What Makes a Good Theory

In 1831 Charles Darwin was 22 years old. He tried going to medical school, but he had to drop out when he figured out that the sight of blood made him physically ill. So his father shipped him off to Cambridge to study theology so he could become a clergyman instead. He got his degree, but while in Cambridge he spent most of his time collecting beetles and taking long walks with his botany professor John Stevens Henslow, rather than actually studying theology. Henslow suggested that he join a surveying voyage to South America. The ship's captain needed a companion and a naturalist for the trip. Someone educated who could document the natural world while the crew charted coastlines. The position was unpaid, the voyage was slated to last two years, and Darwin would be sharing a cabin the size of a closet with several other men while sailing around the world on a ship that was, by all accounts, quite small and prone to violent rocking. Darwin said yes immediately.

The HMS Beagle set sail in December 1831. The plan was to spend two years surveying South America's coastline, and then head home. But the work kept expanding and what was supposed to be two years turned into five. And those five years, Darwin later wrote, determined his whole career.

During the voyage, Darwin did what naturalists did: he collected things. Birds, plants, rocks, fossils, insects. If it existed, Darwin wanted a specimen of it. He shipped crate after crate back to England, each one meticulously labeled, each one representing hours of work that he performed while fighting off constant, debilitating seasickness. He kept meticulous notes, drew detailed sketches, and documented everything he saw. He found fossils that he noticed looked like enormous versions of animals still living on the continent. Giant armadillo-like creatures. Huge sloths. Why would extinct creatures resemble the living ones in the same place and also be so wildly different in size? In Argentina, traveling south, he kept finding slightly different versions of the same bird species. Not dramatically different, just...variations. Why would there be so many species that were almost identical but not quite? Then, in September 1835, the Beagle reached the Galápagos Islands.

The Galápagos are young islands, geologically speaking, volcanic and isolated. And Darwin started noticing that each island had animals that were seemingly slight variations of the animals on the other islands. The mockingbirds were different sizes and had different markings, the tortoises had differently shaped shells, and then there were the finches.

The finches looked similar enough that Darwin initially thought they were all one species with some variation. It wasn't until he got back to England and examined the drawings he had made more carefully, that he realized these weren't variants at all, they were distinct species. And they were distinct in ways that allowed each species to survive on their specific island more effectively. Birds on islands with hard seeds had thick, strong beaks for cracking them open. Birds on islands with insects had thin, pointed beaks for catching them. Birds on islands with cacti had sharp beaks perfectly suited for accessing the fruit. It was as if each island's finches had been custom-designed for their environment. If God had created each species separately, why would he create nearly identical birds but give them slightly different beaks for different islands? Why would extinct South American animals look like giant versions of the living South American ones? Why would species vary slightly as you traveled from place to place? The patterns suggested something that would have been heretical to say out loud in 1836: species weren't fixed. They changed over time. They adapted.

But having the thought and proving it were very different things. Darwin knew that claiming species could change would be professional suicide without ironclad evidence. Maybe even with it. So when he got home in October 1836, he didn't publish anything. He got married, moved to the countryside, and started working. For twenty years.

He spent those two decades obsessively studying everything he could get his hands on. He studied barnacles for eight years straight, cataloging every species he could find, establishing himself as a serious naturalist who did rigorous, careful work. He bred pigeons in his backyard, documenting how artificial selection could produce wildly different varieties from a single ancestral species. He corresponded with breeders, farmers, gardeners, and anyone else he could find who worked with living things and watched them change. And he collected data on everything he could think of: orchids, worms, coral reefs. He was building an argument so comprehensive that when he finally did publish, no one would be able to dismiss it as speculation.

