That question stayed with me after my recent interview with Dr Dov Gebien. I had invited him to discuss his work on sudden infant death syndrome and his hypothesis that, in some infants, the terminal event may involve sustained contraction or dysfunction of the diaphragm.

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I approached the discussion as a specific question about SIDS. But as I listened to the proposed mechanism, I realised the implications could extend well beyond infancy. If a diaphragm can become inflamed, fatigued or mechanically locked in an infant, I have to ask whether the same thing could occur in an adult. More specifically, whether it could explain a small but important subgroup of sudden deaths during sleep, particularly when the heart appears structurally normal at autopsy.

I am not presenting this as established fact. I am showing how I arrived at a hypothesis that I believe deserves proper investigation.

The Label May Be Hiding an Assumption

I think the terminology itself creates a blind spot.

When a young person dies suddenly and no obvious cause is found, the event is often placed within the category of sudden cardiac death or sudden arrhythmic death syndrome. That wording immediately directs attention towards the heart.

I then assume that an undetected electrical disturbance—perhaps ventricular fibrillation—was responsible. That may often be correct. A person can have an inherited channelopathy or electrical instability without visible structural disease at autopsy. I do not dispute that.

But there is an important difference between saying an arrhythmia is possible and saying it has been demonstrated.

When no structural heart disease is found, no rhythm was recorded and no witness observed the physiological sequence, I am looking at an inferred mechanism. The person died suddenly, the heart stopped, and the event was therefore classified as cardiac.

The difficulty is that every terminal event eventually involves the heart stopping.

That does not tell me what failed first.

The Australian Data Raised the First Concern

I looked at prospective Australian and New Zealand data on sudden cardiac death among children and young adults.

The largest diagnostic category was unexplained death.

Other cases had recognisable pathology. Coronary disease, myocarditis, hypertrophic cardiomyopathy, dilated cardiomyopathy and arrhythmogenic cardiomyopathy provide plausible cardiac explanations. Aortic dissection provides a clear vascular one.

But the unexplained category is different.

These were predominantly young people, many of whom underwent detailed postmortem examination. Despite that, no clear cause was identified. Yet the deaths remained framed as cardiac.

What caught my attention was the proportion occurring during sleep. Sudden collapse during exercise fits naturally with certain cardiac mechanisms. Exertion increases heart rate, sympathetic drive and myocardial demand. In someone with an arrhythmogenic substrate, that stress may expose the problem.

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Not because personal suffering makes someone scientifically correct. It does not. But it told me something about the person I was speaking to. Dr Dov Gebien was willing to expose the most damaging part of his own history without protecting his status or polishing his reputation. He could look directly at failure, accept responsibility, and then ask what could be learned from it.

That openness matters in research, because many scientific failures begin with the opposite behaviour. People defend their position, their institution or their expertise long after the evidence has begun to raise uncomfortable questions. Dr Gebien’s experience seems to have stripped away that instinct for self-protection. He asks questions from outside the approved framework because he has already lost professional standing and survived it.

I found that significant, because the interview was ultimately not only about the diaphragm. It was about who is permitted to ask scientific questions.

Emerging SIDS Discovery 2025 - Substack >

When Science Depends on Who Is Speaking

Dr Gebien is not an established SIDS professor working within a major academic programme. He is a clinician with emergency medicine experience, pathology training, and a hypothesis that emerged from listening closely to a patient.

That immediately creates a problem.

Modern science claims to judge ideas by evidence. In practice, ideas are filtered first by hierarchy. Who published it? Which institution supports it? Is the researcher already recognised in the field? Does the mechanism fit comfortably within the existing literature?

If the answers are wrong, the work is often not refuted. It is simply ignored.

That appears to be what happened here. Dr Gebien described years of contacting clinicians and researchers with little meaningful engagement. The exception was Dr Paul Goldwater in Australia, an established SIDS researcher willing to consider the argument, challenge it, and ultimately collaborate.

That is how science should work. Listening is not endorsement. Reviewing a hypothesis does not require accepting it. It requires only enough discipline to separate the quality of the question from the status of the person asking it.

The disturbing point is that the medical establishment often does not reject unconventional science after investigation. It rejects the investigator before the investigation begins.

Goldwater, Paul N., and Dov Jordan Gebien. "Metabolic acidosis and sudden infant death syndrome: overlooked data provides insight into SIDS pathogenesis." World Journal of Pediatrics 21.1 (2025): 29-40.

The Patient Who Could Not Breathe In

The hypothesis began with an unusual clinical history.

A medical colleague described recurrent episodes, beginning in childhood, in which he woke from sleep with severe bilateral chest and rib pain. He felt what he called a powerful bear hug around the chest and could not inhale. Trying harder to breathe in did not help. There was complete resistance to inspiration.

He survived because, as a child, he tried something counterintuitive. He breathed out.

By his account, forced expiration released the pain at once and restored his breathing. The episodes recurred over several years, but he had found a manoeuvre that ended them.

The limitations are obvious. This was a retrospective account, not a monitored event. No diaphragm electromyography, no ultrasound, no respiratory tracing. We cannot prove what happened.

But the description raises a legitimate question. Could this have been a sustained contraction of the respiratory muscles, particularly the diaphragm?

Most people understand cramp in the leg or foot. They do not think of the diaphragm the same way. Yet the diaphragm is skeletal muscle. It can fatigue, become inflamed, twitch, spasm, and develop abnormal patterns of excitation.

A hiccup is already proof that the diaphragm can spasm. The more serious proposal is that, under particular conditions, the muscle might enter a sustained contraction and fail to relax.

If that happened, the lungs would not necessarily be blocked. The brain might still be trying to breathe. The problem would be that the respiratory pump itself had become mechanically fixed.

The Second Pump

Medicine pays enormous attention to the heart as a pump. When the heart fails, circulation stops and death follows quickly.

The diaphragm is the body’s other vital pump.

When it contracts and descends, it creates the pressure change that draws air into the lungs. If it becomes weak, fatigued or fixed in contraction, ventilation can fail even when the airway is open and the respiratory centre is still signalling.

This points to a third category of respiratory arrest that may be under-recognised. We recognise central failure, where the brain stops generating an adequate respiratory signal. We recognise obstructive failure, where airflow is blocked in the upper airway. But there is also pump failure, where the muscles of ventilation no longer work.

That is the conceptual gap Dr Gebien is asking medicine to examine.

Why Sleep May Be the Vulnerable Period

The connection with sleep matters. During rapid eye movement sleep, much of the skeletal musculature is functionally suppressed. This stops us acting out our dreams. The accessory muscles of respiration are affected too, leaving the diaphragm to carry a greater share of the work.

A healthy adult tolerates this. The situation may be different in an infant with immature respiratory muscles, a patient with a viral illness, someone with systemic inflammation, or a person with pre-existing neuromuscular weakness.

If the diaphragm is already fatigued or inflamed, sleep may remove the reserve that normally compensates.

The proposed sequence is not hard to follow. A vulnerable diaphragm enters sleep already under strain. Accessory activity falls. The workload rises. The muscle becomes unstable, fails to relax, or moves into sustained contraction. Ventilation stops, hypoxia develops and cardiac arrest follows.

That remains a hypothesis. It has not been demonstrated during a sudden unexplained death. But it is coherent enough that it should not be dismissed without direct investigation.

Could Some Sudden Adult Deaths Begin With Respiratory Arrest?

This is where the discussion moved beyond SIDS. When adults die suddenly in their sleep, the default assumption is often cardiac arrhythmia. That is reasonable in patients with known cardiomyopathy, coronary disease, inherited channelopathy or structural heart abnormalities.

But what about the person who dies during sleep with no convincing cardiac pathology?

An arrhythmia may leave little evidence at autopsy, so it remains the presumed explanation. Yet primary respiratory arrest may also leave little structural evidence, particularly if the diaphragm is never examined microscopically. A routine postmortem may find a diaphragm that looks normal to the naked eye while missing inflammation, fibre injury or contraction-related changes visible only on histology.

The point is not that diaphragm cramp now explains sudden adult death. That would be an irresponsible leap. The point is that the differential may be artificially narrow, because one of the critical organs of breathing is not investigated adequately.

If an unexplained death occurs during sleep, with a structurally normal heart and no major airway obstruction, I think it is reasonable to ask whether the respiratory pump was examined properly.

At present, the answer is often no.

The Possible Link With Post-Viral Illness

The part of the interview that caught my attention most strongly was diaphragmatic myositis. We recognise myocarditis because the heart is muscle. We recognise skeletal myositis when patients develop weakness, pain and raised muscle enzymes. Yet we seldom ask whether inflammatory muscle injury reaches the diaphragm.

This may be particularly relevant after viral infection.

I repeatedly see patients with post-COVID or long COVID patterns describing breathlessness, chest tightness, lower rib pain, exercise intolerance, or a sense that they cannot take a satisfying breath. The CT is normal. The echocardiogram is normal. Pulmonary embolism has been excluded. Troponin is normal. Lung function does not explain the severity of the symptoms.

The usual conclusion is that nothing major has been found.

That is not the same as showing that nothing is wrong.

If the diaphragm or intercostal muscles are inflamed, weak or failing to coordinate, standard cardiopulmonary investigations may miss it. Oxygen saturation can stay normal at rest. Routine imaging may show nothing. Even creatine kinase can be normal in localised or low-grade muscle inflammation.

This gives a plausible phenotype: breathlessness driven not by lung parenchymal disease but by dysfunction of the respiratory musculature.

Again, plausibility is not proof. Breathlessness and chest pain after COVID have many possible causes, including autonomic dysfunction, dysfunctional breathing, microvascular disease, deconditioning, cardiac disease, pulmonary pathology and anxiety. Diaphragm dysfunction should not replace that differential.

It should be added to it.

How This Could Be Investigated

The next step does not require a grand theoretical programme. It requires targeted measurement.

In symptomatic patients, diaphragm ultrasound can assess excursion, thickening and asymmetry. Respiratory muscle strength can be estimated with maximal inspiratory pressure and sniff nasal inspiratory pressure. Phrenic nerve studies and diaphragm electromyography may help in selected cases. MRI may show muscle oedema or inflammatory change, though accessibility and interpretation remain limiting factors.

The most informative studies would compare patients with unexplained post-viral breathlessness against matched controls, using diaphragm ultrasound, respiratory muscle testing, inflammatory markers and symptom provocation during exertion.

Autopsy practice needs reconsideration too. In unexplained deaths during sleep, systematic diaphragm sampling should be considered rather than relying on gross appearance. Histology should look for inflammation, fibre degeneration, contraction-band injury and previous scarring.

The hypothesis can be tested. It remains uncertain not because testing is impossible, but because the question has not been prioritised.

The Larger Lesson

I came away with two conclusions.

The first is scientific. The diaphragm may be a blind spot in the investigation of sudden respiratory arrest, unexplained deaths during sleep, and post-viral breathing difficulty.

The second is institutional. Science becomes weaker when evidence is filtered through status before it is examined on merit.

Dr Gebien may ultimately be wrong about major parts of this theory. Some cases attributed to diaphragm cramp may turn out to be terminal hypoxia, sleep paralysis, airway obstruction or something else entirely. That is precisely why the work needs investigation rather than passive dismissal.

I do not think the responsible position is to declare that diaphragm contracture explains SIDS, sudden adult death or long COVID breathlessness.

I think the responsible position is this: the respiratory pump has been neglected, the proposed mechanism is biologically plausible, and the tools to investigate it already exist.

The next question is not whether the hypothesis came from an approved expert.

The next question is whether we are prepared to look.

Timecodes

0:00 Intro
1:16 Why Revisit SIDS and Diaphragm Cramp?
3:04 Dr Dov Gebien’s Background, Addiction and Recovery
9:13 “Patient Zero”: Waking Up Unable to Breathe In
13:49 How One Childhood Case Led to a SIDS Hypothesis
15:36 Could Some Deaths During Sleep Be Respiratory, Not Cardiac?
17:00 REM Sleep and Respiratory Muscle Vulnerability
24:33 From Hiccups to Sustained Diaphragm Contracture
30:34 SIDS Risk Factors Through the Lens of Diaphragm Fatigue
37:01 Why Scientific Ideas From “Outsiders” Are Often Ignored
40:37 Dr Paul Goldwater and the Vaccine-Risk Controversy
50:27 Diaphragmatic Myositis, Long COVID and Unexplained Breathlessness
57:07 Risk Stratification and Better Respiratory Monitoring
1:06:26 How Could Diaphragm Injury Be Detected in Adults?
1:09:02 What Future Research and Autopsy Practice Should Examine
1:14:29 Practical Prevention Ideas and Closing Thoughts

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Between 2016 and 2025, Crohn’s disease and ulcerative colitis rose markedly in NHS Hospital Episode Statistics. In my current analysis, Crohn’s disease is up around 48% above the pre-pandemic baseline, ulcerative colitis is up around 73%, and combined inflammatory bowel disease activity is up about 60%. Yet several functional or non-inflammatory gut codes did not rise in the same way. Irritable bowel syndrome went slightly down. Functional intestinal disorders fell. Malabsorption did not show the same rise.

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That asymmetry is why I keep coming back to the gut. Not because the gut is fashionable. Not because every problem reduces to diet. And not because I think inflammatory bowel disease is being created from nothing. I keep coming back because if the intestine were simply seeing “more of everything,” the low-acuity functional codes should have risen too. They did not.

Still, the objection matters. Other gastrointestinal activity also rose. Gallstones rose. Pancreatitis rose. Appendicitis rose. Some hernia codes rose. Several of these are not immune-mediated inflammatory bowel diseases, so their rise forces me to take the broader post-pandemic gastrointestinal activity tide seriously. I cannot lazily say, “IBD rose, therefore COVID caused IBD.” The better question is narrower and more interesting: why are inflammatory bowel codes rising strongly while functional bowel codes are not?

The disciplined interpretation

The strongest interpretation is not that all gut disease is rising. It is more specific than that. The inflammatory bowel disease signal appears selective against functional bowel disease. It is not fully selective against the wider gastrointestinal tide. That distinction matters.

