smaller

An Essay on How Failed Scientific Theories Survive by Getting Smaller

In March 2026, Dr. Tom Cowan was working through a 2013 review paper from Cold Spring Harbor Laboratory on the pathogenesis of meningococcal infection when he made an observation that extends far beyond meningitis.¹ The paper’s central claim — that the bacterium Neisseria meningitidis causes meningitis and septicemia — kept running into the paper’s own admissions. And each time the claim failed, the authors didn’t abandon it. They retreated to a more granular version. When that version failed, they retreated again. Each retreat produced a more sophisticated-sounding sub-claim that would take years to investigate and eventually falsify, by which time everyone had forgotten that the original claim was never established.

Cowan called it “getting smaller and smaller.” He compared it to physics, where the causal agent moves from the neutron to the muon to the sub-muon, each falsification generating a smaller particle to blame. He illustrated it with a story about skunks in exploded houses that distils the logic to its absurd core.

What he identified is not just one failed theory. It is a method — a structural pattern by which institutional science protects failed models from falsification. It operates across medicine, biology, and genetics. And when you follow it to its logical terminus, you arrive at something worse than bad science. You arrive at unfalsifiability — theories that have retreated so far from direct observation that no possible evidence can contradict them.

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How to Explain It to a 6-Year-Old

Someone says the dog broke the vase. But the dog was asleep. Did the dog break the vase? No.

So they don’t blame the dog anymore. They blame something smaller — the dog’s tail, twitching in a dream. But the dog was in another room. Did the tail break the vase? No.

So they go smaller again. They blame the vibrations from the dream-twitch, travelling through the floorboards, reaching the shelf, and knocking the vase off.

Every time you prove them wrong, they don’t stop blaming the dog. They just blame a smaller part of the dog. First the whole dog. Then the tail. Then the vibrations from the tail. And every time the explanation gets smaller, it gets harder to check. You can check if the dog was near the vase. That’s easy. You can’t check invisible vibrations from a dream. That’s the point.

Grown-ups do this with medicine and science. When their explanation doesn’t work, they don’t say “we were wrong.” They go smaller. They blame a smaller part of the same thing, using longer words, until nobody can tell it stopped working a long time ago. This essay is about that trick, and how it has been running for over a hundred years.

The Skunks

A hundred houses on a street. Five are blown up. You investigate and find skunks in all five. You conclude the skunks did it.

Except skunks are also in the other ninety-five houses. The ones that are perfectly fine.

A rational person would abandon the skunk theory. But a person with a career built on skunk research, with grants funded by anti-skunk agencies and a vaccine designed to prevent skunk-related explosions, faces a different set of incentives. So instead of abandoning the theory, they refine it. It’s not all skunks — it’s the skunks with red marks near their eyes. Those are the ones that blow up houses.

You investigate. Some of the red-marked skunks are in the blown-up houses. Some are in the intact houses. Some blown-up houses have skunks without red marks.

A rational person would abandon the red-mark theory. Instead: it’s the subtype of the red mark. It’s the genetics of the skunk. It’s the epitope of the skunk’s genetics. Smaller and smaller and smaller.

The refinements sound more sophisticated at every stage. They buy another decade of research at every stage. And they move further from the original claim — which was simply that skunks blow up houses. Nobody can prove that, but nobody needs to anymore, because the conversation has moved so deep into skunk genomics that the original question feels naive.

This is Cowan’s analogy, and it maps precisely onto meningitis.

The Bacterium That Everyone Carries

Neisseria meningitidis is a real, observable, culturable bacterium. Unlike viruses, there is no dispute about its existence. It can be seen under a microscope, grown on a plate, and identified in patient samples. The question is whether it causes meningitis.

The Cold Spring Harbor paper — authored by a University of Paris research group — states the conventional claim directly: Neisseria meningitidis is responsible for cerebrospinal meningitis and septicemia.¹

Then, in the same paper, the admissions begin.

The bacterium is “a common inhabitant of the human nasopharynx” — a normal saprophytic organism found in the nose of essentially everyone.¹ Only “a small proportion of colonized subjects” ever develop disease. Cowan practised medicine for forty years, including emergency medicine, and may have seen one or two cases.

Koch’s postulates require that the alleged causative agent be present in all people with the disease and absent from all people without it. Neisseria meningitidis fails this at the threshold. It is present in virtually everybody. Multiple other bacteria are also associated with meningitis. The bacterium cannot distinguish sick from well.

