The State of Disease

We see autoimmunity as the immune system gone rogue. Why is this person's immune system attacking their own body? The research focuses on understanding the mechanisms of attack: which tissues are targeted, which inflammatory pathways are activated, what's different about these attacking immune cells. And the treatment follows this research, attempting to turn the immune response off in targeted ways so it stops attacking the body.

But every healthy body has cells that attack its own cells, called autoreactive immune cells, which serve useful purposes like clearing damaged cells and debris. Which means that what's happening in autoimmunity is similar to what we saw in cancer, in that it's a normal cellular process running without its normal controls. In healthy people this process is kept in check by regulatory T cells (Tregs) that suppress them before they can cause damage in healthy tissue. But in autoimmunity, a few things happen simultaneously: Treg production drops meaning there are fewer overall Tregs, and the remaining Tregs function less efficiently, meaning they are less able to regulate the way they’re meant to. And there is something called IL-2, which feeds both Tregs and autoreactive immune cells, which are the ones that always exist to attack your own tissue. And when Tregs are diminished, there's more IL-2 to go around and so the autoreactive cells get a lot more of it, which effectively ramps them up. You end up with a situation that's kind of like removing the police while simultaneously arming everyone in a crowd. The autoreactive cells that are normally suppressed can now attack freely and have more fuel to do so. Which means the question we should be asking is: why does the monitoring fail like we saw in cancer?

So this is what’s happening in autoimmune diseases, and yet we seem surprised that autoimmune diseases cluster together. About 25% of people with one autoimmune condition develop at least one more - and for some conditions, the risk of developing a second is 4 to 10+ times higher than the general population. But when you understand what we just laid out, that autoimmune disease comes from systemic monitoring failure plus autoreactive activation, of course you'd see multiple autoimmune conditions develop. If your entire immune monitoring system is compromised while autoreactive cells are ramped up throughout your body, why would it only affect one tissue type? Or occur in one isolated spot in the body? Ibuprofen doesn’t just target inflammation in your hand, or your gut, it’s system wide because that's how the body works. The mystery isn't why they cluster - it's why we expected them not to.

We have identified between 80 and 100 'different' autoimmune diseases, which as a whole affect 1 in 10 people. We keep discovering new ones every year, adding to the list like we're cataloging species. Hashimoto's thyroiditis. Graves' disease. Type 1 diabetes. Rheumatoid arthritis. Lupus. Sjögren's syndrome. Each one gets its own specialist, its own treatment protocol, its own research funding. As if each one is a separate phenomenon requiring separate explanation. It's like discovering that water can make cotton wet, and wool wet, and silk wet, and declaring you've found 100 different wetting diseases instead of recognizing that water makes things wet.

And autoimmune clustering is just the beginning of a much bigger pattern; disease clustering extends far beyond autoimmune disease. We use the term "comorbidity" when diseases occur together - for example if you have both diabetes and heart disease, or depression and Alzheimer's. We think of "comorbidity" as separate diseases that just happen to coincide. But the clustering is far too consistent and predictable to be explained by chance alone.

In fact, over half of US adults have multiple diagnosed health conditions. It's not unusual to see patients with 5-7 conditions, and older adults having 5+ conditions means an average of 50 prescriptions, 14 different doctors, and 37 visits per year. And they’re clustering in predictable patterns. Depression with stroke, chronic pain, and Alzheimer's. Diabetes with heart disease, depression, and kidney disease. Asthma with cardiovascular disease, COPD, and depression. The more conditions you have, the more likely you are to develop more. When you look at the actual patterns, what you see is that certain diseases cluster in specific constellations. Alzheimer's, congestive heart failure, COPD, diabetes, and cancer cluster together at rates far beyond what chance would predict. About 80% of people with Parkinson's disease will develop dementia during the course of the disease. If you have depression you are about 40% more likely to experience a stroke. The list goes on and on, across every body system you could name.

And neurodegeneration clusters the same way. Alzheimer's and Parkinson's share so much pathology that at autopsy, about 60% of Alzheimer's patients have Lewy bodies - the "hallmark" of Parkinson's. MS patients have about twice the risk of developing Alzheimer's disease. The boundaries between these "different” diseases blur the moment you look closely. We draw boundaries between them, but the bodies keep showing all of them bleeding into each other.