If everything had moved in the same direction — IBS, functional bowel disorders, malabsorption, Crohn’s, ulcerative colitis, gallstones, hernias, appendicitis, pancreatitis — I would be much more cautious. That would look like general healthcare activity, service recovery, coding changes, or delayed access. But that is not the pattern. The inflammatory codes are moving strongly. The functional codes are not.

So the question becomes whether the gut is showing us a shift toward inflammatory disease being unmasked, amplified, or made more complex after the pandemic. This is where I use the word unmasking. I do not think repeated exposure creates inflammatory bowel disease from nothing. That is too simplistic. The data do not prove that, and the biology does not require it. The more plausible model is that people with subclinical gut inflammation, genetic susceptibility, autoimmune tendency, prior gut symptoms, impaired barrier function, or microbiome disruption are being pushed over a threshold they were already close to.

There were already embers. Repeated inflammatory exposure may be petrol on those embers.

Crohn’s and ulcerative colitis are not the same disease

Crohn’s disease and ulcerative colitis are often grouped together as inflammatory bowel disease, but they are not the same condition. Crohn’s is often patchy, can affect different parts of the gut, and can involve deeper layers of the bowel wall. Ulcerative colitis usually affects the colon and rectum, and tends to involve the inner lining in a more continuous pattern.

Different diseases. Different anatomy. Different behaviour. Yet both are rising. That raises the possibility that the common denominator is not one specific diagnosis. It may be a broader inflammatory pressure being applied to vulnerable intestinal tissue — and that tissue then fails in whichever pattern that individual was already predisposed to.

That is the idea I am testing. A framework for broad increased intestinal inflammation.

Why the intestine matters beyond digestion

Most people still picture the gut as plumbing. Food goes in, nutrients are absorbed, waste comes out. That is true, but it is not the important part of this story.

The intestine is one of the body’s largest immune surveillance systems. Every day it has to decide what to tolerate and what to attack. It is exposed to food antigens, bacteria, fungi, toxins, viral particles, immune cells, inflammatory mediators, and the metabolic products of the microbiome. It has to get that judgement right constantly.

If that system becomes destabilised, there is no reason to assume the consequences will remain confined to the bowel. The intestine is a living border between the outside world and the immune system. If that border becomes inflamed, leaky, or immunologically unstable, the effect may extend beyond gut symptoms. It may influence fatigue, joint pain, skin disease, eye inflammation, neurological symptoms, immune flares, and broader inflammatory patterns.

That is why I do not see this as simply a gastroenterology issue. I see the gut as a possible amplifier — not just another organ affected by the pandemic, but one of the places where post-pandemic inflammation may be sustained, multiplied, and exported to the rest of the body.

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Several possibilities had to be considered. A heart attack was plausible. A pulmonary embolism after a long-haul flight was reasonable. A dangerous arrhythmia, severe respiratory failure or another acute cardiovascular event could not be excluded.

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I deliberately waited before discussing the case. I did not want to force a medical explanation onto a situation where the essential facts were still unknown. The subsequent report that he had suffered an aortic dissection changed the clinical question completely.

I was no longer looking at a clot travelling to the lungs or a blocked coronary artery. I was looking at catastrophic rupture of the largest blood vessel in the body.

That matters, because I have been watching aortic disease for several years. Long before this case, I had become concerned that inflammatory changes associated with the COVID era could eventually influence the trajectory of aneurysms, dissections and other major vascular events.

I am not claiming that COVID infection or vaccination caused Lindsey Graham’s death. I do not have the evidence to make that conclusion. What I am saying is that his death draws attention to a disease process I already believed required much closer investigation.

Why Aortic Dissection Is So Catastrophic

The aorta carries blood directly from the left side of the heart to the rest of the body. With every heartbeat it takes a high-pressure pulse and must expand and recoil without tearing. The aortic wall is therefore not a simple tube. It contains elastic tissue, smooth muscle and several structural layers that let it withstand enormous mechanical stress over a lifetime.

In a dissection, a tear develops in the inner lining. Blood is forced into the wall itself, separating its layers and creating a false channel.

Once that begins, it can spread rapidly.

The dissection may cut off blood flow to the brain, heart, kidneys, intestines or limbs. It may rupture into the chest or abdomen. If it ruptures around the heart, blood fills the pericardial sac and stops the heart from filling. If it ruptures freely, blood loss can be overwhelming within minutes. There is no way to compress the aorta from outside the body. Survival depends on rapid recognition, immediate blood-pressure control and, in many cases, highly complex emergency surgery.

This is why someone can appear reasonably well and then deteriorate with extraordinary speed.

In Graham’s case, the reported delay in responders reaching him was therefore clinically significant. I cannot know when the dissection began, when it ruptured, or when cardiac arrest occurred. But with an aortic catastrophe, every minute matters.

The Part of the Aorta Most People Never Hear About

What interests me most is not the tear itself. It is what may have weakened the wall before the tear occurred. Large arteries such as the aorta are too thick to draw all their oxygen and nutrients from the blood flowing through the central lumen. The outer wall is supplied by a network of tiny vessels called the vasa vasorum.

I think of these as the blood vessels that feed the blood vessel.

If the vasa vasorum become inflamed, narrowed, thrombosed or otherwise damaged, the outer aortic wall receives less oxygen. Smooth-muscle cells may become dysfunctional or die. Elastic fibres may deteriorate. The wall may gradually lose its ability to tolerate pressure.

This does not mean inflammation automatically produces a dissection. Most dissections arise in people with recognised risk factors such as hypertension, age-related degeneration, inherited connective-tissue disease, bicuspid aortic valve or an existing aneurysm.

My concern is different.

I am asking whether inflammation affecting the aortic wall or its vasa vasorum could accelerate weakness in people who were already vulnerable. That would not create an entirely new disease. It could take an existing one and make it progress faster.

Why I Keep Returning to COVID

Evidence of vascular inflammation during and after COVID infection has been present since the early stages of the pandemic. PET imaging studies identified inflammatory activity in large arteries, including the aorta, particularly after severe disease.

COVID is not simply a respiratory infection. It can affect endothelial cells, coagulation, immune regulation and vascular tissue. It can trigger thrombosis, complement activation, macrophage recruitment and persistent inflammatory signalling.

I have also examined reports of myocarditis, pericarditis and aortic inflammation following vaccination. Individual case reports cannot establish population-level causation, but they can offer histological clues for patterns of inflammation.

One reported case, in a previously healthy young man, described myocarditis, pericarditis and fatal aortic dissection 16 days after mRNA vaccination. What mattered was not the timing. It was the reported inflammation involving the aortic wall and the vasa vasorum.

For me, that provides a possible pathological template. It suggests a mechanism by which an immune response to spike exposure through infection or vaccination, might affect the small vessels supplying the aorta.

A plausible mechanism is not proof and that distinction is critical.

But when a plausible mechanism exists alongside a changing population mortality pattern, I do not believe the responsible response is to dismiss the question. I believe it is to investigate it properly.

Balbona, E. J., et al. "Case of Myocarditis, Pericarditis, and Fatal Aortic Dissection following Covid-19 mRNA Vaccination." Biomed Sci Clin Res 3.3 (2024): 01-08.

Case Of Myocarditis Pericarditis And Fatal Aortic Dissection Following Covid19 Mrna Vaccination

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The Mortality Trend Does Not Reassure Me

Recent US mortality data show that deaths involving aortic dissection declined for a period, then began rising again before the pandemic. The increase did not begin in 2020, and COVID cannot explain the entire trend.

But the pandemic years create an additional question.

COVID disproportionately affected older people and those with hypertension, diabetes, obesity and cardiovascular disease, the same broad population in which aortic-dissection risk is concentrated. A substantial number of vulnerable individuals died during the acute pandemic. Under ordinary circumstances, I might have expected this mortality displacement to flatten subsequent aortic-dissection mortality, at least temporarily.

Instead, the upward trajectory continued.

That does not prove acceleration. Changes in diagnosis, coding, survival, imaging and population structure may all contribute. But I do not think it should be waved away without deeper analysis.

My hypothesis is that repeated inflammatory vascular injury may be accelerating aortic disease in a subset of susceptible people. I do not know the size of that subset. I do not know the speed of progression. I do not know whether infection, vaccination, repeated spike exposure or other pandemic-related factors matter most.

Those uncertainties are precisely why research is required.

What I Would Want From the Autopsy

A routine statement that someone died from an aortic dissection is not enough to answer the question I am asking.

I would want the aorta examined systematically by an experienced cardiovascular pathologist, with multiple samples taken from the tear, the surrounding intact wall, the ascending aorta, the arch, the descending thoracic aorta and apparently normal regions.

I would want careful assessment of the elastic layers, smooth-muscle cells, medial degeneration, fibrosis, microhaemorrhage and the vasa vasorum.

Most importantly, I would want to know whether inflammatory cells were present in intact tissue away from the rupture. Inflammation immediately beside a catastrophic tear may simply be secondary to haemorrhage and tissue destruction. It cannot automatically be read as evidence of pre-existing inflammatory disease.

I would want immunostaining to identify macrophages, T cells, B cells, plasma cells, complement deposition and microthrombi. I would want infection excluded and tissue retained for molecular testing.

Even then, a single autopsy could not prove a pandemic-wide phenomenon. But it could identify a pattern worth comparing across a larger case series.

That is how meaningful science begins: not with certainty, but with careful observation, reproducible pathology and a question that can be tested.

What People Can Do Now

While the research continues, the established risk factors still matter. Everyone with hypertension should know their blood pressure and take responsibility for controlling it. Smoking should be stopped. Diabetes, cholesterol and established vascular disease should be managed properly.

Anyone with a family history of aneurysm or dissection should ask whether screening is appropriate. People with Marfan syndrome, bicuspid aortic valve, inherited connective-tissue disorders or a known aneurysm need structured surveillance.

Stimulant drugs that sharply raise blood pressure create an avoidable risk, particularly in someone with existing aortic disease.

The emergency warning also needs to be understood. Sudden severe chest, back or abdominal pain—particularly if it is tearing, ripping or unlike anything experienced before—requires immediate emergency assessment.

This is not a condition to watch at home.

A Signal Is Not a Conclusion

Lindsey Graham’s death is a tragedy. It should not be turned into proof of a political or medical narrative that the evidence cannot support. But neither should the chance to learn from it be discarded because the questions are uncomfortable.

I see this case as a signal, not a conclusion.

I see an established lethal disease, a rising mortality trajectory, evidence that COVID can affect large blood vessels, and a biologically plausible pathway involving inflammation of the aortic wall and the vasa vasorum.

What I do not yet see is the systematic pathological investigation required to connect those pieces responsibly. That is where the next stage of research must go: fewer assumptions, better autopsies, more detailed vascular pathology, serious comparison between pre-pandemic and post-pandemic cases.

When someone dies suddenly, I cannot change the outcome. But I can ask whether the tissue left behind holds information that might protect someone else.

That, for me, is the purpose of examining this case.

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From the beginning, the subject was almost impossible to discuss. The structures were labelled a conspiracy. The embalmers were dismissed. The photographs were questioned. And because doctors and pathologists were not reporting the same thing, many people assumed it could not be real.

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That argument has become increasingly difficult to sustain.

The discussion has moved beyond whether embalmers are genuinely seeing these structures. The questions that matter now are what they are made of, when they form, why they appear to have become more common since 2021, whether they can develop before death, and what biological mechanism could create such material inside the vascular system.

To explore this, I spoke with two people who have approached the mystery from very different directions: Tom Haviland, who has spent four years systematically surveying embalmers around the world, and Dr Shankara Chetty, whose clinical reasoning throughout the pandemic has centred on understanding disease mechanisms through careful observation of unusual patterns.

What emerged went far beyond conventional clotting.

How One Question Became a Four-Year International Investigation

Tom Haviland did not begin as a clotting researcher or medical scientist. He is a retired US Air Force major with degrees in mathematics and electrical engineering and a master’s degree in computer resources and information management.

His involvement began after watching the documentary Died Suddenly in 2022. The film included testimony from embalmers who said they were removing unusual white fibrous structures from the deceased.

Tom was initially sceptical.

But one statement caught his attention. An embalmer named Wallace Hooker reportedly showed photographs of the structures to approximately 100 embalmers at a professional conference in Ohio. When he asked how many had encountered similar material, almost the entire room reportedly raised their hands.

Rather than accept the claim, Tom contacted the Ohio Embalmers Association. Within 24 hours he had spoken to its vice president, Woody Wilson, who confirmed that he too had encountered these structures. That was the moment Tom decided the observation needed systematic investigation.

With the assistance of Laura Kasner, he developed an international survey and distributed it through funeral director associations and directly to more than 1,700 funeral homes worldwide. Across four annual surveys between 2022 and 2025, 808 embalmers participated.

The results were striking. Embalmers across multiple countries reported unusual white fibrous structures, often describing them as distinctly different from the conventional blood clots they had seen earlier in their careers. This work has now progressed to publication, in a paper examining self-reported observations of these structures in embalmed corpses across five countries between 2022 and 2025.

That does not resolve the mystery. But it moves the discussion beyond a handful of isolated photographs.

Haviland, Thomas F., Laura Kasner, and Daniel Santiago. "Self-Reported Observations of Unusual White Fibrous Structures in Embalmed Corpses: Multi-Year Survey Results from Embalmers in Five Countries, 2022–2025." International Journal of Innovative Research in Medical Science (IJIRMS) 11.07 (2026).

Why Embalmers Are Uniquely Positioned to See This

One of the central questions I raised was why embalmers would see these structures when doctors and pathologists apparently do not. The answer may lie in the embalming procedure itself.

To preserve a body, an embalmer introduces embalming fluid into the vascular system while removing blood. Before the pandemic, Tom explained, this could usually be achieved through a single injection site. But when a body contains these fibrous structures, some embalmers report needing multiple access points — neck, axilla, pelvis and legs — because the vascular system is obstructed.

According to Tom, a procedure that once took an hour to an hour and a half can now take two to two and a half hours when these structures are extensively present.

This is critically important.