But it wasn’t just that he was worried he didn’t have enough evidence, he was also scared. His wife Emma was deeply religious, his friends were religious, Victorian England was religious. And the church believed that God created every individual creature just as it existed today. The idea that instead life evolved and adapted went directly against everything the church believed and taught at the time, which made it both scientifically controversial, and socially and professionally dangerous. The last book suggesting species could change had come out in 1844 by Robert Chambers, who published anonymously because he was afraid of backlash. And as he feared, critics tore it apart. It was mocked, and dismissed as unscientific. Darwin’s former mentor Adam Sedgwick called it a foul book and wrote a scathing critique in The Edinburgh Review attacking it. The book was called ignorant, reckless, and accused of corrupting morals, and Chambers kept his authorship secret for the rest of his life. Darwin watched that happen and decided he wasn't ready. Not yet.

He wrote out his theory first in a 35-page sketch and then in an expanded 231 page paper, and showed these initial drafts to his close friend Joseph Hooker, swearing him to secrecy, and told his wife that if he died, she should publish it. And then he just…kept working. Collecting more evidence, anticipating objections, writing and rewriting, on and on and on. His friends kept urging him to publish; Lyell and Hooker both insisted he had enough, that he needed to get it out before someone else did. But Darwin kept saying not yet. Not yet. I need more evidence.

By 1858, he was finally writing what he called his "big book" on natural selection, thousands of pages to make his argument as comprehensive as possible. And he was maybe two years away from finishing, when on June 18, 1858, a letter arrived from halfway around the world.

The letter was from Alfred Russel Wallace, a naturalist collecting specimens in the Malay Archipelago. Wallace had enclosed a short essay and was asking Darwin to review it and, if Darwin thought it was good enough, pass it along to Charles Lyell for possible publication. When Darwin read the essay, his stomach dropped. Wallace had figured it out. Not just evolution, which Darwin knew other people were starting to circle around, but natural selection. The exact mechanism Darwin had been sitting on for twenty years. Wallace had arrived at the same conclusion independently, and he'd done it in a twenty-page essay that Darwin said later could not have been a better short abstract of his own work. Even the terminology matched the chapter headings Darwin had been working on. After two decades of careful preparation, someone else had gotten there too.

Darwin sent the essay to Lyell immediately. "Your words have come true with a vengeance," he wrote. Lyell had been warning him this would happen if he kept waiting, and now, here it was. Darwin was beside himself, and not just about priority. Wallace had sent the essay to him in confidence, trusting Darwin to help him get it published. What was he supposed to do? Sit on it while he rushed out his own book? He couldn't do that. But if he forwarded it for publication as Wallace requested, he'd lose credit for twenty years of work.

Darwin left the decision to Lyell and Hooker. "I would far rather burn my whole book than that he or any man should think that I had behaved in a paltry spirit," he wrote. They came up with what seemed like a fair solution: a joint presentation to the Linnean Society, which was and is one of London's most prestigious scientific organizations for naturalists. They would present Wallace's essay alongside excerpts from Darwin's sketch and an 1857 letter Darwin had written to the botanist Asa Gray outlining his theory. Both documents predated Wallace's essay, which Lyell and Hooker could verify. This way both men would get credit for the independent discovery, Darwin's priority would be established, and Wallace's work wouldn't be suppressed.

On July 1, 1858, the papers were read before the Linnean Society with neither Darwin nor Wallace in attendance. Darwin's infant son had just died, and Wallace was in the Malay Archipelago, completely unaware the presentation was even happening. But when Wallace eventually learned about it months later, he was genuinely delighted. He'd been included in a major scientific presentation alongside Darwin, and that was backed by the most respected naturalists in England. He never expressed any bitterness about the arrangement, not then or later. He was just happy to have contributed.

So natural selection, now one of the most important discoveries of all time, was presented publicly, finally, after twenty years of sitting on it. And what happened after? Pretty much nothing. The Linnean Society's president would later remark that 1858 had been a year in which nothing particularly revolutionary had occurred. The papers were published in the society's journal in August, and the scientific world essentially yawned. One of the most important scientific papers ever published, and it was met with near-total indifference.

What got noticed was what came next. Wallace's letter had finally forced Darwin's hand. He couldn't sit on his theory any longer. Someone else had gotten there independently, which meant the idea was in the air, which meant if he didn't publish soon, someone else might beat him to it entirely. So Darwin abandoned his massive encyclopedic "big book" and started writing what he called an "abstract." A condensed version that would get the essential ideas out quickly. He worked frantically for thirteen months, and on November 24, 1859, On the Origin of Species was published.