When researchers analyzed 10 million patients to look at the pattern of comorbidities, they identified very well-defined disease clusters. Metabolic syndrome clusters together: obesity, high cholesterol, hypertension, diabetes. Autoimmune and inflammatory conditions cluster together. Mental health disorders cluster with chronic pain. Cardiovascular diseases cluster together. The pattern is there, clear and consistent, across millions of people. We see the pattern, but since we treat each disease as its own discrete entity with its own specialist, we never step back far enough to see what's creating the cluster.

Disease state

So let's do that now. If we look across all of medical research, and then step back so we can see the full picture, it becomes clear that there's a specific physiological state that precedes all chronic disease. Medicine has identified some of its markers: high blood sugar, hypertension, inflammation, and obesity, and noticed these appear upstream of hundreds of conditions. But we stopped there, treating these markers as causes rather than symptoms. We never asked what was upstream of those markers. What could explain why they were happening in the first place?

Let’s think about a volcano for a minute. A volcano erupts and it creates a lava flow and ash. We aren't studying the lava at the base of the volcano as different from the lava 2 miles away, in different departments. We aren't studying the ash and wondering what could produce this weird substance without connecting it back to the volcano. We all intuitively understand that would be ludicrous. We look first to the volcano. (the body in this case: it’s the thing that's producing all of these disparate results.) What caused the eruption? What was happening over time that caused the pressure to build up the way it did. The way a volcano explosion affects the surrounding landscape depends on the features of that landscape, but no one is studying how it affects trees vs how it affects lakes vs how it affects grass as though those are different things. It's all: what was in the blast radius when the volcano went off and how do we FIRST stop the lava flow, and THEN clean up the rubble.

But when it comes to disease we’re instead studying how the grass was affected by the lava flow down to the molecular level in one department, and how the lake was affected by the lava in another department. Both are independently seeing lava upstream of their diseases. But they aren’t talking to each other, and they aren’t looking at the volcano. If we were looking at the body as the originator then we would be looking for what was similar in each disease, not looking at them each as their own separate mystery.

When we look at the full picture to see where disease actually begins, maintains itself, and progresses, a clear physiological state emerges. The chemicals being maintained in this state cause Tregs to downregulate and become less effective which leads to autoimmunity. In cancer, this same chemical state suppresses the NK cells and cytotoxic T cells that normally eliminate aberrant cells thus stopping the abundance of cells that leads to the natural selection process that produces cancer. And when we look below at all the rest of our chronic disease categories, we will see it cleanly explains them as well.

From here forward we'll call this upstream disease state pathostasis. Patho meaning disease, stasis meaning steady state. Pathostasis is the disease state medicine has been meticulously documenting piece by piece but has never assembled whole.

So what exactly is pathostasis? It’s a coordinated biological response that has existed in every vertebrate animal for 500 million years, and is one of the most conserved systems in all of evolutionary biology. It's what happens when the animal’s adaptive and useful acute threat response, which is designed to activate briefly then resolve once a threat passes, gets stuck on.

Every value in this table is in our research data, our medical textbooks, our curriculum, we’ve just never been able to look across silos and recognize that this chemical configuration IS the chronic disease state, not a risk factor for it or a contributor to it, but the actual mechanism itself.

While in this state, due to prolonged exposure to these chemical changes that our bodies weren’t evolved to maintain, your clearing systems fail, your immune system dysregulates, inflammatory processes go haywire, and disease develops. And though it seems random: why did person A get cancer while person B got depression? What we can tell from the data is that it isn't as random as it may seem. Let’s think about it mechanistically. Imagine a chain. If a chain were to get rusty and weathered, and someone dropped something heavy on it, is it just going to break where the thing hit it? Or is it going to break at its weakest point - where there's the most rust, where the latch is damaged, where it's been rubbing against something? It can be either or both. Where your system got the blow, and/or where there was already damage or vulnerability. This is what we see happening with the development of disease; it shows up where there's already vulnerability - genetic predisposition, prior damage, existing strain, or it develops where it received the blow, like lung cancer in smokers. And then, once that system starts failing, those failures create more stress on adjacent systems in that same cluster, and the next most vulnerable point in that system breaks.