This is the first fork in the road. The theory could be abandoned. It is not.

The Retreat Begins

The paper states that the mechanisms by which the bacterium moves from the nasopharynx to the blood and brain “remain mostly unexplained and will not be approached in this review.”¹

Consider what that means. This is a review paper on the pathogenesis of meningococcal infection. The central question — how a bacterium that everyone carries, and that causes no problems in 99.99% of carriers, occasionally invades the brain and kills someone — is the only question that matters. The paper declines to address it.

The next admission: “The reason why disease occurs in some individuals and not others remains unclear, but human genetic polymorphism is likely to be important.”¹

The bacterium couldn’t explain it. The mechanism couldn’t explain it. So the explanation retreats into the host’s genetics — a speculative claim with no demonstrated causal pathway.

Then smaller still. Not all meningococci have the same “pathogenic potential.” Analysis of multi-locus sequence typing reveals “distinct phylogenetic clonal complexes,” some of which are more likely to be found in sick patients than in asymptomatic carriers.¹ The skunks with the red marks.

Then smaller. Within those clonal complexes, “the presence of a prophage” — a virus-like element that inserts into the bacterial chromosome — “has been responsible for a large proportion of invasiveness.”¹ Now the bacterium is itself allegedly infected by something even smaller, and that’s what transforms it into a killer. No proof. No demonstration. Speculation layered on top of speculation to rescue a model that failed at the first postulate.

And then the paper reveals something that should stop the entire enterprise: “Neisseria meningitidis interacts only with human cells, and there is no animal model of meningococcal sepsis.”¹

The bacterium that supposedly kills teenagers cannot be shown to cause disease in any animal, under any conditions, in any laboratory anywhere in the world. Mouse and rat models show some bacterial survival in fluids but do not produce the disease.

All pathogenesis hypotheses are “derived from post mortem studies of patients who died from meningitis.”¹ The entire model is built on finding bacteria at the scene of damage and concluding they must have caused it. Firemen at the fire.

Bacterium → subtypes → clonal complexes → host genetics → prophage elements. Five retreats from a claim that was never proven, spanning decades of research, consuming careers and funding and institutional credibility — always further from evidence, never closer.

The Biggest Retreat of All

Cowan articulated this pattern in the context of meningitis, but its most consequential instance is much larger. It is the historical move from bacteria to viruses.

Koch’s postulates were formulated in the late nineteenth century to prove that a specific microorganism causes a specific disease.² They require that the organism be found in all cases, absent from all controls, isolated in pure culture, and shown to reproduce the disease when introduced into a healthy host.³ These are not arbitrary demands. They are basic logic — the same logic you’d use to determine whether a hammer drives a nail or whether a frog eats flies.

Bacteria kept failing the postulates. Koch himself abandoned the first postulate when he found carriers of cholera and typhoid fever who never got sick.³ By the mid-twentieth century, bacteria were turning up in healthy and sick people alike, and purified cultures often failed to reproduce the disease. The theory that specific bacteria cause specific diseases was in serious trouble.

This was a fork in the road. The germ theory could have been abandoned. Instead, the establishment went smaller.

Viruses are approximately one thousand times smaller than bacteria.³ They cannot be seen with a light microscope. They cannot be grown in pure culture on a plate — they reportedly require living cells to replicate. They cannot be isolated from a patient’s fluids using the same straightforward methods that work for bacteria.

In 1937, Thomas Rivers modified Koch’s postulates for viruses.³ The modifications are revealing. Rivers dropped Koch’s first postulate entirely — the requirement that the organism be found in all sick people — because many people suffering from allegedly viral illnesses do not harbour the supposed pathogen.³ The postulate was dropped not because it was illogical, but because the evidence kept contradicting the theory. Rather than questioning the theory, they loosened the rules.

Even with loosened rules, Rivers’ postulates have never been fully satisfied for any viral disease.³ The establishment’s own literature acknowledges this. The response has not been to question whether viruses cause disease. The response has been to loosen the rules further, replace direct observation with indirect inference, substitute cell cultures for patient isolates, and declare Koch’s postulates “obsolete.”³

Cowan and others have documented extensively what happens in viral “isolation.”⁴ ⁵ Cell cultures are starved of nutrients, poisoned with antibiotics, and inoculated with patient material. When the cells break down — the so-called cytopathic effect — the breakdown is attributed to a virus. Control experiments using identical procedures without patient material are not performed. When Stefan Lanka’s group finally ran those controls, they got the same cytopathic effect with no patient material at all.⁵ The cell breakdown was caused by the culture conditions, not by any pathogen.