A pathologist performing a conventional postmortem does not flush the entire vascular system this way. A clinician does not inspect long sections of major vessels directly. The embalmer may therefore occupy a unique observational window that no other profession routinely has.

I have always found it surprising that this point receives so little consideration. That doctors are not seeing these structures does not mean embalmers cannot be. They are doing something entirely different.

Are These Structures Forming Before Death?

Shankara made clear that he believed at least some of these structures were likely to have formed ante-mortem — before death. His reasoning rested partly on their distribution and morphology. Some appear to form long casts of particular vessels, complete with branching extensions corresponding to vascular tributaries. The question then becomes obvious: how could a structure several feet long exist inside a major vein without producing catastrophic obstruction?

This was one of the most fascinating parts of our discussion.

Shankara proposed that the structures may not initially obstruct the entire vessel. Blood could continue flowing around them while they gradually develop along the vascular wall. That would explain how an individual might carry an extraordinary structure through a large vessel without the symptoms expected from an acute, completely occlusive thrombosis.

We also discussed material reported from living patients. In one case shared with me by a whistleblower, images appeared to show pale material removed from the inferior vena cava during a procedure. I have always been careful to say that I cannot independently corroborate the full clinical history, because I do not know the identity of the source. Even so, the images raised an important question: if comparable structures are genuinely being recovered from the living, a purely postmortem explanation becomes inadequate.

The critical scientific challenge is to document such cases properly.

What Are These Structures Actually Made Of?

The word “clot” may itself be misleading.

When most doctors think about a thrombus, we think of fibrin, platelets and blood cells. Yet these white fibrous structures are often described as rubbery, elastic and remarkably resistant to manipulation.

Previous analyses have suggested an unusual protein composition. My own interest deepened when proteomic findings showed unexpectedly high levels of haemoglobin components, alongside fibrin-related and inflammatory proteins.

That raised an immediate question: why would haemoglobin be present in such high concentrations inside a pale, fibrous vascular structure?

Haemoglobin should normally be contained within red blood cells. If large quantities of globin proteins are being incorporated into these structures, something must first be happening to the red cells themselves.

That observation opens an entirely different biological pathway.

The Red Blood Cell Connection

I explored whether red-cell damage could be central to understanding these structures.

COVID-19 has been associated with abnormalities affecting red blood cells, including immune-mediated haemolysis in some patients. Once red cells are damaged or destroyed, haemoglobin and globin chains can be released into the circulation.

But free haemoglobin is potentially toxic, so the body has sophisticated mechanisms to clear it. This is where macrophages and monocytes become important.

Certain circulating monocytes act as scavengers, clearing damaged red cells, haemoglobin and cellular debris. I have become increasingly interested in whether a particular immune phenotype involving thrombospondin-related monocyte activity could be relevant here.

The possibility I raised was this: what if a single immune cell is simultaneously processing damaged red-cell material, altered fibrin proteins and spike-related material?

Could these normally separate biological processes converge inside the same immune environment?

And could repeated exposure then drive an abnormal immune response against modified globin or fibrin structures?

This is not yet proven. But it offers a coherent explanation for something that otherwise makes little sense: the incorporation of substantial haemoglobin-related protein into a large, pale, fibrous structure.

Could the Immune System Be Building the Structure?

This became one of the central ideas in our discussion.

I have increasingly wondered whether we should stop thinking of these structures as conventional clots that simply grow abnormally large. Perhaps, in at least some cases, we are dealing with an immune-mediated protein assembly occurring within the vascular system.

Imagine damaged red blood cells releasing haemoglobin. Imagine fibrinogen undergoing structural modification. Imagine persistent or repeated exposure to spike protein from infection or another source. Now place those components within an activated immune environment of monocytes, macrophages, platelets, neutrophils and endothelial injury.

The result may not be a conventional thrombus at all.

It may be a composite structure incorporating proteins from several different biological systems.

That could explain why proteomic studies have identified such an unusual mixture of fibrin-related proteins, haemoglobin chains, inflammatory proteins and other components.

The key question is whether these proteins are merely trapped passively within the structure or actively participating in its formation.

That distinction is fundamental.

The Spike Protein Question

Inevitably, the discussion turned to spike protein. This remains one of the most controversial aspects of the subject, but it cannot be excluded simply because it is politically uncomfortable.

There is experimental evidence that spike protein can interact with fibrin and alter clot architecture. There is also evidence that spike can persist in tissues and immune cells after infection. The broader question is whether repeated exposure could contribute to an environment in which abnormal protein aggregation, endothelial dysfunction, immune activation and altered coagulation converge.

I do not think the right question is simply, “Did COVID cause these clots?” or “Did vaccination cause these clots?”

Those questions are too crude.

The better question is whether repeated spike exposure — from infection, vaccination, or both in different individuals — could act as one component in a multi-step process involving immune priming, red-cell injury, altered fibrin, abnormal protein aggregation and impaired clearance.

If so, susceptibility would almost certainly vary between individuals. That may be one reason why some people develop profound abnormalities while others apparently do not.

Has India Observed Unusual White Clots?

One particularly interesting part of the discussion centred on observations emerging from India. Unlike many Western countries, India deployed a range of COVID-19 vaccine platforms rather than relying predominantly on mRNA technology, including adenoviral vector vaccines, inactivated whole-virus vaccines and others. This naturally raises an important scientific question. If similar white fibrous structures are being reported across populations exposed to different vaccine platforms, then perhaps our focus should move beyond a single product or technology. We discussed whether the common denominator might instead be prolonged or repeated exposure to spike protein itself, irrespective of how that exposure occurs, or whether the wider inflammatory and immune responses triggered by different platforms could converge on similar biological pathways.

At this stage, we simply do not know the answer. It remains entirely possible that the phenomenon is related to repeated spike exposure from infection, vaccination, or both, but it is equally plausible that differences between vaccine platforms, adjuvants, lipid formulations, vector biology or the immune responses they generate may influence risk in different ways. Rather than assuming a single explanation, we felt that the observations from countries using multiple vaccine technologies provide an opportunity to compare biological outcomes across platforms. If similar clot structures are consistently identified despite fundamentally different vaccine designs, that would point researchers towards shared downstream mechanisms. If important differences emerge, they may help identify which biological pathways are most relevant. Either way, the international experience offers a valuable natural experiment that deserves careful scientific investigation rather than assumption.

Could Repeated Exposure Be the Critical Event?

The idea of immune priming grew more important as our conversation progressed. The first exposure may not create the final pathology as it may instead establish an altered immune state.

If, during that initial exposure, immune cells encounter spike protein alongside damaged haemoglobin, altered globin chains or structurally modified fibrin (for example adduction changes through charged lipid nanoparticles), those proteins could become incorporated into the immune response.

Then comes re-exposure as the immune system meets spike again — but this time within an environment already primed with modified self-proteins.

Could the response then expand beyond spike itself?

Could it begin targeting altered globin chains, fibrin or other proteins present during the original inflammatory event?

This would create a sequential process rather than a single catastrophic event and that distinction matters, because these structures may take time to develop.

The Amyloid and Prion-Like Question

The discussion also entered more challenging territory: whether some components of these structures have amyloid or prion-like properties. This does not mean people with these structures have Creutzfeldt-Jakob disease. That would be an unjustified leap as the process would have to be occurring in the brain.

The more precise question is whether proteins within the structures have misfolded into beta-sheet-rich configurations, and whether some possess seeding behaviour — the capacity to promote further misfolding.

This matters because fibrin itself can undergo amyloid-like structural changes under certain inflammatory conditions. Spike-derived peptides have also demonstrated amyloidogenic properties experimentally.

If abnormal protein conformations are present, it could explain the structures’ extraordinary physical properties: their strength, elasticity, persistence and possible resistance to normal fibrinolysis. It could also mean these are not simply excessive coagulation, but a form of pathological protein assembly.

That would fundamentally change how we think about them.

Why the Absence of Symptoms Is So Important

One of Shankara’s most important observations concerned the apparent lack of symptoms in some individuals reported to have extensive structures. A person can apparently die with a long fibrous structure occupying a major vessel without that structure being identified as the immediate cause of death.

At first glance, that seems impossible.

But if the structure develops slowly along the vessel wall while preserving a channel for blood flow, it becomes more conceivable. The danger might arise only when it reaches a critical size, changes shape, fragments, triggers secondary thrombosis or interferes with flow in a vulnerable location.

Which raises another possibility: perhaps we are seeing only the end stage of a much longer process. If that is true, there may be living individuals with earlier forms of these structures who remain completely undiagnosed.

That is one of the most serious implications of the entire discussion.

The Problem of Medical Silence

Tom spoke about the frustration of embalmers who feel their observations have been ignored. I understand why scientists are cautious as extraordinary claims require strong evidence. Photographs are not enough and surveys cannot establish causation. Self-reported observations are vulnerable to selection bias and samples collected after death create obvious problems of interpretation.

All of that is true but none of it justifies refusing to investigate.

The scientific response to an unusual observation should not be automatic belief. Nor should it be automatic dismissal. It should be measurement and investigation of the phenomena.

If hundreds of embalmers across several countries report structures they consider unusual, the obvious response is to establish a proper collection protocol and determine exactly what they are.

The failure to do this has allowed speculation to fill the vacuum left by absent research.

What Needs to Happen Next

By the end of our discussion, one point was clear: the next phase has to be far more rigorous.

We need fresh samples collected under controlled conditions, ideally before embalming fluid is introduced. We need precise anatomical documentation of where each structure was found. We need the medical history of the individual — recent infections, vaccination history, medications, inflammatory disease, malignancy and cause of death.

We need proper control samples: conventional ante-mortem thrombi, ordinary postmortem clots and pre-pandemic specimens wherever they are available. We need blinded histology, proteomics, spectroscopy, electron microscopy and biochemical assessment.

We need to know whether the structures contain intact cells, cellular remnants, fibrin, fibrinogen, globin chains, immunoglobulins, complement, platelet proteins, neutrophil proteins, extracellular matrix components or amyloid-like material.

And critically, we need to know whether every structure now being called a “white clot” is actually the same biological entity.

My suspicion is that they may not be so easy to classify.

We Have Moved Beyond the First Question

For years, the debate was dominated by one question: are these white fibrous structures real?

I think we have moved beyond that.

Embalmers have reported them and surveys have documented those reports. Samples have undergone preliminary biochemical investigation. Published papers are beginning to appear.

The question now is what these structures actually represent.

Are they unusual postmortem clots? Vascular casts? Abnormal thrombi? Immune-mediated protein assemblies? Amyloid-rich fibrin structures? Or are we grouping several completely different pathological entities under one name?

We do not yet know, but after years of following this subject, I believe the most important mistake we could make would be to assume that because something sounds extraordinary, it therefore does not deserve investigation.

Science advances when observation forces us to reconsider what we thought we already understood.

The embalmers made the observation. Tom Haviland documented the signal. Shankara Chetty asked how such structures could form in living circulation.

Our task now is to connect those observations to the underlying biology.

Because if these structures are forming before death, if they are developing slowly within the circulation, and if they represent an abnormal convergence of immune activation, red-cell damage, fibrin modification and protein aggregation, then the implications extend far beyond the embalming room.

That is the question we now have to answer.

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At face value, this looks like a contradiction. How does someone trying so hard to slow ageing and improve health end up with an autoimmune disease attacking the stomach lining? Many people will reduce this to a lifestyle story, or a vaccine story, or a “biohacker gets humbled” story. I think all of that misses the more important clinical pattern.

The question that interests me is not whether Bryan Johnson developed autoimmune gastritis. It is whether he represents a wider category of people whose immune systems were already predisposed to autoimmunity, and in whom something then disturbed the balance enough to make another autoimmune condition visible.

That is where this becomes important.

Autoimmunity Is Often Already There Before It Is Diagnosed

One of the mistakes we make in medicine is treating autoimmune disease as if it appears from nowhere. Clinically, that is rarely how I think it behaves.

In many patients, autoimmunity is more like a smouldering fire. The person may look well. Their blood tests may be mostly reassuring. They may not yet have the full clinical syndrome. But beneath the surface there can already be immune tension: inflammatory cells pushing in one direction, regulatory cells trying to hold them back.

This is where regulatory T cells matter. I think of them as the immune system’s peacekeeping force. Their role is not to eliminate inflammation, but to stop the immune system from turning its weapons against the body. When that regulation works, a person can appear stable. When it fails, the underlying inflammation can suddenly become clinically obvious.

That is the crucial point. The inflammation may not have suddenly appeared. The control system may have failed.

Why Thyroid Disease Matters

In Bryan Johnson’s case, the important background detail is that he was already known to have autoimmune thyroid disease. That matters, because autoimmune diseases cluster. One autoimmune condition increases the likelihood of another, because the underlying problem is not only the organ being attacked. It is the immune system’s tendency to lose tolerance.

Autoimmune thyroid disease and autoimmune gastritis are not random strangers. They are recognised to overlap. So when I hear that someone with autoimmune thyroid disease later develops autoimmune gastritis, I do not think, “This is completely unexpected.” I think, “This person may already have had an autoimmune tendency, and something may have unmasked another part of it.”

That is different from claiming one exposure caused everything. I am not saying that. I am saying the immune terrain matters. A person with existing autoimmunity is not the same as a person with no autoimmune history. That distinction should have mattered during the pandemic, and it still matters now.

The Sacchi Study Was a Warning Signal

This is why the Sacchi study remains important to me. It was a small Italian study of healthcare workers, and it was criticised for its size. But its strength was never size. Its strength was timing.

The researchers had blood samples before vaccination, then followed participants after mRNA vaccination. That design is very difficult to recreate after the fact. Once a population has already been vaccinated or infected, you cannot go back and reconstruct a clean baseline.

In the Sacchi study, 77 healthcare workers with no known prior COVID infection and no known autoimmune disease were analysed. The key point is this: among those who were ANA-negative at the start, 22 of 52 developed new ANA antibodies during follow-up. That is about 42% of the initially ANA-negative group. Across the whole analysed cohort, it was 22 of 77, or 28.57%.