The first printing of 1,250 copies sold out immediately. The book was readable, comprehensive, and packed with evidence from every field Darwin had been quietly studying for two decades. He made a carefully argued case built on thousands of observations of his and others that all pointed to one unifying mechanism: natural selection. Organisms vary, and some of those variations make them more likely to survive and reproduce, and over time, this process produces all the diversity of life on Earth. Not separate acts of creation, as was the prevailing belief, but one continuous process of descent with modification. And the response was explosive. Religious leaders were outraged; the idea that humans descended from animals was blasphemy. Cartoons appeared in newspapers showing Darwin with the body of an ape. Public debates erupted, the most famous of which was the 1860 confrontation at Oxford between Thomas Huxley, who became known as "Darwin's bulldog" for his fierce defense of the theory, and Bishop Samuel Wilberforce. Darwin himself stayed home, citing illness. Some historians think his convenient illnesses during controversy were genuinely stress-related. Others suspect he preferred to let his defenders take the heat while he kept working.

But the scientific community's response was more complicated than simple rejection. Many scientists accepted that evolution had occurred because the evidence for change over time was overwhelming once you looked at it. What they resisted was natural selection as the mechanism, because to them it seemed too random and undirected. There was even a period called "the eclipse of Darwinism" where alternative mechanisms were seriously explored, such as Lamarckian inheritance, where traits you acquire throughout your life like large muscles can be passed down to your children. Orthogenesis: that evolution is predetermined; organisms are "programmed" to evolve toward increasing complexity or a specific endpoint. And saltationism: that evolution happens through sudden large jumps rather than gradual change. It wasn't until the 1930s and 1940s, when Mendel's work on heredity was integrated with Darwin's natural selection, that natural selection finally became widely accepted as the primary driver of evolution. That was seventy years after On the Origin of Species was published. Seventy years of debate, resistance, and alternative theories before Darwin was fully vindicated.

Darwin had everything he needed to publish by 1844. All the observations were there. Breeders had known for centuries that selection could change organisms. Fossils showed species had changed over time. Everyone could see that organisms varied. The pieces were sitting in plain sight across different fields. Darwin's contribution was connecting them, seeing that artificial selection, natural variation, the struggle for existence, and the fossil record were all part of one process. And even with mountains of evidence, even with twenty years of meticulous preparation, even after demonstrating that his theory explained everything from species distribution to orchid structure to ancient extinctions, it still took seventy years for the scientific establishment to fully accept it. Not because the evidence was weak, but because the implications were too disruptive. And because it overturned fundamental assumptions about how life worked, humanity's place in nature, and the role of divine creation. At its most basic, it took so long because accepting it meant rethinking everything.

So here we are, looking at pathostasis. And it may seem almost too simple. Too neat. One mechanism explaining hundreds, thousands, of diseases? Surely if this were true, someone would have noticed by now. Surely this would have been figured out already. The same thing people said about evolution when they first encountered it - if species really changed over time, wouldn't we already know that?

But history shows us that the most important scientific discoveries often hide in plain sight, waiting for someone to connect pieces that everyone else keeps in separate boxes. And history also shows us that when those connections finally get made, the resistance can be fierce, and it can last for years. Not because the new theory is wrong, but because accepting it means admitting we've been looking at the problem wrong all along.

What’s unique about pathostasis is that it’s not proposing anything that doesn’t already exist in thousands of peer reviewed studies. We aren’t claiming to have discovered a mechanism medicine hasn't documented. Every arrow in the pathostasis tree — every hormone, every cascade, every downstream effect — comes from peer-reviewed medical research. The Level 0 chemicals are measured in standard labs. The Level 1 and 2 mechanisms are in medical textbooks. Thousands of researchers across decades documented these pieces. What's new isn't any individual piece. What's new is seeing that they fit together.