This is why cardiovascular diseases cluster with kidney disease and stroke risk, for example. Hypertension develops because your blood vessels are constricted due to the elevation of norepinephrine, epinephrine, vasopressin and cortisol from pathostasis, and then the damage from that creates more load on your heart, and heart disease develops. Then that heart damage affects your kidney’s ability to function optimally, and kidney disease develops. The vascular damage affects your brain, and stroke risk increases. It's not four separate diseases. It's progressive failure in an already-compromised vascular system, each failure creating conditions for the next.

The same pattern plays out in metabolic clusters. The chemical cocktail of pathostasis creates the exact conditions for diabetes: increased glucose production, and insulin tolerance/resistance. When this is expressed, this metabolic dysfunction affects the cardiovascular system, and heart disease develops. The inflammatory state from both affects more metabolic processes. The pattern cascades through related systems, all connected through the same metabolic infrastructure that was vulnerable to begin with.

Autoimmune conditions cluster together, which makes sense because if your immunity is already a weak point, then it’s easier for further autoimmune diseases to tack on to the first. Again, these are not separate diseases randomly occurring in the same person; they're progressive failure in an interconnected body system.

This explains everything we find puzzling about comorbidity. It explains why "comorbidity" rates are so absurdly high - they're not actually CO-morbidity, they're the same morbidity expressing in related systems. It explains why treating each disease separately downstream doesn't stop new ones from developing - because you're not addressing the upstream state that's causing the failures.

So let’s look at how this plays out across the spectrum of diseases. To read this tree, you can look at the letters on the chemicals in Level 0, and the numbers on the level 1 and 2 disorder/disease mechanisms, and see how those map to the example diseases below. This tree shows that chronic diseases cascade down from level 0 chemistry. Levels 1 and 2 map out commonly studied cascade pathways medicine has documented but never unified. The disease list is a representative snapshot, not an exhaustive list.

You will notice how 'real' diseases, 'functional' disorders, and 'psychiatric' conditions all trace back to the same Level 0 chemicals? That's because these divisions never existed in biology, only in medical specialization. An emergency room doctor, a psychiatrist, and a rheumatologist could all be treating the same patient for what are defined as three different diseases, chest pain, depression, and arthritis, when in fact they're all looking at different expressions of the same Level 0 chemistry.

So let’s walk through what we're looking at here. At the very top, Level 0 is the chemical picture of the body in pathostasis like we showed in the first chart, and it explains in a clean domino effect, every single chronic disease we know about. Notice how cortisol (A) appears in almost every disease pathway? Or how immune dysfunction (mechanisms 8, 9, 10) shows up everywhere? These are the common threads we missed by studying diseases separately. In levels one and two we are showing byproducts of level zero, downstream cascades that medicine talks a lot about and sees causing a lot of other stuff.

Inflammaging

And we have gotten SO CLOSE. Sort of. Here are a list of the terms medicine has used to connect siloes:

Inflammaging: when they see increased inflammation in aging. Metaflammation: chronic low-grade inflammation from metabolic disease. “Metaflammation is characterized by the same mechanisms underpinning inflammaging.” Was a sentence published in Nature endocrinology about the effects of inflammaging.

Psychoneuroimmunology: the field studying psychology, neurology, and immunology. Neurogastroenterology, Gut-brain axis, Immunometabolism. Cardiovascular-kidney-metabolic syndrome: The American Heart Association proposed this name because heart, kidney, and metabolic disease keep appearing together. And after naming it they almost immediately moved to start including the liver as well. Researchers have started calling Alzheimer’s “type 3 diabetes” because they found insulin resistance in the brain.

Whenever they look across they see the connections, that’s where all these mashups come from. It’s like saying we have a toe-ankle axis, or an esophageal-stomach axis. The body is connected, it was always connected, they just haven’t had the opportunity to step all the way back to study it as such. So let’s walk through what we see when we do.

Diabetes

You can think of diabetes as the poster child for pathostasis. It is literally just: what happens in the body when these chemicals are elevated and stay elevated? Diabetes. Let’s walk through it.

Elevated cortisol (A), epinephrine (C), and glucagon (E) at Level 0, these chemicals tell your body to produce glucose because threat means you need immediate energy. So that gives you chronic hyperglycemia (5).

That excess glucose forces insulin production higher and higher, trying to shuttle all that glucose into cells. But over time, those cells build a resistance (tolerance, because most any receptor that’s being flooded in the body will downregulate its uptake) to insulin's signal.

So now that you've built up a tolerance to insulin, the pancreas has to work overtime trying to overcome that tolerance by producing even more insulin. This chronic overstimulation eventually exhausts the pancreatic beta cells that produce insulin.