That distinction matters. It is not a small detail. If someone was already antibody-positive at baseline, they cannot become newly positive. The proper clinical question is what happened to those who were negative at the start.

I need to be clear: ANA positivity does not mean someone has an autoimmune disease. I would never make that leap. Many people carry autoantibodies without any clinical autoimmune diagnosis. But it is equally lazy to pretend new autoantibody formation means nothing. It is a biological signal. It tells us the immune system has shifted.

The Sacchi study did not prove autoimmune disease. It showed movement toward measurable autoreactivity after repeated immune stimulation.

Sacchi, M. C., et al. "The onset of de novo autoantibodies in healthcare workers after mRNA based anti-SARS-CoV-2 vaccines: a single centre prospective follow-up study." Autoimmunity 56.1 (2023): 2229072.

The Spike Question Is Broader Than Vaccination

This is where the public discussion goes wrong. People divide into camps. One side says the vaccine must be responsible, while the other says the vaccine could never be responsible. Both positions are too simplistic.

My concern has always been broader than vaccination alone. The spike protein was central to the disease process in COVID-19, and I was focused on autoimmunity very early in the pandemic, because I did not believe severe COVID was merely a viral pneumonia. It involved immune dysregulation, macrophage activation, delayed or impaired interferon responses, tissue injury, and autoimmune-type mechanisms.

That understanding made me cautious about using the same spike protein as the target for repeated immune stimulation across entire populations. The question was never whether vaccination could produce antibodies. Of course it could. The question was whether repeated spike-directed stimulation could, in susceptible individuals, disturb immune regulation.

Infection can do this. Vaccination may do this in some people. Recurrent infection combined with repeated immune stimulation may do it more strongly in certain cohorts. That is the more serious model, and focusing only on the vaccine misses the fact that SARS-CoV-2 infection itself can also disturb immune balance.

So if someone already has autoimmune thyroid disease, and then experiences repeated immune perturbations through infection, vaccination, inflammation, stress, or other triggers, it is biologically plausible that another autoimmune condition becomes clinically visible.

That is the argument. Not certainty. Plausibility.

What I Think May Have Happened

In Bryan Johnson’s case, my clinical research interpretation is that he may have had an autoimmune-prone immune system already. His thyroid disease was the visible part. The later autoimmune gastritis may have been another expression of the same underlying vulnerability.

Something then shifted the balance. It may have been infection. It may have been spike-directed immune stimulation. It may have been repeated immune exposures. It may have been the natural progression of autoimmune clustering. I do not know, and anyone claiming to know with certainty is overstating the evidence.

But I do think this case fits a pattern: a person with pre-existing autoimmunity develops another autoimmune condition after a period of major immune challenge.

That is exactly the kind of pattern medicine should be tracking carefully.

The Failure Was the Lack of Honesty

The deeper problem is not immunology. It is trust.

Bryan Johnson has said he regrets taking the COVID vaccine, because he wanted to trust the systems producing the science, and felt they influenced him rather than simply giving him the data. That is a powerful statement, because it captures what many people now feel.

I have said this repeatedly: the public should have been told the truth. They should have been told what was known, what was uncertain, who was clearly high-risk, who was low-risk, and where the gaps were. That would have been honest medicine.

Instead, the public was given a slogan. “Safe and effective” became a political instrument rather than a careful scientific statement. Once mandates entered the picture, uncertainty became inconvenient. If you want to mandate an intervention for healthy, low-risk people, you have to present it as virtually risk-free. That was never a scientifically mature position.

The price of that approach is now being paid in public trust.

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Why This Still Matters

Some people want to move on from these questions. I think that is impossible. Autoimmune diseases do not disappear because society grows tired of the pandemic. If spike-related immune dysregulation, recurrent infection, or repeated immune stimulation has contributed to autoimmune unmasking in some people, this issue will keep surfacing.

The right response is not panic. It is not denial. It is investigation.

I want proper longitudinal studies of people with autoimmune backgrounds before and after major immune exposures. I want better tracking of autoantibodies, regulatory T-cell function, inflammatory markers, and clinical outcomes. I want medicine to stop pretending that absence of proof is proof of absence.

The Sacchi study should have triggered serious follow-up. It should not have been dismissed for being small. In science, some small studies matter precisely because they ask the right question at the right time.

The Real Lesson

Bryan Johnson’s case does not prove that COVID vaccination caused autoimmune gastritis. I would not make that claim. But it raises a question that should have been taken seriously from the start: what happens when a person with autoimmune vulnerability is exposed to repeated immune disruption?

That is the missing category. Not everyone is the same. Not every immune system responds the same way. A healthy young person, an elderly person with comorbidities, and a person with existing autoimmune disease should never have been treated as if they carried identical risk-benefit profiles.

This is where medicine failed. It flattened individual risk into population messaging. It treated scientific uncertainty as a communications problem. It expected trust without earning it through transparency.

That cannot continue.

If people like Bryan Johnson, who have every incentive to measure, optimise, and understand their own biology, are now questioning the systems that advised them, then medicine has a serious problem. The answer is not to mock them or silence them. The answer is to return to science, data, humility, and proper clinical reasoning.

Because the autoimmune question is not going away.

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Not because I wanted the numbers to be bad. Quite the opposite. But everything I have looked at over the past few years points the other way. In the UK hospital data I have analysed, I keep seeing rising admissions for hypertension, heart failure, myocarditis, atrial fibrillation, endocrine disorders, inflammatory conditions, ulcerative colitis and a range of other chronic problems. That is not a population becoming dramatically healthier.

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So when the CDC reported a record-low age-adjusted mortality rate, the question was not simply whether the number was correct. It was: what was driving it?

Overall mortality can mislead you. A headline can be technically true and still point your attention in the wrong direction.

The Difference Between a Rate and Reality

The first thing to separate is the age-adjusted mortality rate from the total number of deaths.

The age-adjusted rate fell. That is true. But total deaths actually rose, from just over 3.07 million in 2024 to just over 3.09 million in 2025. That distinction matters. An age-adjusted rate tells us how mortality compares after accounting for population structure. It does not mean fewer people died.

This is where people are misled. Read only the headline and you might conclude the country is healthier. Drill into the causes of death and a very different picture emerges.

The fall was not because heart disease disappeared. It was not because cancer declined. It was not because stroke, diabetes, kidney disease, Alzheimer’s or chronic respiratory disease suddenly improved.

Many of those categories went up.

Mortality in the United States: Provisional Data, 2025

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What Actually Drove the Improvement

The biggest driver was a fall in unintentional drug overdose deaths.

That matters, and it is good news. Overdose deaths rose sharply from 2019 to 2022, then fell significantly. By 2025 they had dropped by around 14% in a year, reaching the lowest level since 2019.

But here the interpretation becomes critical. Overdose deaths disproportionately affect younger and middle-aged adults, so a fall in that category pulls the age-adjusted rate down hard. When deaths drop in younger groups, the rate moves strongly.

That does not mean the chronic disease burden has improved. It means one major category of premature mortality has improved.

That is not the same thing.

What the Chronic Disease Numbers Are Saying

Beyond the overdose story, the pattern was concerning.

Heart disease was up. Cancer was up. Stroke was up. Chronic lower respiratory disease was up. Alzheimer’s was up. Diabetes and kidney disease were up. Most strikingly, influenza and pneumonia rose by more than 17% and moved from the 11th to the 8th leading cause of death.

That is not broad health improvement. It is statistical improvement driven by a fall in one category, while the deeper chronic disease pattern remains unresolved.

This is why the public needs to be careful. The danger is not that the CDC number is false. The danger is that people read it falsely. They hear “lowest death rate ever” and assume the health crisis is over.

The numbers underneath say something else.

The Influenza Signal Matters

The influenza and pneumonia increase is especially important.

A 17% rise is not a minor fluctuation. Something changed in the interaction between respiratory viruses, population vulnerability and immune resilience.

I am not saying the flu virus itself became dramatically more lethal. That would be too simplistic. But if flu and pneumonia deaths rise sharply without evidence of a uniquely lethal strain, we have to ask a different question.

Why is the population more vulnerable?

The factors could be many: an intense season, lower vaccine uptake, delayed treatment, older and more comorbid patients, post-pandemic immune disruption, the lingering impact of repeated respiratory exposure.

But clinically, I cannot ignore the broader pattern. Respiratory infection does not only kill through pneumonia. It destabilises cardiovascular disease. It raises stroke risk. It precipitates heart failure. It unmasks frailty. It tips people with chronic illness over the edge.

So I do not see influenza and pneumonia as an isolated category. I see it as a marker of population vulnerability.

The Mortality Debt Problem

There is another issue that is often ignored: mortality debt.

During the pandemic, many frail and vulnerable people died earlier than they otherwise would have. Death is not repeatable. People can only die once. If a period of excess mortality removes a large number of frail individuals, then in a purely statistical sense you might expect mortality to fall afterwards.

That does not mean the remaining population is healthier. It may simply mean many of the most vulnerable have already died.

This is why I am cautious about celebrating a record-low rate too quickly. After years of excess mortality, some rebound is expected. The real question is whether mortality is falling below where it should be after that prior loss, or whether chronic disease is still rising beneath the surface.

From what I can see, the chronic disease signal remains deeply concerning.

The Pattern I Think We Are Seeing

The pattern looks like this.

Overdose deaths fell. COVID deaths fell. Those two changes improved the headline.

But chronic disease deaths kept climbing, and influenza and pneumonia rose sharply. The acute pandemic-era spike may be unwinding while the deeper health burden stays intact.

This is the distinction people are missing.

The population may be dying less from certain acute causes while becoming more chronically ill.

That is not a contradiction. It is exactly how modern public health can fail while still producing a reassuring headline. We can cut deaths from one category and still have rising disease burden elsewhere. We can improve emergency response to overdose and still have worsening metabolic, cardiovascular, inflammatory and respiratory health. We can lower the age-adjusted death rate and still have a population that is more medically fragile.

That is the false comfort in this story.

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Why This Matters

If policymakers take the headline at face value, they will miss the warning.

They may assume the country is recovering. They may assume the pandemic impact has passed. They may assume chronic disease is simply following an expected ageing curve. The data do not allow that complacency.

The correct response is not panic. It is precision.

We need to know who is dying, from what, at what age, and after what sequence of illness. We need to understand whether respiratory infections are triggering cardiovascular and neurological deaths. We need to look at admissions, not just deaths. We need to distinguish fewer fatal overdoses from better underlying health.

Most of all, we need honesty. If the population is still becoming more chronically ill, a record-low mortality rate should not be used as a sedative. It should be a prompt to ask better questions.

The Bottom Line

I do not look at this data and see a healthy population.

I see a mortality headline pulled down by fewer overdose and COVID deaths, while chronic disease continues to rise underneath. That is a very different story.

The record-low rate is real. But it is not the full truth.

The acute mortality surge may be easing. The chronic disease burden is still moving in the wrong direction. If we ignore that because the headline looks reassuring, we will miss the chance to understand what is happening to the population before the next wave of consequences becomes impossible to deny.

The data are telling us something.

We should not look away.

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Not because the condition is not real. Quite the opposite. I think the term has become too small, too vague, and too politically loaded for what we are actually trying to understand. Many people hear “Long COVID” and immediately place it into a box. Some think of fatigue. Some think of anxiety. Some think of a post-viral syndrome. Some simply switch off because they are tired of the entire subject.

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But when I look at the science now, I do not think the most important question is whether symptoms have lasted a long time after COVID. The more important question is this: what if COVID has left a persistent injury pattern in the smallest blood vessels of the body?

That is why I prefer the phrase post-COVID vascular damage. It is not perfect, but it moves us closer to mechanism. It forces us to ask what is happening in the microcirculation, in the capillaries, in the tissue-level blood flow that standard tests often fail to capture.

The Battleground Is Smaller Than We Thought

In my discussion with Dr Beate Jaeger and Joachim Gerlach, the central idea was simple but deeply uncomfortable. The main battleground may not be the large arteries, the obvious organs, or the routine scans. It may be the microcirculation.

Capillaries are the final delivery system. They are the smallest vessels, the point at which oxygen and nutrients actually reach the cells. You can think of them as the last tiny pipes supplying each street in a city. If the main water pipe is open but the last few metres are blocked, the house still has no water.

This is why the post-COVID picture can be so confusing. A patient may have a normal oxygen saturation, a normal echocardiogram, a normal CT scan, and routine blood tests that do not explain the severity of their symptoms. But if the capillary network is impaired, the body can still be failing at the level that matters most: tissue oxygen delivery.

The paper we discussed separates this into two forms of microvascular rarefaction. One is functional rarefaction, where the capillary is still there but blood does not flow properly through it. The other is structural rarefaction, where the capillary itself may be damaged or lost. That distinction is crucial. A blocked vessel may reopen. A lost capillary is a very different problem.

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Microclots Are Not the Whole Story

For several years, much of the discussion has focused on microclots. That was necessary, because microclots gave us a way to understand why patients could feel profoundly unwell despite normal routine investigations.

But I think we now have to go beyond microclots alone.

The model that is emerging is more complex. There may be platelet activation, fibrin amyloid microclots, neutrophil extracellular traps, red blood cells becoming less deformable, endothelial inflammation, pericyte constriction, and macrophage activation all feeding into the same problem. Blood does not simply clot or not clot. It becomes rheologically abnormal. It becomes harder to move through the smallest vessels. It becomes inflammatory.

This matters because a red blood cell is roughly the size of the capillary it needs to pass through. It must deform to squeeze through that space. If the red cell becomes stiff, if the vessel entrance constricts, if platelets are activated, or if fibrin structures are forming inside that system, then oxygen delivery begins to fail even before we see obvious organ damage.

That is the pattern clinicians are not trained to look for.

Why the Patient Looks Well Until They Don’t

One of the most important clinical observations is that many patients do not collapse immediately. They deteriorate over weeks and months. They may describe a mild infection, a day or two of feeling unwell, then apparently recover. Two or three weeks later, something shifts. Fatigue appears. Exercise tolerance collapses. Palpitations start. Brain fog appears. They cannot understand why they have moved from functioning to struggling.