The move from bacteria to viruses follows the identical logic as the move from Neisseria meningitidis to its prophage elements. The original claim failed. Rather than abandon it, the establishment went to a smaller, more elusive entity — one that conveniently cannot be independently verified using the methods that exposed the failure of the original claim. And within virology itself, the same retreat continues. The virus → the genome → the spike protein → the variant. Always further from anything directly observed in a sick person.

The Pattern in Cancer

The oncogene theory of cancer, launched in 1973, claimed that mutations in specific genes controlling cell growth were the cause of cancer.⁶ Find the mutated gene, fix it, cure the cancer. The War on Cancer was declared. Funding poured in.

Fifty-two years later, there is not one mainstream therapy for common cancers based on the oncogene theory.⁶ The primary conventional treatments remain surgery, chemotherapy (which kills cells indiscriminately), and radiation (which also kills cells indiscriminately). None of them have anything to do with genes.

The retreat followed the pattern. First it was one oncogene per cancer. When that failed — tumours turned out to have thousands of heterogeneous mutations, different in every cell, different between patients with the same diagnosis — the theory retreated to “multiple interacting mutations.”⁷ Researchers examining cells from a single tumour found not a clone of identical mutant cells but a chaotic mixture, each cell carrying its own unique set of mutations.⁷ Cowan uses the image of a bombed building: every house has a kitchen, so you find blown-up pots and pans in most cases, but the wreckage is different everywhere you look.⁶ The mutations are the wreckage, not the bomb.

BRCA, the breast cancer gene — probably the most famous oncogene in public consciousness, the one that drove Angelina Jolie’s double mastectomy — is worth examining closely. A 2018 Lancet Oncology study found no significant difference in overall survival between breast cancer patients carrying BRCA mutations and those without them.⁸ A 2015 meta-analysis of sixty-six studies concluded that it is “not yet possible to draw evidence-based conclusions about the association between BRCA1 and/or BRCA2 mutation carriership and breast cancer prognosis.”⁹ Some BRCA polymorphisms may actually be protective.¹⁰

Even Gleevec — the targeted therapy for chronic myelogenous leukaemia, hailed as the proof of concept for the entire oncogene paradigm — has an awkward footnote. Two other commonly used drugs produce the same dramatic remission in CML, and neither affects the oncogene supposedly responsible. All three drugs share a molecular three-dimensional shape, which has left researchers wondering whether Gleevec’s effectiveness has a simpler explanation than its alleged genetic target.⁷

Oncogene → multiple oncogenes → thousands of heterogeneous mutations → surrogate markers that don’t even measure survival. The original promise — find the gene, fix the gene, cure the cancer — dissolved decades ago. The conversation moved on. The funding moved on. The failure stayed.

The Pattern in Cystic Fibrosis

Cystic fibrosis is presented to every medical student as the textbook example of a proven genetic disease.¹¹ One mutation on one gene on chromosome 7 produces one defective protein in a transmembrane receptor, and that causes the disease. Clean. Simple. Settled.

Except it’s not one mutation. It’s hundreds. Cowan examined the literature and found that researchers have identified literally hundreds of different mutations in the same gene, all allegedly producing the same diagnosis.¹¹ But the patients don’t have the same symptoms. Some have poor lung function. Some have normal lung function. Some have poor digestion. Some have normal digestion. The prognoses vary enormously, and forty years of trying to correlate specific mutations with specific outcomes has produced, in Cowan’s assessment, almost nothing.¹¹

One gene → one mutation → hundreds of mutations → no clear genotype-phenotype correlation. The original simplicity — this mutation causes this disease — has dissolved into a thicket of complexity that serves primarily to justify continued funding and maintain the framework.

Where the Pattern Terminates

Follow the “getting smaller” strategy far enough and you arrive at a specific destination: unfalsifiability.

Cowan documented this endpoint in a discussion of DNA chimerism.¹¹ The mainstream model holds that DNA is the hereditary material — your unique code, identical in every cell, passed faithfully to your offspring. Paternity and forensic testing rest on this claim. When a DNA test shows that a mother’s DNA does not match her own biological children — cases that have been documented — the theory faces a direct falsification.