When they fail, insulin production drops; that's F at Level 0, depleted insulin, which also leads to weight loss, which should be a hint that weight gain itself is downstream of something else. Early disease causes weight storage (gain), late disease causes weight loss. This insulin drop combined with the ongoing glucose elevation from A, C, and E, plus the inflammation from mechanism 10, you get the full picture of Type 2 diabetes at position 13 in Level 2. It's not a separate disease entity, just pathostasis playing out. The tree shows exactly how A, C, E, F → 5, 10 → 13. Every step is documented in medical literature.

Obesity: symptom not cause

Notice obesity is on the level 2 list, secondary cascades. This means it’s a symptom of disease, as we just saw with diabetes, not the cause. In fact, why don't we look at obesity a little more closely; use obesity as a case study to see how this tree can shake out the truth that we’ve been missing, since it's blamed for so much. We see that a lot of disease happens in people who are 'overweight,' and so we conclude that weight gain causes disease. So how well does it correlate?

27% of thin people have metabolic profiles that look just like what medicine thinks is caused by obesity. They actually label them “metabolically obese normal weight” which is…something. We are so sure weight is the cause that we label people obese who aren’t to make sense of the contradictory data.

And then there are the obese people who are perfectly healthy. 35% of them. They call them “metabolically healthy obese”.

So we’ve got over ¼ of thin people who are sick in the way we attribute to being CAUSED by fat, and ⅓ of obese people NOT being sick in the way we think is caused by fat, and the response is to…label them a different category and continue believing fat causes disease.

We've noticed that belly fat specifically correlates with certain diseases, so we declare belly fat is especially dangerous, rather than asking WHY the body would preferentially store fat around organs during certain conditions. But JUST losing weight doesn’t actually help. In 2004 when Klein et al. removed 28-44% of abdominal fat via liposuction, they found no change in insulin sensitivity, no change in inflammatory markers, and no change in blood pressure, glucose, insulin, or lipid concentrations. And this was about 12% of overall body fat removal. They then tracked these same people for 1.5 to 4 years after the liposuction and these same results persisted. If fat were really causing disease, wouldn't you expect losing it to provide some consistent benefits?

Given that losing fat alone doesn’t seem to change much, and being fat is neither enough nor necessary to cause disease, let's think about what's actually happening at Level 0 and Level 1 when weight gain occurs in pathostasis. You have elevated glucagon (E) and cortisol (A) driving chronic hyperglycemia (5). Your body is producing more glucose than it needs because your threat response thinks you need immediate energy available. That glucose has to go somewhere. Insulin’s job is to get the cells to open the door and let in glucose, so when glucose rises like this, initially, insulin rises as well, to shuttle it into cells. But just like your body needs more and more alcohol to get you drunk the more you drink, the more insulin the system has, the more insulin is needed to perform the same amount of glucose shuttling. So the cells become tolerant (medicine calls this resistance) to insulin's signal, and now you have high glucose and high insulin circulating in your bloodstream. Insulin does two other things as well. It promotes fat creation, and stops fat from breaking down. So when there are chronic high levels of insulin in the blood it makes it very easy to gain weight and very hard to lose it.

And cortisol which is also elevated in pathostasis specifically promotes visceral fat accumulation - fat around your organs. In acute danger having readily accessible energy stores near your vital organs makes evolutionary sense. You might need that energy fast. The problem is that when you’re in pathostasis and these chemicals persist, your body just keeps packing fat into your midsection month after month, year after year. You're stuck in storage mode without an efficient release mechanism.

So where did this idea come from then? If there isn’t really any medical basis for it? It turns out the idea of body fat as the cause of disease came from one guy. The same guy who proposed that eating fatty foods was bad. In the 1950s, a physiologist named Ancel Keys started pushing what he called the diet-heart hypothesis, which posited that eating saturated fat raises cholesterol which he thought caused heart disease. He had access to data from 22 countries and in an effort to prove his idea, he only used data from the 6 that supported his hypothesis. Rather than reexamine his idea once he saw the data didn’t cleanly fit, he just ignored the findings that didn’t match. He was ridiculed by the scientific community for his antiscientific methods. Two epidemiologists even published a devastating critique pointing out that Keys had data from 22 countries but only used 6, and that he was studying a "tenuous association" rather than proof of causality. In it they also showed that if he had included all 22 countries the correlation essentially disappeared. In fact they were even able to show that if you picked a different set of 6 countries you could show the exact opposite effect that he was trying to prove. After being ridiculed he wanted to prove his detractors wrong, so he decided to conduct a study. But he used the same cherry picking methods from his original study, chose 7 countries where the data best fit what he wanted to see, used cohorts that weren’t representative of their countries, used inconsistent measurement methods, and through this research “proved” his hypothesis. This somehow worked and got him onto the board of the American Heart Association, and eventually on the cover of Time magazine in which he promoted "the evils of fat" including both body fat and dietary fat as one unified evil.