The problem is that we are still thinking in old timelines. We look for the acute infection. We look for the obvious complication. We do not always trace the delayed immune-vascular effect back to the preceding viral exposure.

I see this repeatedly in medicine. The event and the consequence are separated by time, so the connection is missed. If a patient has a stroke or cardiac event two weeks after a mild respiratory illness, the infection is often treated as irrelevant. If a patient becomes housebound after a viral episode that seemed trivial, we may look for psychological explanations rather than ask whether the microcirculation has changed.

That is a major blind spot.

The Difference Between Damage and Dysfunction

I think we need to be very careful here. Not every post-COVID symptom means permanent capillary loss. That would be too simplistic and probably wrong.

Some patients may have primarily functional obstruction. Their capillaries remain present, but blood flow is impaired by microclots, platelet activation, inflammatory constriction, or red-cell stiffness. These patients may have a better chance of meaningful recovery if the process is identified early and treated appropriately.

Others may develop structural damage. That is the more concerning possibility. If capillaries are actually lost, the tissue they supplied may also be compromised. This is most frightening in tissues with poor regenerative capacity, such as myocardium and brain. Once fibrosis begins, or once highly specialised cells are lost, we are no longer talking about simple fatigue. We are talking about lost reserve.

This is the hypertension analogy I keep coming back to. Before hypertension was properly understood, people watched it silently damage the heart, kidneys, eyes and brain. By the time treatment started, some of the injury was already irreversible. I worry that post-COVID microvascular disease may be following a similar pattern. We are watching symptoms without measuring the right pathology.

Why One Protocol Will Not Solve This

One of the reasons the system struggles with this illness is that medicine wants clean protocols. One diagnosis. One mechanism. One drug. One outcome measure.

But this condition does not behave like that.

Some patients are predominantly vascular. Some are neurological. Some are gut-driven. Some have dysautonomia. Some have viral persistence. Some have autoimmune features. Many overlap. That means a single trial of a single drug against a vague label like “Long COVID” is almost guaranteed to disappoint.

This does not mean treatment is impossible. It means phenotyping is essential. We need to know whether the dominant problem is clotting, endothelial inflammation, macrophage activation, viral persistence, mast-cell activation, mitochondrial dysfunction, autoimmunity, or loss of microvascular reserve. Without that, we are not treating patients. We are guessing.

Dr Jaeger’s presentation emphasised how severe cases may require layered approaches: correcting deficiencies, addressing platelet activation and coagulation abnormalities, considering antihistamine strategies in selected patients, and in extreme cases using H.E.L.P. apheresis or related extracorporeal approaches. The important point is not that every patient needs this. Most do not. The important point is that the sickest patients show us the biology more clearly.

The Clinical Community Has to Wake Up

The most dangerous response now is the desire to move on.

I understand the fatigue. The public is tired. Doctors are tired. Institutions are tired. But biology does not care whether we are tired. If a mechanism continues, the consequences continue.

What concerns me most is the quiet accumulation of damage. A patient does not need to become critically ill to lose function. An older person who was independent may become housebound and everyone says, “They are just getting old.” A younger person who was athletic may become unable to exercise and is told to pace themselves. A patient with wound complications, poor healing, inflammatory flares, or unexplained vascular symptoms may never have the dots connected.

The missing link may be the microcirculation.

What I Think This Means

I do not think post-COVID illness is one disease. I think it is a family of overlapping pathologies triggered by SARS-CoV-2 and shaped by the patient’s underlying biology.

But I increasingly think the microvascular component may be one of the most important parts of the puzzle. It explains why symptoms can be systemic. It explains why routine tests can be normal. It explains why exertion exposes the problem. It explains why the brain, heart, muscles, lungs and gut can all appear involved without a single obvious organ diagnosis.

Most importantly, it explains why early recognition matters.

If we identify functional obstruction early, there may be a window to restore flow and prevent progression. If we ignore it until structural rarefaction has occurred, we may be trying to reverse damage that should never have been allowed to accumulate.

That is the uncomfortable message. The smallest blood vessels may be carrying the biggest clue.

Timecodes

00:00 — Opening: Why post-COVID vascular damage matters
07:00 — The new paper: microvascular damage and capillary erasure
10:01 — Organ damage vs persistent post-COVID illness
13:26 — Why H.E.L.P. apheresis entered the discussion
15:30 — Early cases: clots, children, and clinical turning points
20:10 — Mapping the full disease: spike persistence and clotting
25:00 — Platelet activation, amyloid fibrin, and endothelial damage
29:50 — Why single-drug trials miss a multi-pathway disease
40:00 — Severe cases in young athletic patients
44:40 — Heparin and H.E.L.P. apheresis: proposed mechanisms
49:20 — Antivirals, immune reactivation, and glycocalyx support
54:50 — Capillary loss and tissue hypoxia: the key concept
59:00 — Case evidence: perimyocarditis, fibrinogen, and oxygenation
1:04:50 — Why early detection matters before irreversible loss
1:10:40 — Clinical silence, wound complications, and moving on too soon
1:15:00 — What needs to happen now: family doctors, reinfections, and mitigation

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But immunology is not that simple.

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I was not arguing that systemic immunity was irrelevant. I was arguing that it was incomplete. A virus that enters through the upper airway has to be confronted at the upper airway. If the main protection is generated in the bloodstream, there is already a timing problem. The virus has gained access through the nose and throat before the strongest immune response has even arrived.

That was the point I felt was being missed.

The immune system is not one uniform defence system. It is organised into compartments. I have systemic immunity in the blood. I have mucosal immunity in the nose, throat, lungs and gut. I have immune surveillance in the skin and other surfaces. Each compartment has its own logic, and each infectious threat has to be considered according to the route by which it enters the body.

For SARS-CoV-2, the key battlefield was always the mucosal surface of the upper airway.

Why This Never Made Sense to Me

The contradiction was obvious. SARS-CoV-2 replicates quickly in the nose and throat. It spreads efficiently from person to person before many people even realise they are infected. Yet the dominant vaccine strategy was built around intramuscular injection, which mainly trains systemic immunity.

That can help reduce severe disease. It can help the body respond once the virus has moved deeper. It can reduce the risk of the most catastrophic outcomes in vulnerable people. I have never had difficulty understanding that argument.

But preventing severe disease is not the same as stopping circulation.

If a virus can establish itself in the upper airway before systemic immunity fully engages, then it can still replicate, transmit, and continue to evolve. This is why I always felt the promise of transmission control through injectable vaccines alone was biologically weak. It assumed that blood-based immunity could compensate for weak front-line mucosal protection.

That is not how a fast upper-airway virus behaves.

The nose and throat need a rapid local response. One of the key components of that response is mucosal IgA. IgA is not just another antibody. It is part of the immune defence at the surface where the virus first lands. If that response is weak, the virus has an opportunity to gain a foothold.

Once it has gained that foothold, the problem changes.

The Timing Gap

The timing issue is critical.

If SARS-CoV-2 enters through the upper airway and mucosal IgA is weak, the virus can replicate locally in the first day or two. During that time, the person may feel little or nothing. But the virus is not waiting politely for the systemic immune system to catch up.

It can move deeper into the respiratory tract. It can expose tissues to spike protein. In some individuals, it can trigger broader inflammatory and immune responses. By the time the blood-based immune system has increased antibodies and begun to contain the infection, the virus may already have established itself.

This is the gap.

People often say, “But vaccinated people still have antibodies.” That is not the whole question. The real question is where those antibodies are, what type they are, how quickly they respond, and whether they are specific enough for the variant now circulating.

Systemic immunity may reduce the severity of disease after infection has begun. But mucosal immunity helps determine whether the virus gets the chance to establish infection in the first place.

That distinction was blurred during the pandemic. It should not have been.

What This New Paper Shows

A recent Nature Communications paper looked at intranasal boosting in SARS-CoV-2 vaccine-imprinted mice. The paper is technical, but the core message is straightforward.

The researchers studied mice that had been primed with Wuhan-1 spike-based vaccines and then boosted with Omicron-matched vaccines. They compared different strategies: intramuscular priming and intramuscular boosting, intramuscular priming and intranasal boosting, intranasal priming and intramuscular boosting, and intranasal priming and intranasal boosting.

The important finding was that intranasal boosting produced stronger variant-specific responses in key compartments. It improved mucosal responses. It improved XBB.1.5-specific antibody responses. It also helped overcome some of the imprinting created by earlier Wuhan-spike exposure.

That matters because imprinting changes the way the immune system responds to later variants.

Once the immune system has been trained strongly against the ancestral spike, later exposure to a new variant does not occur on a blank slate. The immune system tends to recall what it already knows. It produces cross-reactive responses. Those responses may bind, but they may not be the most useful response against the current variant.

This is why the paper is so important. It does not simply show that intranasal vaccines are interesting. It shows that route matters. It shows that the immune compartment matters. It shows that systemic boosting and mucosal boosting are not equivalent.

Intranasal boosting induces variant-specific responses in SARS-CoV-2 vaccine-imprinted mice

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The Problem of Imprinting

Immune memory is usually a strength. But in a rapidly changing virus, memory can become a constraint.

If the immune system keeps being pulled back toward an older version of spike, it may struggle to generate the precise response needed against the current variant. This is what I mean when I talk about immune imprinting. The immune system is not failing to respond. It is responding through the pathway it was trained to use.

That distinction is essential.

The problem is not always a lack of immunity. Sometimes the problem is the wrong shape of immunity. Sometimes the response is broad but poorly targeted. Sometimes it is systemic when it needs to be mucosal. Sometimes it is cross-reactive when it needs to be variant-specific.

In the paper, the strongest mucosal IgA signal was not generated by repeating the same injectable logic. It came when the mucosal compartment was directly engaged. That is exactly what I would have expected if the original weakness was anatomical.

We trained the immune system in one compartment while the virus was exploiting another.

What I Think Was the Strategic Mistake

I do not think the serious argument is that COVID vaccines did nothing. That is too crude, and it misses the point.

The serious argument is that the vaccine strategy was incomplete from the start.

It prioritised systemic protection against severe disease, but it was presented and operationalised as if it could also provide durable control of infection and transmission. Those are different goals. They require different immune architecture.

For high-risk individuals, systemic protection may have had a rational role, especially early in the pandemic. But using that same logic across the whole population, including people with prior infection and younger low-risk groups, created a different problem. It trained large populations against ancestral spike through an injectable route, while the virus continued to evolve and circulate through the mucosal surface.

That is the weakness that now needs to be acknowledged.

Not emotionally. Not politically. Scientifically.

If the goal was to stop a fast-spreading upper-airway virus, mucosal immunity should have been central from the beginning. Intranasal vaccines, broader antigen strategies, early antiviral approaches, and protection of high-risk groups should have been considered as part of a more nuanced strategy.

Instead, the world built a platform around injection and then seemed surprised that infection continued.

Why This Still Matters

This is not a historical argument. It matters now because SARS-CoV-2 is still circulating.

The public has largely moved on, but the virus has not. Repeated infection still carries risk. For some people, that risk may be vascular. For others, neurological, inflammatory, immune-mediated, or metabolic. I am not comfortable with a casual acceptance of repeated infection as if it is biologically trivial.

I see too many unusual patterns. I see too many subtle presentations. I see too much evidence that this virus can disturb the immune system in ways that do not always announce themselves immediately.

That is why I keep coming back to the same point. If the virus repeatedly gets past weak mucosal protection, the body is repeatedly forced into systemic immune engagement. For some people, that may be tolerated. For others, it may become the beginning of a longer inflammatory cascade.

This is what I have called the COVID storm: not always dramatic at the start, not always obvious, but capable of creating downstream immune disruption.

The Lesson I Take From This

The lesson is simple. The entry point matters.

I cannot design a serious respiratory virus strategy while ignoring the mucosal immune system. I cannot pretend that blood antibodies alone are sufficient for a virus that replicates quickly in the nose and throat. I cannot ignore immune imprinting when repeated exposure to related spike antigens shapes the response to future variants.

This new paper does not answer every question. It is a mouse study. It does not prove every downstream clinical implication in humans. But it strengthens the central argument I made in 2021: an intramuscular-only strategy was never going to be enough to control a rapidly spreading mucosal virus.

The uncomfortable truth is that this should have been studied and acknowledged much earlier.

I think the next phase requires honesty. We need to stop pretending that the original strategy was complete. We need to distinguish protection against severe disease from control of infection. We need to take mucosal immunity seriously. And we need to recognise that if the virus continues to circulate, the health consequences may continue to accumulate.

I said this would be a problem in 2021.

I am saying in 2026 that it is still a problem.

And until we face the anatomical and immunological mistake at the heart of the strategy, I do not think we will understand why this virus has been so difficult to control.

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Susan did not arrive at COVID with a reflexive distrust of vaccines or medicine. That would be too easy to dismiss. She spent forty-five years in biotech, working on regulatory approvals, quality control, global clinical trials, vaccines, biotherapeutics, and medical devices. She understood the industry from the inside.

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That is why I wanted this discussion (Timecodes below).

We have reached a dangerous point where the public conversation around COVID has become almost useless. On one side, people say everything was safe, effective, necessary, and settled. On the other, people feel betrayed, censored, harmed, and ignored. Between these positions sits the more important question: what actually happened to the systems meant to protect public trust?

Susan’s answer is not emotional. It is procedural. She is asking whether the normal questions were asked, whether the normal safeguards were applied, and whether the public was given enough to make a truly informed decision.

The Insider Who Did Not Start as an Outsider

The first thing I wanted to establish was Susan’s credibility and her relationship to the vaccine industry.

This matters because the lazy response to any criticism of pandemic vaccination policy is to label the person anti-vaccine. That label does not fit Susan. It does not come close.

She spoke with real pride about her time at Connaught Laboratories. One example she gave was BCG, originally developed against tuberculosis and later used in a very different context as an immune-based treatment for bladder cancer. That story shows how she thinks. She understands immunology not as a slogan but as a practical clinical tool. She understands that a biological product can be beneficial, that immune stimulation can be useful, and that regulatory approval, manufacturing data, clinical trials, and quality control all carry weight.