This matters for how you evaluate the theory. We don’t need to evaluate whether cortisol suppresses Tregs — it’s in the immunology literature. We don’t need to evaluate whether chronic catecholamine elevation causes vasoconstriction — it's in every physiology textbook. The question isn't whether the pieces are real. The question is whether the assembly is correct.

So before we go any further, let's look at this theory the way science is supposed to work, by asking: what makes a theory good? What separates revolutionary science from wishful thinking or speculation? And when we apply those same criteria that eventually validated germ theory, evolution, and plate tectonics to both medicine's current framework and to pathostasis, which explanation actually holds up? And when we apply these criteria, we're not asking whether the pieces are correct, they have all been meticulously and carefully documented over decades by medicine themselves. What we're asking is does the synthesis of medicine’s own data make more or less sense than the way medicine is interpreting it.

Karl Popper established the criteria for what separates science from non-science. His framework is taught in every scientific methodology course and used in courts. When you need to know if something is actually science or just speculation, you use Popper's criteria which consists of these five things: falsifiability, parsimony, predictive power, integrative power, and mechanistic rigor. So let's apply them and see what pathostasis offers compared to medicine's current framework.

Falsifiability

A good theory should make predictions that could be proven wrong

An overly simplified example of something that is unfalsifiable would be the idea that “everything happens for a reason.” This can never be disproven because any outcome can be explained as "this happened because it was supposed to happen.” Whereas for gravity, if you dropped a ball and it fell upward, that would falsify the theory. So in order to be considered falsifiable, which is the gold standard for any scientific theory, there must be things that could make the theory wrong. Let’s look at medicine first.

Medicine's framework:

Medicine has no concept of healing chronic disease. They call it "remission" when it happens, they assume it’s waiting in the wings. And there is no outcome that can prove them wrong. If someone heals they either say they could get sick again at any time, or they say it must have been a misdiagnosis, they must have never been sick. They wave away anything that doesn't fit their narrative of chronic diseases being incurable. This is the definition of something being "unfalsifiable" which is one of the worst offenses in the sciences.

And then there are the things that are falsifiable, and that actually are proven wrong through the data, that medicine steadfastly continues believing anyway: Medicine claims being overweight causes disease, but weight loss alone doesn’t change disease outcomes. People who are thin still get sick, people who are ‘overweight’ are perfectly healthy. And yet none of those things factor into them revisiting their theory, they just keep saying fat is bad. Medicine believes that Alzheimer's patients' neurons are dying, and yet they have lucid periods where all of their lost function comes back for a few hours at a time. Instead of revisiting their theory to see if it actually holds up they just say it's a paradox. Medicine becomes unfalsifiable in their hand waving away anything that doesn't fit their theory. They say things like "it's multifactorial", meaning it's complex, which allows anything and nothing to fit in anywhere. Anything that fits their data they tout, anything that doesn't they ignore, deny, or call it an anomaly or a paradox or multifactorial or complex. But if you have the right theory, there aren't anomalies. There are no fossils in the fossil record that don’t fit Darwin’s evolution. Gravity works the way we expect it to all of the time. We don’t occasionally see things fall upwards or sideways. That's not what you see when a theory is right, you see things following the rules.

There's no observation that can prove medicine's framework wrong because it doesn't actually predict anything. It just describes and names, becoming more and more complex the more they find.

Pathostasis:

For pathostasis, if you can find a single chronic disease where the documented physiological mechanisms in medicine's own literature don't trace back to the Level 0 stress hormones, then the theory fails.

It has a specific, testable prediction, as science demands.

When trying to disprove a theory, sometimes people will do so without engaging with the actual theory, so to be clear, to scientifically test whether pathostasis holds up, requires that you actually use the equation. You can’t falsify Pythagorean theorem without actually applying the equation as intended; you can't "disprove" it by saying "I thought of a triangle where it doesn't work" without actually measuring the sides and doing the math. So if someone tries to falsify pathostasis without actually engaging by tracing the chemicals to the disease in question, then that’s not falsifying, that’s hand waving. But if you use the chemical tree and trace it down and it doesn’t fit, then that breaks the framework.