The response is not to question whether DNA functions as advertised. The response is chimerism: in some people, and nobody knows how many, the DNA has somehow changed. It doesn’t match the offspring, but it’s still the hereditary material. The theory is confirmed. And when the DNA does match? The theory is also confirmed. Every possible result — match or mismatch — is absorbed by the model.

A theory that cannot be contradicted by any evidence is not a theory. It is a doctrine. And doctrine is where “getting smaller” leads when it runs out of room to retreat.

How It Works

The method runs on two engines.

The first is specialisation. The person studying the prophage elements of Neisseria meningitidis is not the same person who was supposed to prove that the bacterium causes meningitis. They inherited the assumption. They’ve never examined it. It’s the foundation their career is built on, and foundations are not things you dig up. This is true at every level: the virologist doesn’t question whether viruses exist, the oncogeneticist doesn’t question whether genes cause cancer, the CF researcher doesn’t question whether one gene produces one disease. They were trained within the refined framework. The unresolved question underneath them was “resolved” before they were born — not by evidence, but by institutional momentum.

The second is time. Each cycle of retreating and refining takes five to twenty years. Three or four cycles consume a century. The people who asked the original question are dead. As Cowan observed: you can “run that out for a hundred or so years, and everybody eventually forgets about the original claim.”¹

This is not a flaw in the system. This is how the system operates.

What Gets Lost

While the theories get smaller, the questions that might actually matter don’t get asked.

A thirteen-year-old girl in Sussex develops meningitis. She was vaping. Vaping devices deliver aerosolised nicotine, propylene glycol, heavy metals, and carcinogens directly through the nasal passages — a delivery route that leads toward the brain.¹ The medical establishment does not investigate the toxins. It investigates the bacterium that everyone already carries. It blames saliva shared on vaping devices for transmitting an organism that every human nose already harbours. It uses the case to justify injecting more children with vaccines containing, among other things, propylene glycol.¹

Nobody asks whether the girl was poisoned, because the question has already been answered — a century ago, by a theory that was never proven, through a process of getting smaller that made the original failure invisible.

Bacteria are found at sites of tissue damage because that is where biological work is being done — breaking down waste, processing toxins, participating in the body’s restorative processes. Their presence at the scene is not evidence of causation. It is evidence of response.

But you’d have to step outside the framework to see that. And the framework has spent a hundred years making itself look like the ground.

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References

1. Coureuil M, Join-Lambert O, Lécuyer H, Nassif X. Pathogenesis of meningococcemia. Cold Spring Harbor Perspectives in Medicine. 2013;3(6). University of Paris group. As discussed by Dr. Tom Cowan, Meningitis Science News Webinar, 25 March 2026.

2. Koch R. The etiology of tuberculosis. Reviews of Infectious Diseases. 1982;4(6):1270-1274.

3. Cowan T, Fallon Morell S. The Contagion Myth: Why Viruses (Including “Coronavirus”) Are Not the Cause of Disease. New York: Skyhorse Publishing; 2020.

4. Cowan T. Breaking the Spell: The Scientific Evidence for Ending the Covid Delusion. 2023.

5. Lanka S. Control experiments for cell culture procedures, as documented in Cowan (2023) and discussed in multiple Cowan webinars, 2024-2026.

6. Cowan T. Interview with Jesse Chappus on cancer, oncogene theory, and the failure of targeted genetic therapies. Podcast transcript, project files.

7. Cowan T. Cancer and the New Biology of Water: Why the War on Cancer Has Failed and What That Means for More Effective Prevention and Treatment. White River Junction, VT: Chelsea Green Publishing; 2019.

8. Copson ER et al. Germline BRCA mutation and outcome in young-onset breast cancer (POSH): a prospective cohort study. Lancet Oncology. 2018;19(2):169-180.

9. Van den Broek AJ et al. Worse breast cancer prognosis of BRCA1/BRCA2 mutation carriers: what’s the evidence? A systematic review with meta-analysis. PLOS ONE. 2015;10(3).

10. Lin C et al. The case against BRCA 1 and 2 testing. Surgery. 2011;149(6):731-734.

11. Cowan T. Webinar, 11 March 2026. Discussion of cystic fibrosis genetics, DNA chimerism, and unfalsifiability. Otter.ai transcript, project files.