So when someone like Susan raises concerns, the honest response is not to dismiss her. It is to ask what she saw that made her concerned.

The First Crack in Confidence

What struck me most was that Susan did not describe an instant conversion from trust to distrust.

That is important. Many people imagine that those who questioned the pandemic response were always suspicious. In Susan’s case, the concern built slowly. She watched events closely, volunteered in the health system, sat on committees, worked with Ontario Health Teams. She was not standing outside throwing stones. She was inside the machinery, observing it.

Then the contradictions began to accumulate.

The first was the mRNA platform. When the public was told vaccines could be developed in record time, Susan assumed this meant a more traditional approach. That made sense to her, because traditional platforms can be adjusted when a new strain appears. Influenza vaccines are updated every year using established manufacturing systems. When she realised that two of the major COVID products were mRNA-based, her concern increased.

This is where the public discussion often becomes confused. The question is not whether mRNA is a vaccine in the broad regulatory sense. The deeper question is whether the biological behaviour of the platform is similar enough to traditional vaccines to be regulated, monitored, and communicated in the same way.

A traditional vaccine delivers an antigen. The body responds to it, and the dose can be measured by what is in the vial. With mRNA, the product delivers instructions, and the body’s own cells produce the antigen. That creates a different set of questions.

Where does the lipid nanoparticle go? Which cells take it up? How much spike protein is produced, and for how long? Does every person produce the same amount? What happens in people with inflammatory, autoimmune, vascular, or pregnancy-related risk states?

Those are not fringe questions. They are exactly what should matter when a technology moves from a development programme into mass use.

Why Dose Is Not a Simple Issue

One of the clearest points Susan made was about dose.

With a conventional vaccine, potency testing is central. The manufacturer must show that each vial contains a defined amount of antigen, and regulators can verify it. A person may respond differently depending on their immune system, but the administered dose itself is measurable.

With mRNA, Susan’s concern is that the injected dose is not the same as the biological dose.

That distinction matters. The amount of mRNA in the vial can be measured, but what the body produces afterward may vary. One person may produce little antigen, another much more. The duration of production may vary. The tissue distribution may vary. The inflammatory context of the host may vary.

This does not prove harm. That is not the point. The point is that it creates uncertainty, and uncertainty should lead to better surveillance, not stronger reassurance. If the biological dose varies between individuals, safety monitoring needs to be designed with that in mind.

This is where I think the pandemic response failed intellectually. The system treated uncertainty as something to manage through messaging rather than investigate through rigorous follow-up.

The Problem with Saying Billions Received It

One argument often used in defence of the COVID vaccines is that billions of doses were given, and if there were major safety issues, they would surely be obvious by now.

At face value, that sounds reasonable. But it only holds if the surveillance system is sensitive enough to detect the signal. If the system depends on passive reporting, clinician recognition, patient persistence, and official willingness to investigate temporal associations, then signals can be diluted or missed.

I have seen this clinically. When a patient has a stroke, myocarditis, arrhythmia, autoimmune flare, cancer diagnosis, or vascular event after vaccination, the immediate question is causality. And causality is difficult. If the patient already had risk factors, the event is attributed to background risk. If it is rare, it is dismissed as coincidence. If the mechanism is not established, the suspicion is called speculative.

That is precisely why pharmacovigilance exists. The threshold for an individual clinician to prove causation is very high, so the system must look for patterns. It should ask whether certain diagnoses rise in defined windows after exposure. It should compare vaccinated, unvaccinated, boosted, and recently infected cohorts. It should examine timing, recurrence, clustering, and biological plausibility.

The tragedy is that this can still be done. In health systems with linked vaccination and hospital data, retrospective analysis is possible. The lack of appetite for that work is part of why public trust continues to erode.

The Pregnancy Question

One of the most uncomfortable areas we discussed was pregnancy.

From a public health perspective, I understand why pregnancy became a concern during COVID. Pregnant women, especially in the third trimester, may be at higher risk from respiratory illness. No serious person should dismiss that.

But from a regulatory and ethical perspective, the question is different. If pregnant women, lactating women, women trying to conceive, and people with autoimmune conditions were not adequately studied in the original approval process, how was the public supposed to understand the uncertainty? Were vaccination clinics given the full information? Were patients given real informed consent? Were exemptions considered? Were frontline staff allowed to communicate nuance?

Susan’s account was striking. She described being involved in setting up vaccination clinics and asking basic questions about consent forms and product information. Her concern was that the public were given the benefit message but not always the uncertainty message.

That is where trust breaks. People can tolerate uncertainty. What they cannot tolerate is being told certainty existed when it did not.

How Trust Breaks

I often say trust is like glass. Once broken, it cannot be glued back together by another press conference.

The pandemic did not damage trust only because people disagreed with policy. It damaged trust because many felt that questions were treated as threats.
- They felt that doubt was diagnosed rather than answered.
- They felt that scientific uncertainty was replaced by institutional confidence.
- They felt that adverse events were minimised before they were properly investigated.

Susan’s diary matters because it captured this process in real time.

Memory is unreliable, and institutions know it. Public anger fades. Official narratives become cleaner with time. People forget the sequence of events. They forget what was said before the message changed. They forget which claims were made with certainty and then quietly abandoned.

A diary resists that. Susan kept handwritten records through the pandemic, documenting meetings, news events, policy decisions, personal experiences, family losses, exclusion, censorship, and the care of her mother. That does not make every interpretation correct, but it makes the record valuable.

It gives us sequence. And sequence matters, because public trust was not lost in one event. It was lost step by step.

The Danger of Grandfathering a Platform

One of Susan’s most important warnings was about what she called the grandfathering of technology.

Once a platform is accepted as safe, future products using it may face a much easier path. The antigen or target can change, but the underlying delivery system is treated as already established.

That may be reasonable when the platform is genuinely well understood. It becomes dangerous if the original platform was accepted under emergency conditions, with unresolved questions about distribution, persistence, immune effects, lipid nanoparticle behaviour, long-term safety, and population-level risk stratification.

This is where the COVID issue becomes bigger than COVID. The mRNA platform is not going away. It is being explored for influenza, RSV, cancer, and other conditions, and some of those applications may prove valuable. I do not dismiss the technology itself. In cancer, a personalised immune strategy may make biological sense in a way that is very different from repeated mass vaccination of healthy populations.

But if the platform is going to expand, the unanswered questions need to be answered. Not messaged. Answered.

That means proper distribution studies. Proper long-term follow-up. Proper risk stratification. Proper pharmacovigilance. Proper informed consent. Proper humility.

Without that, the public will not see innovation. They will see evasion.

Why Forgetting Is Not an Option

One of the most powerful parts of the conversation was not technical. It was personal.

Susan said she cannot forget, because she wrote it down. That is the point of the diary. It resists the emotional and institutional pressure to move on.

There is a temptation now to say the pandemic is over and that revisiting it is unhelpful. I think that is wrong. We do not revisit the pandemic to remain angry. We revisit it because the same systems remain in place. The same incentives remain in place. The same regulatory dependencies remain in place. The same financial pressures remain in place. The same fear-based communication strategies could be used again.

If we do not understand how trust was lost, we will not know how to rebuild it. And pretending there was no problem will not rebuild anything.

What I Think Must Happen Now

I do not think the way forward is endless blame. That may be emotionally satisfying, but it will not repair the system. The way forward is harder.

I think regulators need to revisit the assumptions made during the pandemic. I think industry needs to recognise that public trust cannot be demanded; it has to be earned. I think adverse event surveillance must become far more active and transparent. I think linked health data should be used to investigate signals that remain unresolved. I think informed consent must return to medicine as a serious ethical process, not a bureaucratic formality.

Most importantly, we need to separate two things that were dangerously fused during the pandemic. We can support medical innovation and still demand better evidence. We can recognise the potential of new platforms and still question how they were deployed. We can believe vaccines have had historic value and still insist that every product, every platform, every population, and every risk-benefit calculation be evaluated honestly.

That is not anti-science. That is science.

Susan Langlois’ diary matters because it forces us to face an uncomfortable truth: trust was not lost by accident. It was lost because too many questions were brushed aside at the very moment they most needed answering.

If we are serious about the future of medicine, we cannot let that happen again.

Timecodes

0:00 Opening: Why Susan’s Perspective Matters
2:25 Susan’s Biotech, Regulatory, and Ontario Health Background
4:40 Forty-Five Years in Vaccines: BCG, Insulin, and Approvals
8:09 Asking Hard Questions to Protect the Industry
9:20 What Industry Insiders Are Saying Behind the Scenes
13:09 Reassessing Vaccine Risk-Benefit After COVID
15:55 Is mRNA Being Treated Like a Traditional Vaccine?
19:04 The 2013 Regulatory Distinction: Vaccine vs Genetic Product
23:30 “Billions Received It”: Dose, Potency, and Safety Signals
27:00 Emergency Release, Consent, Liability, and Shortcuts
29:49 Placebo Evidence and the Limits of Passive Surveillance
37:34 Pregnancy, Exemptions, and Missing Consent Information
41:50 Broken Trust, Public Inquiries, and Regulator Independence
45:08 mRNA Potential, Platform Risk, and Grandfathering
54:36 Lab-Leak Questions, Incentives, and Industry Opportunity
56:22 Susan’s Diaries, Censorship, and Rebuilding Trust

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What happens to post-pandemic health research if the current opening for discussion begins to close again?

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That is my concern. Not politics, not personalities, not whether someone likes RFK or dislikes him. My concern is whether medicine will still be allowed to ask the difficult questions that patients are forcing us to ask.

Over the past few years, something clear happened. The range of what could be discussed publicly narrowed. Certain subjects became almost impossible to raise without being labelled misinformation. Question vaccine policy, natural immunity, early treatment, adverse events, immune dysregulation, post-COVID syndromes, or unusual pathology after the pandemic, and you could quickly find yourself pushed outside acceptable discussion.

That was not healthy science. It was a managed narrative.

Why RFK Matters, Even If You Disagree With Him

I know RFK is controversial, and that many people disagree with him on many issues. That is not my point.

My point is that his presence changed the atmosphere. It became easier for people who had challenged the consensus to speak. The censorship did not feel as suffocating. Conversations once dismissed outright could at least be brought into the open.

That matters. I do not have to agree with everything a person says to recognise that they may have shifted the public space in a useful direction. In medicine this is important, because progress often begins when someone asks an uncomfortable question before the system is ready to hear it.

Dr Shankara Chetty put it plainly when we spoke. RFK gave a voice to people who felt the accepted pandemic narrative was not strong enough, not honest enough, or not clinically complete. I think that is true. The frustration many clinicians felt was not a desire for chaos. It was that they were seeing patterns in patients that did not fit the official story.

And when doctors are seeing things in real patients, the worst response is to silence them.

The Trust Problem Was Already There

One argument now being made is that public trust in institutions such as the CDC has fallen because of RFK. I think that looks at the issue the wrong way round.

Did RFK damage trust, or did he expose the fact that trust had already been damaged?

The distinction matters. Trust is not destroyed because someone asks questions. It is destroyed when institutions make claims that later prove incomplete or misleading, when safety concerns are dismissed before they are properly investigated, when scientific debate is replaced by public messaging.

If trust in public health has fallen, it is not enough to blame the person pointing to the cracks. We have to ask why those cracks were there in the first place.

This is not about attacking public health. It is about recognising that public health cannot survive without honesty. Once people sense that uncomfortable evidence is being hidden or managed, confidence collapses.

The Problem With Consensus Medicine

One word became almost sacred during the pandemic: consensus.

Consensus has value when it reflects accumulated evidence. It becomes dangerous when it hardens into a boundary around thought, used to prevent new evidence from being examined. That is where I think we went wrong.

I am not suggesting every claim made outside the mainstream was correct. Some were poor, exaggerated, or unsupported. But that does not justify shutting down the entire space of inquiry. Bad arguments are not defeated by censorship; they are defeated by better evidence.

What concerned me was that serious clinical questions were treated as if they were inherently illegitimate. That is not science. Science requires disagreement, scrutiny, and the humility to admit that our first explanation may not be sufficient.

This is especially true after a pandemic. A pandemic is not only an infectious event. It is an immunological, vascular, neurological, and societal event. It does not end when the acute crisis passes. The consequences can unfold across organ systems for years.

What I Am Seeing Clinically

This is why I keep returning to the clinical patterns.

Across post-pandemic health, I am seeing unusual signals — changes that do not fit neatly into the old frameworks. Patients describe illnesses that look viral at the start but then do not behave like ordinary viral illness. Some develop fatigue and headache with little else. Some appear to recover, then deteriorate two weeks later. Some develop gut, autonomic, neurological, clotting-type, or inflammatory relapses that make no sense if we think only in the old way.

When a doctor sees a patient and cannot explain what is happening, that is not an abstract academic inconvenience. It is one of the worst positions to be in clinically. You are sitting in front of someone who is suffering, and the usual diagnostic boxes are not enough.

This is where post-pandemic research must go. It has to move beyond slogans and look seriously at immune dysregulation, microvascular injury, persistent antigenic stimulation, gut immune activation, mast cell patterns, neuroinflammation, and clotting abnormalities. These may not apply to every patient or explain every case. But they are plausible, visible, and clinically important enough to deserve proper investigation.

Post Pandemic Dashboard (top 3 conditions) >

The Missing Evidence: Tissue Pathology

There is one thing I keep coming back to: autopsies.

Everything is an opinion until we have tissue pathology.

If I could have spoken directly to RFK about what needed to be done, that is what I would have emphasised. We need systematic post-pandemic pathology. We need to know what is happening in the tissues — why people are getting sick, why some deteriorate unexpectedly, and why certain organ systems appear affected in patterns clinicians did not commonly see before.

This matters most in vaccinated cohorts, post-COVID cohorts, repeatedly infected cohorts, and those with unexplained deterioration. I am not saying we begin with conclusions. I am saying we begin with tissue.