And people will argue that you can be stressed and not get a chronic illness or perfectly calm and get a chronic illness, which we will address in the next section. But that’s not the theory. The theory is that all chronic diseases trace back to the chemicals at Level 0. That is falsifiable.

Parsimony

A good theory should explain more with less

Medicine treats chronic diseases as separate entities. It catalogs over 100 distinct autoimmune diseases, multiple types of cardiovascular disease, various cancers, different neurodegenerative conditions - each with its own specialty, its own research journals, its own treatment protocols. Each disease has well-documented downstream mechanisms but murky upstream causes. When the origin is unclear, medicine labels it 'multifactorial' - a sophisticated way of saying 'we see associations but don't understand causation.' It's a framework for categorizing disease, not explaining it. Explaining less with more.

Pathostasis: All chronic diseases trace back to one stable physiological state. That state produces direct physiological chemicals, which directly and clearly cascade into many secondary disease mechanisms, which express as specific diseases depending on individual vulnerabilities. Different diseases aren't different problems, they're different expressions of the same upstream process hitting different vulnerable systems. One mechanism, unlimited expression. Explaining more with less.

This is what parsimony demands - when you have two theories that both explain the observations, choose the simpler one. Medicine requires hundreds of separate etiologies. Pathostasis requires one.

Evolution produces staggering complexity, but the mechanism is dead simple. People see the complexity of the output of these processes and assume the explanation must match in complexity. But it never does. The explanation is always a simple engine that runs for a long time and produces elaborate results.

The history of science isn't "we slowly accumulated more and more complexity until we understood everything." It's the opposite. We accumulated complexity, complexity, complexity - and then someone came along and said "what if it's just this one thing" and the whole edifice collapsed into elegance.

Heliocentrism. Evolution. Germ theory. Plate tectonics. Every single one replaced a complicated mess of special cases with a single unifying principle.

Every generation thinks they're the ones who finally got it right. The doctors who believed in humors weren't stupid. They were working within the best framework they had, and that framework had internal logic and institutional support and centuries of tradition. They would have found the idea that tiny invisible organisms cause disease laughable. Ridiculous. Obviously wrong.

And we tell that story now like "of course germs are real, how silly they were" - without ever turning the lens on ourselves and asking: what are we absolutely certain about right now that will look exactly that silly in 100 years?

But what’s difficult for paradigm shifts to take hold is that they require giving something up. Accepting germ theory meant giving up miasma and humoral medicine. Accepting pathostasis means giving up the idea that each disease is its own special puzzle to solve. People don’t like giving things up, especially if they’ve built their identity or career around them.

So we end up in this weird place where complexity signals sophistication, when historically it’s been a signal that you’re missing something. When we thought the universe revolved around the earth, with every new finding we had to add another epicycle, another specific and complex explanation, a bandaid to an incorrect theory. Once we figured out we were actually revolving around the sun, all the bandaids were stripped away, no longer needed once we had the right answer.

Which version is doing that here?

Predictive Power

A good theory should make testable predictions.

It should tell you what you'll observe before you observe it, which allows for scientific testing to be constructed and executed. For example we should see pathostatic chemicals before we see disease onset.

Pathostasis predicts disease clustering patterns that medicine observes but can't explain. It predicts which diseases will cluster based on shared mechanisms. It predicts that addressing the root cause will produce improvements across multiple "separate" conditions simultaneously. It predicts that load reduction will improve outcomes across the board.

It predicts genetic expression patterns - why some people with "disease genes" never get sick, why others get sick without the genes, and why genetic diseases only express under certain conditions.

These aren't post-hoc explanations, they're predictions the theory generates that can be tested.

Medicine's framework mostly describes associations without predicting them. But the overarching theory seems to be a vestige of germ theory, where they’re still looking at things through the pathogen model, assuming that if they can remove or kill the thing they can see, that will cure the disease. For example, medicine predicted clearing amyloid plaques would cure Alzheimer's. They spent billions of dollars over decades of research, and created drugs that had minimal to no benefits, they found patients with plaques that had no Alzheimer’s, and patients without plaques with severe Alzheimer’s. Their prediction was clearly wrong, but did that lead them to revise it? No. The majority of Alzheimer’s research and treatment is still focussed around amyloid plaques.