Keys was also the person who named BMI Body Mass Index, which later got adopted by the NIH and then used by the world health organization to recognize obesity as an epidemic. BMI actually came from one statistician in the 1830s who was trying to define “the average man”. To determine this he gathered data of Scottish and French military men’s height and weight, and came up with a formula that he felt represented it: weight/height^2. This was just based on his observation that these European military men didn’t tend to get wider as they got taller. So no actual medical or even scientific basis and it wasn’t intended for medical purposes. It was just a curious statistician trying to figure out the mathematical correlations between human physical characteristics. But when Keys renamed it the Body Mass Index, it somehow took hold, and now every doctor's office in America uses it to determine if people are diseased.

Which means many people labeled 'overweight' by these arbitrary standards aren't sick at all. They're just larger than a formula designed around 19th century European military men said they should be. Their blood markers are fine, their energy is fine, their bodies are functioning exactly as they should. We even have a name for it, “medically healthy obese”. Meaning we know fat doesn’t always cause issues. And yet because of this deeply entrenched belief we continue to pathologize normal human variation in body size. Meanwhile, the people who ARE sick, the ones actually in pathostasis, aren't sick because they're storing fat. They're storing fat more than healthy people because they're sick.

So this one guy single handedly vilified body fat, dietary fat, coined BMI leading to it becoming a clinical measurement tool, and convinced everyone cholesterol was bad—all without any actual evidence. And the question isn't really why this one guy thought these wrong things; people think wrong things all the time. The question is how and why we bought in, amplified his wrongness, and protected it for seven decades. And why it's all still largely believed and implemented today across the globe. Semmelweis had the right data and was dismissed because it didn’t fit the framework. Keys had the wrong data and was amplified because it did.

Keys was the co-principle investigator on a study meant to prove his hypothesis. They studied over 9000 people in controlled settings where they could actually measure dietary compliance, from 1968-1973, and they found two key things. One, that lowering saturated fat did in fact reduce cholesterol. And two, that reducing cholesterol didn’t reduce heart death. In fact the participants in the study who had greater reductions in cholesterol had higher risk of death. The inverse of what his hypothesis predicted. So what happened with this study? They just…never published it. It sat in the lead investigator Ivan Frantz’s basement until his son found it in 2011. When asked why they never published it Frantz said “We were just disappointed in the way it came out.” The most rigorous study ever done to test his hypothesis proved it was wrong, and they didn’t like the results so they just sat on it. Frantz’s son helped get it published in 2016, but by then it was all so institutionalized there was really no reversing course. It got published and completely ignored.

What research has shown is that cholesterol is actually good for you and necessary for immune function and brain function, and many other vital processes; every cell membrane requires it. It is so vital that 80% of your cholesterol is produced “in house” in your body. When you are in pathostasis your body produces more of it because it’s so beneficial, but we saw elevated cholesterol in sick people and assumed correlation meant causation. And we have spent decades trying to lower people’s cholesterol. Statins are a front line drug for people with heart disease and statins do actually provide benefits. And we assume this is because of the cholesterol lowering function, but statins also reduce inflammation and improve endothelial function. When we use drugs that ONLY reduce cholesterol, we see no benefits at all on cardiac health. When ezetimibe (a non-statin cholesterol lowering drug) was added to statins, it lowered cholesterol even further but showed no additional mortality benefit. Same with PCSK9 inhibitors, they lower cholesterol dramatically but don't reduce death rates. The drugs that lower cholesterol without the anti-inflammatory effects don't save lives. Statins which have anti-inflammatory effects do. The mechanism we attribute the benefit to isn't actually the mechanism producing the benefit.