Tissue pathology has a way of cutting through argument. It can confirm, refute, or refine our models. It can show whether we are dealing with myocarditis, micro-scarring, endothelial injury, microvascular occlusion, immune infiltration, or something we have not yet properly characterised.

Without that, too much remains opinion. And opinion is not enough.

The Danger If the Window Closes

My concern is that if RFK leaves, or if the political and institutional environment shifts again, everyone becomes more cautious. Researchers, journals, clinicians, platforms.

That is how censorship often works. It does not always require direct prohibition. Sometimes it only requires a signal.

People begin to ask whether a topic is worth the risk. Researchers choose safer questions. Doctors avoid public discussion. Journals hesitate to publish controversial findings. Institutions return to familiar narratives because they are easier to defend.

And then patients lose. The patients with persistent symptoms, with unexplained vascular events, with neurological deterioration, with post-viral immune dysregulation — all the patients who do not fit clean diagnostic categories. That is the cost of closing the window.

COVID Is Not Just Historical

One mistake we are making is treating COVID as a historical event.

For many people, COVID is something that happened in the past. Lockdowns happened. Vaccines happened. Variants happened. Then the world moved on.

Clinically, I do not think the story is over. We are still studying the consequences in real time. The virus has changed. Population immunity has changed. Clinical presentations have changed. Testing has changed. Public attention has changed.

That means many people may be experiencing post-pandemic immune effects without recognising them. They call it flu. They call it burnout. They call it ageing or stress. Sometimes it is those things. But sometimes it is something more specific: an immune system that has not reset properly after repeated inflammatory exposures.

That is why the research matters.

The Question Medicine Must Answer

The question is not whether RFK is right about everything. He is not the issue. The issue is whether medicine is allowed to ask the questions that patients’ symptoms are demanding.

Can we investigate vaccine injury without being labelled anti-vaccine? Can we investigate Long COVID without reducing it to psychology? Can we investigate unusual cardiovascular patterns without pretending they are all coincidental? Can we investigate microvascular clotting, immune dysregulation, gut persistence, and neuroinflammation without waiting for permission from a consensus that may already be behind the clinical reality?

That is the real test. If science is strong, it should not fear difficult questions. If public health is trustworthy, it should not need censorship to protect itself. If medicine is honest, it should be willing to say: we do not yet know, but we must investigate.

Where I Think We Go From Here

The next phase has to be built around disciplined clinical inquiry. Not reckless claims, not political loyalty, not blind trust in institutions. We need open discussion, serious pathology, better phenotyping, transparent data, and clinicians willing to describe what they are seeing. We need to separate poor speculation from legitimate dissent, and to recognise that some of the most important medical discoveries begin as observations that initially make people uncomfortable.

That is why this moment matters. If RFK remains, the opportunity is to push for tangible research — especially tissue pathology and serious post-pandemic surveillance. If he leaves, the responsibility does not disappear. It moves back to the clinicians, researchers, and patients who refuse to let these questions be buried.

We cannot afford to go back to silence. People are still getting sick. Doctors are still seeing patterns they cannot explain. And the worst thing medicine could do now is pretend that asking difficult questions is the danger.

The real danger is refusing to ask them.

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When I spoke again with Geert Vanden Bossche, I wanted to put the question many people are now asking, openly or quietly: is COVID over? Hospitals are not overwhelmed. Intensive care units are not full of COVID patients. Most people who get infected describe something mild — fatigue, headache, a sore throat, a short-lived viral illness. (Timecodes at end)

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At face value, that sounds reassuring. But I have never been comfortable with face value when the pattern underneath does not make sense.

Geert’s argument is that we are not looking at a normal transition into endemicity. We are looking at something far less stable. The virus is still circulating, still being detected, still evolving. Different variant families continue to co-circulate, and none has settled into the stable pattern we would expect if this had truly become like seasonal influenza.

That is the point I think people are missing. The danger may not be that COVID looks the way it did in 2020. The danger may be that it has changed its clinical presentation while continuing to press on the immune system.

Why This Does Not Look Like Influenza

The public has been encouraged to think of COVID as similar to influenza, and I understand why the comparison is attractive. It places COVID in a familiar box. We know influenza. We expect winter waves, we expect the vulnerable to be at highest risk, and we accept that some years are worse than others.

But COVID does not fit that pattern.

I do not see a clean seasonal rhythm. I see circulation across the whole year. I see infections that are mild at the time, followed by complications weeks later that neither patient nor doctor links back to the infection — fatigue, headaches, relapses, vague inflammatory presentations, and later deterioration labelled as a chest infection, sepsis, cardiovascular instability, or simply “one of those things.”

That is clinically dangerous, because once the acute illness becomes unimpressive, the causal link becomes invisible.

In a true endemic phase, we would expect the virus to stop behaving as if it is still searching for an evolutionary solution. That is not what we are seeing. It has not gone. It has not settled. It keeps moving, but its gains are getting smaller.

That is not reassurance. It may be a warning.

The Illusion of Stability

The most important concept Geert raised was the idea of a metastable state, and this is the part a lay audience needs to grasp.

A situation can look stable from the outside while demanding enormous effort to hold that balance. Imagine a bucket with water flowing in and a hole letting water escape. If the level stays roughly the same, you might call the system stable. It is not. Water is constantly entering and leaving; the apparent balance depends on a dynamic process continuing in the background.

That is how Geert sees the current relationship between SARS-CoV-2 and population-level immunity. The virus is still transmitting. The immune system is controlling it enough to reduce severe disease in many people, but not eliminating it. The response is not sterilising. The result is a tense equilibrium in which both sides are still adapting.

I find that important because it explains how we can have mild acute disease and continuing concern at the same time. Mild symptoms do not prove the system is safe. They may simply show that the immune system is still suppressing the visible part of the illness.

Where Geert and I See the Problem Slightly Differently

I pushed Geert on something I have been turning over from the clinical side. My concern is that repeated infection may be slowly weakening immune function across parts of the population — not dramatically overnight, but progressively, until people become less able to respond properly and present with infections or inflammatory complications that are never clearly recognised as COVID-related. My worry is that the chronic process is doing more damage than we acknowledge.

Geert accepted the logic but placed the emphasis differently. In his view the immune system is not exhausted. It is still powerful — and that is part of the problem. It exerts enough pressure to keep acute disease mild in many people, but not enough to eliminate the virus, and that suboptimal pressure keeps driving viral adaptation.

The distinction matters. If the immune system were simply defeated, the story would be straightforward. But if it is strong enough to constrain the virus without clearing it, the virus is being forced into a narrowing evolutionary space. It must keep transmitting while its usual routes for immune escape become less efficient.

This is where Geert’s warning turns serious.

The Evolutionary Bottleneck

Earlier in the pandemic, each major variant brought a substantial gain. The virus grew more infectious and found ways around prior immunity. Omicron was a major shift — a dramatic change in the spike protein and widespread breakthrough infections.

Geert is now describing a different pattern. Variant families such as BA.3.2 may carry significant genetic changes, yet they are not gaining the decisive advantage earlier variants achieved. They compete. They fluctuate. They do not clearly win.

That suggests the virus may be approaching an evolutionary bottleneck — spending more energy for less return. It accumulates mutations, but those mutations no longer deliver the same leap forward. The immune pressure remains while the obvious escape routes narrow.

Geert’s concern is that, faced with that constraint, the virus may stop relying on incremental spike mutations and find a different solution altogether. He has suggested that changes in glycosylation — the sugar structures on the viral surface — could allow more efficient escape from immune pressure. In simple terms, the virus may change its disguise rather than alter individual parts of its structure.

That is the point at which a phase transition becomes possible.

A Hyperacute Presentation Would Not Be Subtle

The obvious question is how we would know if Geert’s feared transition had happened. His answer was blunt: we would not miss it.

He is not describing a slightly worse winter wave or a gradual rise in positive tests. He is describing a rapid, hyperacute pattern of severe disease in highly vaccinated populations, driven by a variant that can break through the adaptive immune responses now holding disease in check.

I want to be careful. This is a hypothesis, not an established outcome — but a hypothesis that deserves to be understood before it is dismissed.

Geert is not saying every vaccinated person would be affected. He is saying that if this transition occurred, the severe hyperacute cases would fall predominantly among those whose immune systems had been shaped by repeated vaccination and breakthrough infection, with possible exceptions among unvaccinated people who had previously had severe COVID.

That would be a very different clinical signal from anything we have seen. If it emerged, it would be hard to explain away as ordinary influenza, sepsis, or respiratory infection.

The Window We May Be Missing

The most striking part of the conversation was not the warning itself but the implication that there may still be a window to intervene.

Geert’s argument is that viral load in highly vaccinated countries is currently low. The virus is under pressure — still present, but not spreading at the levels seen earlier in the pandemic. In his view that creates a narrow opportunity, where population-level antiviral intervention might reduce circulation before the virus finds a more dangerous solution.

This is not about an individual taking a tablet and assuming the problem is solved. The evolutionary dynamics are playing out at population level, so any serious intervention would have to be coordinated at that level too.

That is the difficulty. It would require public health authorities to admit that COVID is not over. It would require a humility that has been largely absent. It would mean acknowledging that the current quiet may not be safety but unresolved instability.

I do not see much appetite for that conversation.

Why I Think This Conversation Matters

I do not believe a physician’s role is to comfort the public with simple narratives. My role is to look at patterns and ask whether the explanation on offer is good enough.

Right now, I do not think “COVID is like flu” is good enough. I do not think “hospital admissions are low” is good enough. I do not think “most infections are mild” is good enough. These may be true on the surface, but they do not explain ongoing viral evolution, chronic presentations, recurrent immune stimulation, or the strange clinical patterns many of us keep seeing.

The uncomfortable truth is that a disease can become less visible while becoming harder to interpret.

That is why I wanted this discussion with Geert — not because every prediction must be accepted, but because serious hypotheses deserve serious examination. If he is wrong, the way to show it is through careful immunology, virology, surveillance, and clinical correlation. Not ridicule. Not silence. Not pretending the pandemic ended because people grew tired of it.

I keep returning to one clinical principle: when the visible symptoms no longer match the underlying biology, the biology eventually wins.

If COVID is truly settling into harmless endemicity, the data should show it clearly. But if we are watching a metastable equilibrium — a tense balance between viral evolution and population immunity — then this quiet period may be the most important phase to understand.

The mistake would be to wait until the pattern becomes obvious. By then, the chance to act may already have passed.

Timecodes

0:00 Introduction: Why Bring Geert Back Now?
2:41 Geert’s Background in Vaccines, Immunology and Global Health
6:32 Speaking Out Against the Industry Narrative
9:40 Is COVID Really Over? Why Geert Says No
12:53 Wastewater, Viral Evolution and the False Endemicity Claim
14:54 Why COVID Is Not Behaving Like Seasonal Flu
18:35 The Lab-Origin Question and the Furin Cleavage Site
24:52 Why Geert’s Timeline Was Wrong — and Why the Theory Remains
29:51 HIVICRON, Mild Symptoms and Later Clinical Collapse
32:04 Chronic Immune Pressure, Suboptimal Immunity and Persistent Infection
36:46 World Cup Mixing, BA.3.2 and Variant Families
39:04 The Evolutionary Bottleneck: Why New Variants Are Gaining Less
41:06 Glycosylation: The “Easy Solution” the Virus May Find
46:53 Could a Hyperacute COVID Variant Be Mislabelled as Something Else?
50:52 AI, Scientific Reasoning and Testing Geert’s Hypothesis
55:53 How Would We Know the Dangerous Transition Has Begun?
1:10:56 Antiviral Intervention, Zinc Ionophores and the Missed Opportunity
1:15:51 Final Reflections: Why Geert May Stop Speaking Publicly

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When I saw the video from Tulsi Gabbard, released on her final day as Director of National Intelligence, I understood immediately why so many people reacted strongly. She was not making a vague political accusation. She was pointing to documents, communications, intelligence assessments, whistleblower testimony, and alleged suppression of dissent around one of the most important questions of the pandemic: where did SARS-CoV-2 come from?

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I have not gone through every document line by line. That work has to be done carefully. But even before that, there is an issue that cannot be ignored. For years, anyone who raised the possibility of a laboratory origin was treated as reckless, unscientific, or conspiratorial. Accounts were suppressed. Careers were placed at risk. Serious people learned to stay quiet.

That is not how science should behave.

Science does not advance by protecting a preferred narrative. Medicine does not protect patients by shutting down uncomfortable questions. If the origin of the virus was uncertain, the honest position was always uncertainty. Instead, many were told that natural origin was effectively settled and that lab origin was irresponsible speculation.

That now looks much harder to defend.

Full Tulsi Gabbard video here >

The Question Was Never Only About Origin

The mistake many people are making is to reduce this entire story to one question: did Fauci cause COVID?

That is too crude. It is emotionally satisfying, but it is not analytically sufficient.

The real question is bigger. If NIAID-funded research was connected to coronavirus work in Wuhan, and if senior figures in that ecosystem also influenced how the intelligence community interpreted COVID origins, then we are looking at a profound conflict of interest. The same institutional world that may have had exposure to the origin question may also have helped decide which experts were trusted to answer it.

That is the issue.

When I assess a patient, I am always looking for conflicts in the history. Who benefits from a particular interpretation? What is being emphasized? What is being ignored? What does not fit? Pattern recognition matters because disease rarely announces itself politely. You have to notice the contradiction before the diagnosis becomes obvious.

The contradiction here was present from the beginning. A highly unusual coronavirus emerged in a city with a major coronavirus research institute, yet the public was steered away from asking whether those facts were connected. That did not prove a lab leak. But it justified serious investigation.

Instead, the question itself became contaminated.

Why the Medical Community Struggled With This

I understand why many doctors struggled to process this.

Anthony Fauci was not a fringe figure. For decades he was woven into the intellectual structure of Western medicine. Many physicians studied from textbooks in which his work formed part of the infectious disease framework. He became a symbol of scientific authority. To question him was not merely to question one person. For many clinicians, it felt like questioning the hierarchy of medicine itself.

That is precisely why this is so difficult.