Medicine predicted lowering cholesterol would prevent heart disease. As we saw, lowered cholesterol not only doesn’t prevent heart disease, it leads to worse death outcomes. Did this incentivize them to come up with a new hypothesis? No. Cholesterol levels are still being medically managed.

If you have a correct theory, and information comes to light that doesn’t fit what you thought, when you dig in further it should further clarify the theory, not muddy the waters. Sometimes things are wrong, and that can lead you to a better truth. But medicine doesn’t have a correct theory, so they just keep adding more and more complexity without adding any more truth.

Neurodegeneration: dormancy vs death

Neurodegenerative diseases are clustered together by one overarching disease marker: neuronal death. Medicine thinks they all cause neurons to die, thus the grouping. But the way that medicine measures neuronal death is by staining certain markers within the cells to see how many are left. And it turns out what this is actually measuring is whether cells are metabolically active, not whether they exist at all. If a cell was dormant, rather than dead, it wouldn't show up on their tests.

Pathostasis predicts that the neurons are dormant due to hypoperfusion, not dead. If you starve a cell of blood and oxygen, it can shut down and wait for the resources to come back.

Lucid periods in Alzheimer's patients, where someone who hasn't recognized their family in months suddenly knows everyone's name and recalls old memories perfectly, would be seemingly impossible if the neurons encoding those memories are dead, but could make a lot of sense if it was caused by dormant cells being turned back on for a while because the blood flow returned.

Here are some other things that don’t make sense if neurons are dead: Good days and bad days across all these conditions. Stress making symptoms worse, and relaxation making them better. Exercise helping across all neurodegenerative conditions. The dramatic placebo responses in Parkinson's we talked about in chapter 2, where patients produced real dopamine and reduced their tremors by 70%. Dead dopaminergic neurons don't start producing dopamine because you believed in a sugar pill. Dormant ones might.

And there are documented cases of ALS reversal, where patients who met full diagnostic criteria — including EMG-confirmed denervation — recovered completely. Their motor function returned. Follow-up EMGs were normal. But because medicine doesn’t have a template for reversing or healing from chronic disease, they assumed these patients must have been misdiagnosed. Which as we discussed above, means the current medical model is unfalsifiable, which is the cardinal sin in science.

So a testable hypothesis that came out of the pathostasis framework is this: neurons that appear dead by current measures may be recoverable if perfusion is restored before true cell death occurs. Which if true would mean that these diseases could be reversible under the right conditions. Which is what those ALS reversals indicate.

This is a testable prediction. And the anomalies medicine keeps dismissing as paradoxes or misdiagnoses are exactly what you'd expect if it's true.

Integrative Power

A good theory should unify observations that previously seemed unrelated or contradictory. It should resolve paradoxes.

Pathostasis does this repeatedly - not by generating new data, but by correctly interpreting medicine's own research.

Disease clustering: Medicine observes that autoimmune diseases cluster but can't explain why. Pathostasis predicts this exactly - they're not separate diseases, they're the same upstream cascade hitting different tissues based on individual vulnerability.

Genetic penetrance: Medicine can't explain why identical mutations express so differently. Why one person with the Huntington's gene get sick at 40, another at 80, another never (we will cover the documented reality that not everyone with Huntington’s gene gets the disease in the next chapter). They call this "incomplete penetrance" and "variable expressivity" - naming the mystery without solving it. Pathostasis explains it: genes load the gun, pathostatic load pulls the trigger.

Cancer metastasis: Medicine knows surgery triggers metastasis. Medicine knows wound healing involves cell migration. Medicine knows cancer cells become migratory. But they treat these as separate phenomena. Pathostasis connects them: surgery triggers wound healing signals → epithelial unjamming → dormant cancer cells become fluid and migratory → metastasis. One mechanism, documented at every step.