One of the most common criticisms you will hear about new theories or ideas is that 'correlation doesn't equal causation' and yet here we've built an entire treatment paradigm around mistaking a symptom for a cause. We saw a correlation - obesity occurs alongside disease - and declared it causal, with no mechanistic explanation for why having more adipose tissue would cause such diverse conditions. Having more fat cells doesn't cause diabetes any more than having a runny nose causes a cold. They're both just observable symptoms of an upstream process.

Cancer

We already walked through cancer in detail. Now look at how it maps: the immune suppression (8) and impaired clearance (17) we spent a chapter on trace straight back to Level 0 — elevated cortisol (A), cytokines (N), histamine (M). The Warburg metabolism shows up at mechanism 7, but as we discussed, it's a marker of stressed cells, not a driver. The real pathway is A, C, N, H → 8, 10, 17. Everything we discovered in chapter three is right here in the tree.

Neurodegenerative diseases

Remember how we saw neurodegeneration clustering earlier - Alzheimer's and Parkinson's sharing so much pathology that half of Alzheimer's patients have Lewy bodies at autopsy, MS patients developing Alzheimer's at 2-4x the normal rate?

Let’s step back like we’ve been talking about and see if there are any clues to follow. If we step back and look at what the research shows across all of these conditions, the same thing comes first in every single neurodegenerative condition: reduced blood flow (hypoperfusion). Hypoperfusion precedes neurodegeneration in Alzheimer's, Parkinson's, ALS, Huntington's, MS, and frontotemporal dementia.

The pathostatic chemicals we've been tracking - norepinephrine, epinephrine, vasopressin, cortisol - all cause vasoconstriction at mechanism 1. That's their job during acute threat: shunt blood toward muscles and away from non-essential functions. But when these chemicals stay elevated chronically, the vasoconstriction becomes chronic too. And the brain regions that get hit first are the ones supplied by small terminal vessels, the last stops on the vascular supply chain, or the areas with the highest metabolic demands and the least backup blood supply.

And we already know hypoperfusion causes dementia. That's what vascular dementia IS - cognitive decline from reduced blood flow. They diagnose it all the time. They even have a category called 'mixed dementia' for when they can't cleanly separate what's vascular from what's Alzheimer's, because the boundaries blur so often. So they know hypoperfusion causes cognitive decline. They know Alzheimer's shows hypoperfusion before plaques appear. Each specialty documented hypoperfusion in their own disease, published it in their own journals, and never looked across.

We think the neurons are dead, it’s right in the name “neurodegeneration. But these diseases are full of things that shouldn't be possible if the standard model is right. Lucid periods in Alzheimer's patients who suddenly recognize their family after months of confusion. Good days and bad days across all these conditions. Stress making symptoms worse. Exercise helping. The dramatic placebo responses in Parkinson's where patients reduced tremors by 70%.

If the neurons are dead, none of this should happen. Dead cells don't come back because you had a good day or believed in a sugar pill. But we don’t have another explanation, so these observations get filed away as anomalies rather than clues.

We have been trying to clear amyloid plaques and Lewy bodies, treating these protein aggregates as the cause of neurodegeneration. But patients can have extensive plaques with no cognitive symptoms, and severe dementia with minimal plaques. The proteins aren't causing the disease. They're accumulating because the clearing systems we talked about in chapter 3 are failing, for the same reason they fail everywhere else in pathostasis: the body's resources are being redirected toward survival, not maintenance.

Hypoperfusion is just one clue. One that you can see when you step back and see what these related diseases have in common. And this is where we need the regular medical model to step in and drill down into this idea. If it comes up empty we step back and look again. But this requires us to take new ideas seriously. Vasoconstriction has been studied…a bit. But it’s hard to get funding when something doesn’t fit what people already think. We have spent decades and tens of billions of dollars trying to clear amyloid plaques, the prevailing theory for Alzheimer's, which has produced exactly zero effective treatments. Meanwhile vasoconstriction has received almost no funding and has therefore barely been studied.

· · ·

Everything we just walked through has been meticulously documented in pieces for over a century. Every mechanism. The elevated hormones, the physiological effects, the cascading failures, all of it measured and published in thousands of studies across every medical specialty. The pieces are all there, we just hadn’t before stepped back far enough to see it's all connected.

But as we established above, correlation isn’t causation. So let’s look next to see what’s been documented about what comes first. Disease, or pathostasis.