Neurodegeneration paradoxes: Medicine defines Alzheimer's and Parkinson's by neuronal death - progressive, irreversible, incurable. But as we saw in chapter 4, the neurons aren't dead. They're dormant from hypoperfusion, and hypoperfusion precedes degeneration in every single neurodegenerative disease. This explains why lucid periods happen, why stress worsens symptoms, why exercise helps, why placebo can trigger dopamine activity in Parkinson's patients. Dead cells don't come back online because you believed in a sugar pill. Dormant cells do, whenever perfusion improves.

Treatment paradoxes: Why do GLP-1s improve outcomes across dozens of "separate" diseases simultaneously? Why does reducing inflammation help both diabetes and depression? Why do stress reduction techniques show benefits across multiple conditions? Medicine has no framework to explain this. Pathostasis predicts it: reduce the root cause, improve all downstream effects.

These clear explanations emerged because once you have the universal law, it organizes the truth. If you don't understand gravity, then you may have one explanation for why we don't float off the earth and another for why two objects of different weight fall at the same speed. Once you have the equation, you can start asking more relevant questions, and all the pieces fall into place.

And luckily for us, medicine has so clearly documented every single bodily process, that now that we have the right equation, the right fundamental law, when we ask the right questions, the answers just present themselves cleanly. One after the other.

Medicine has no equivalent. Each specialty documents its own findings in its own journals, and no one steps back to see how they connect. Cardiology doesn't talk to rheumatology. Oncology doesn't talk to neurology. The same upstream pattern shows up across every field, documented in thousands of papers, and no one puts it together because the framework assumes these are separate diseases requiring separate explanations.

Mechanistic Rigor

A good theory shouldn't just say "this and that are associated." It should specify how, step by step, cause produces effect through documented biological mechanisms.

Every step in the pathostasis cascade uses documented mechanisms. The hormones at Level 0 are measured in standard medical labs. The Level 1 and 2 cascades are recognized disease mechanisms. This isn't speculation, its integration of existing knowledge into a coherent framework. Think about what we walked through with diabetes. Using the pathostasis framework, it’s not mysterious, a moral failing, or even dietary. Pathostatic chemicals signal the body to do exactly what we see in diabetes, sustained high glucose leading to high insulin leading to insulin tolerance/resistance, leading to weight gain, and eventually as we saw in late stage diabetes, to insulin depletion and weight loss. It maps perfectly.

Medicine sees high glucose and thinks it might be diet, or weight issues, or other vague lifestyle issues. They treat it by continuing to flood the system with more insulin which makes the tolerance/resistance even more acute. They have theories about what causes it, and when things don’t fit they just hand wave them away.

Medicine talks about "risk factors" and "associations" and "mechanisms unclear." They find what's broken without explaining what broke it. Pathostasis shows the breaking in progress, mechanism by mechanism.

. . .

Of all the criteria for a good theory, parsimony is often considered the most important - the simplest explanation that accounts for all the data is usually correct. So stepping back and looking at them as a whole, what requires fewer assumptions?

Option A: One unified mechanism - time spent in the pathostasis - that manifests differently based on genetics, duration, intensity, and which system fails first.

Option B: Hundreds of separate diseases with mostly unknown causes that just happen to cluster together in predictable patterns and all correlate with stress through unclear mechanisms and respond to similar interventions for unexplained reasons.

The answer seems obvious. But if pathostasis is so clearly supported by medicine's own data, why hasn't it been recognized? Why are we still treating hundreds of separate diseases instead of one underlying mechanism?

The objections will come, just as they came for Darwin. Some will be scientific, some institutional, some purely reactive. But there's one objection that towers above all others - the one that seems so obvious it might have occurred to you already:

Of course sick people show the same dysregulated hormones we see in pathostasis, being ill IS stressful to the body. How do we know pathostasis causes disease rather than disease causing pathostasis?

It's a fair question. Maybe THE question. Because if we can't prove the direction of causation - if we can't show that pathostasis comes first - then this entire framework collapses.

So let's look at what happens when we track people from childhood, before any disease develops, and see what actually comes first...