Medicine has a weakness it rarely admits. It teaches us to respect authority, but not to interrogate authority when authority itself becomes part of the problem. We are trained to follow guidelines, trust specialist bodies, and defer to public health institutions. That works when the system is functioning honestly. It becomes dangerous when the system has conflicts it refuses to examine.

If the allegations in these documents are correct, this was not merely a scientific error. It was an institutional failure of truth-seeking.

The Public Anger Is Real — But Anger Is Not Enough

I also looked at the public comments reacting to this release, and they were revealing.

People are furious. They are not responding to one set of documents. They are reacting to years of accumulated distrust: AIDS-era grievances, AZT, remdesivir, hydroxychloroquine, ivermectin, vaccine mandates, censorship, vaccine injury, lab leak denial, and the sense that no one in authority ever pays a price.

That anger is real. It should not be dismissed.

But anger is not evidence. Rage is not analysis. If we allow this moment to become only about punishing one man, we will miss the larger diagnostic opportunity.

I am not interested in joining a mob. I am interested in understanding what happened. That means separating what is proven from what is alleged. It means asking who funded what, who knew what, who shaped the expert panels, who suppressed dissent, who benefited, and who should have spoken but stayed silent.

That is the standard we must apply.

The Bigger Question Is What This Means Biologically

There is another reason this matters, and it is the part too many people still do not want to face.

If SARS-CoV-2 was natural, one line of reasoning follows. If it was shaped by laboratory work, a different level of concern follows. That does not mean deliberate release. It does not mean a bioweapon. But it does mean we have to ask harder questions about the biology of the virus.

What exactly was created? What properties were enhanced? What did the spike protein do that made this virus so unusual? Why did it have such systemic effects — vascular injury, immune dysregulation, clotting abnormalities, neurological symptoms, gut persistence, prolonged post-infectious syndromes?

These questions were never peripheral. They were central.

This is why I said early on that if the spike protein was the most immunogenic and potentially dangerous part of the virus, then using that same spike as the dominant template for global immune training demanded extraordinary caution. That concern does not depend on politics. It depends on immunology.

If the virus was manipulated in ways that increased infectivity or altered host interaction, then the spike was not just a convenient vaccine target. It was a biological risk signal. That distinction matters.

We Still Have a Circulating Problem

The most dangerous phrase in public health today may be: “the pandemic is over.”

I understand why people want it to be over. They are exhausted. Governments are exhausted. The medical profession is exhausted. But exhaustion is not resolution.

We still have a circulating virus. We still have repeated infections. We still have people developing chronic symptoms. We still have unexplained shifts in population health — immune, vascular, neurological, renal, cardiac, and autoimmune patterns that require serious investigation.

My concern is not theoretical. I have spent time examining hospital episode statistics across enormous datasets, looking for the discrepancies and disease trajectories that might help us understand what is happening to population health. I do not accept that these patterns can be waved away because they are inconvenient.

This is where ideological thinking becomes clinically dangerous. If someone has already decided that COVID is over, they will not see the signal. If someone has already decided that vaccines cannot be questioned, they will not see the signal. If someone has already decided that lab origin is impossible, they will not see the signal.

Medicine cannot work like that.

Post Pandemic Dashboard (top 3 conditions) >

Do Not Let the Fauci Story Become a Distraction

There is a real risk now that everything becomes focused on Anthony Fauci.

I understand why. If these documents show what they are alleged to show, his role must be examined seriously. If sworn testimony was contradicted by internal communications, that is not a small matter. If intelligence assessments were shaped by conflicted scientific advice, that is not a small matter. If dissenting analysts were intimidated or marginalized, that is not a small matter.

But this cannot be only one man.

No individual, however powerful, creates an entire pandemic response system alone. There were institutions, agencies, scientific journals, media platforms, pharmaceutical interests, intelligence officials, public health bodies, and professional organizations involved in shaping what could and could not be said.

That is the deeper pathology.

If we turn Fauci into the sole villain, the system survives. If the system survives without reform, this can happen again.

What I Believe Must Happen Now

I believe three things must happen.

First, the documents must be reviewed carefully and publicly. Not emotionally. Not selectively. The timeline matters. The funding matters. The communications matter. The intelligence process matters. The expert selection process matters.

Second, the medical profession must admit that it failed to defend uncertainty. Too many clinicians accepted narrative certainty where the evidence was incomplete. That is not science. That is institutional conformity.

Third, we must return to the biological problem itself. The origin question is not merely historical. It affects how we understand the virus, the spike protein, the immune response, long COVID, vaccine consequences, repeated infection, and the population health trajectory still unfolding.

This is why I feel no joy in saying that many of us were right to ask these questions. There is no satisfaction in it. Too much time has been lost. Too many people were harmed. Too many legitimate questions were suppressed. Too many clinicians were taught to look away.

The Real Work Begins Now

I do not want us to replace one dogma with another.

I do not want natural-origin certainty replaced by lab-leak certainty without evidence. I do not want institutional denial replaced by uncontrolled rage. I do not want a serious biological and intelligence failure reduced to slogans.

What I want is harder.

I want the documents examined. I want the conflicts mapped. I want the funding traced. I want the intelligence process reconstructed. I want whistleblowers protected. I want the biological consequences investigated without ideological filters. I want medicine to become brave enough to admit when it protected authority instead of pursuing truth.

The public is angry because people sense that something was hidden from them. The medical profession should be more concerned still, because if that is true, then we did not merely misunderstand a virus. We allowed the boundaries of acceptable thought to be managed while the disease process continued to evolve in front of us.

That is the real scandal.

The question now is not simply whether SARS-CoV-2 came from a lab.

The question is whether we are still willing to follow the evidence wherever it leads.

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I hear this again and again.

“Am I breaking down?” “Why do I feel terrible when my tests are normal?” “Is anyone actually watching what is happening to our health?”

The uncomfortable truth is that many doctors are asking similar questions. Why are people presenting differently? Why are complications appearing in unusual ways? Why do some patients behave clinically worse than expected?

I come at this from a particular angle. I have spent six years studying COVID, immune dysregulation, clotting, endothelial injury and long COVID, and I understand how hospitals work. Over the past few years I have been taking apart Hospital Episode Statistics, tracing disease trajectories across millions of data points.

That combination matters, because the signal is invisible if you only look at one disease at a time.

Why I Look at Hospital Codes

Every time someone is admitted to hospital, their diagnosis is coded. These ICD codes are not perfect, but they are one of the most powerful ways we have to view health at the population level.

I have been looking across 2016 to 2025 and asking a simple question: what changed after the pandemic?

Cardiovascular disease, neurological disease, kidney disease, liver disease, eye disease, immune-related patterns, surgical complications — layer by layer, the same problem keeps appearing. Something has shifted.

Not everything is rising, and that matters. If this were simply better coding or more hospital activity, I would expect everything to move together. It does not. The patterns look biologically coherent: vascular, immune, metabolic and renal signals keep surfacing in ways that deserve far more attention.

The code I want to focus on here is T82.4.

It refers to complications involving vascular dialysis catheters, particularly blockage or thrombosis in a catheter used for haemodialysis. In plain terms, this is where the line that carries blood out of the body, through a dialysis machine, and back again becomes obstructed or fails.

What a Dialysis Catheter Does

A dialysis catheter is not a minor device. It sits directly in the blood system and must allow large volumes of blood to move smoothly in and out of the body.

For many patients it is a temporary or medium-term solution while a longer-term arteriovenous fistula is arranged. These lines are often tunnelled under the skin, commonly in the upper chest, and may stay in place for months.

For dialysis to work, the catheter must stay patent. If a lumen blocks, blood cannot be drawn properly. Sometimes a clot can be broken up with medication. Sometimes the catheter has to be removed and replaced — another procedure, another risk, another disruption to care.

So when I see a rise in T82.4, I do not see a statistical code. I see dialysis access failing. I see patients needing extra procedures. I see a possible sign that blood flow, clotting and vascular access are becoming more problematic.

The Pattern That Caught My Attention

The rise in T82.4 is not a small fluctuation. The data show a substantial post-pandemic increase, particularly when T82.4 is recorded as the primary diagnosis — which usually means it was the main reason for the hospital episode.

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The official account held that she suffered a severe arrhythmia linked to cardiac inflammation following Mycoplasma infection. On the surface, that is medically possible. Mycoplasma pneumoniae is a recognised bacterial pathogen. It usually affects the lungs. It can, rarely, involve the heart. It can be associated with myocarditis.

But medicine is not meant to stop at what is possible. Medicine is meant to ask what is probable, what fits the pattern, and what else should be considered.

That is where this case becomes important.

I am not approaching this from a position of certainty. I do not have her medical records. I cannot confirm her vaccination timeline, laboratory findings, imaging, or histology. What I can do is examine the reasoning and ask whether the publicly accepted explanation is strong enough to exclude other possibilities.

My concern is that it is not.

Who She Was Matters

Before discussing the medicine, it is worth remembering who Princess Bha was. She was the eldest daughter of the King of Thailand — a lawyer, diplomat, and public servant who championed justice, human rights, and the welfare of women prisoners through the UN Bangkok Rules. She was not simply a name in a medical story. She was a deeply respected figure, and her death carried enormous significance.

That is precisely why this case deserves careful thought.

She reportedly collapsed while training dogs in December 2022. She suffered a cardiac arrest or severe arrhythmic event, was resuscitated, remained unconscious, and never recovered. The public explanation became Mycoplasma-associated myocarditis.

The question is not whether Mycoplasma can cause myocarditis. The question is whether that explanation is sufficient given how abruptly this occurred.

Professor Bhakdi claimed that Princess Bajrakitiyabha had received a third COVID injection before her collapse, saying she was “perfectly well” earlier that day and then suffered cardiac arrest later. He described meeting Thai contacts after arriving in Thailand on 31 December 2022, including people he characterised as close to the royal family and government, and argued that the public diagnosis of Mycoplasma myocarditis did not make clinical sense to him. His central point was that he believed Mycoplasma myocarditis could not plausibly develop within hours and cause sudden cardiac arrest, whereas he considered vaccine-associated myocarditis a more plausible explanation

X video post - RefugeOfSinners(ROS) here >

What Mycoplasma Usually Looks Like

Mycoplasma pneumoniae is often called “walking pneumonia” because many people remain active while infected — managing a dry cough, fever, fatigue, or mild chest symptoms while continuing their daily lives. It is fundamentally a respiratory illness, and most people recover without complication.

Rarely, it can involve other systems: skin, blood, nervous system, and heart. When cardiac involvement occurs, myocarditis becomes possible. I am not dismissing that. The condition exists, and dismissing it would be medically wrong.

But there is an important clinical distinction to hold in mind. In most severe cases with extra-pulmonary complications, the patient is already significantly unwell. Heart involvement tends to be part of a broader systemic picture, not a sudden isolated event in someone apparently healthy enough to be outdoors training dogs.

That is a different clinical pattern. Not impossible — medicine humbles anyone who speaks in absolutes — but not the cleanest fit either.

The Case Report That Raises the Real Issue

To understand the problem more precisely, I looked at a published case report of Mycoplasma myocarditis involving a 29-year-old man who presented with sustained supraventricular tachycardia and acute heart failure.

At first glance, this appeared to validate the Mycoplasma-myocarditis connection. But looking more closely, it raised more questions than it answered.

This man had experienced palpitations and abdominal fullness for four days before attending hospital. He was breathless, hypoxic, tachycardic, with basal crackles and pulmonary oedema on imaging. His heart was enlarged. The echocardiogram showed an ejection fraction of 30%, moderate valve regurgitation, and regional wall motion abnormalities.

That last finding matters. A significantly dilated left ventricle does not usually appear overnight. Those findings may fit myocarditis, but they can equally suggest a prior or underlying cardiac process that has then decompensated under the stress of an acute illness.

This is where clinical reasoning becomes essential. If a patient has Mycoplasma markers and myocarditis simultaneously, it is tempting to join the dots and call it Mycoplasma myocarditis. But correlation is not causation. Mycoplasma may have been the primary driver. It may equally have been a trigger, an association, or simply the stress that pushed an already vulnerable heart over the edge.

That distinction is being missed.

Radaelli, Marco, et al. "Mycoplasma myocarditis presenting with sustained SVT and acute heart failure without signs of myocardiocytolysis and extra‐cardiac disease." Clinical Case Reports 12.5 (2024): e8851.

The Missing Differential

In medicine, we use differential diagnosis because symptoms rarely arrive with labels attached.

If a patient is breathless, we do not immediately assume infection. We work through heart failure, pulmonary embolism, arrhythmia, anaemia, metabolic derangement, and more. The differential is not a formality — it is the mechanism by which we protect ourselves from premature closure.

That is why I found it significant that in this 2024 case report, vaccination status was not discussed. That omission matters. The case occurred in the post-pandemic era, after widespread COVID vaccination and repeat boosters. I am not asserting that vaccination caused that man’s myocarditis. I am saying it should have appeared in the differential.

A more complete clinical question would be: could prior myocardial injury, immune-mediated inflammation, or vaccine-associated myocarditis have left the heart vulnerable, with Mycoplasma then acting as the stressor that tipped the patient into failure? That possibility makes more clinical sense to me than assuming a previously normal heart became severely dilated and regionally dysfunctional within days on the basis of Mycoplasma alone.

The same reasoning applies to Princess Bha. If she had received a recent booster — and I stress I cannot confirm that — then vaccine-associated myocarditis should not be dismissed from the differential. Not because it is proven. Because it is medically relevant.

The Pathology We Are Not Doing

There is another piece of this picture that I believe is critical.

A Japanese autopsy study examined patients who had died from unexplained cardiac arrest and found multiple tiny scars distributed throughout the myocardium. What stood out was the observation that across decades of clinicopathological conference experience, this pattern of multiple micro-scars outside the context of myocardial infarction had not previously been seen.

That is extraordinary.

If we are encountering unexplained arrhythmias and sudden cardiac deaths, and if post-mortem histology is revealing an unusual pattern of micro-scarring, the scientific response should be immediate and intense. We should be asking whether this is new, whether it is related to infection, immune dysregulation, vaccination, reinfection, microvascular injury, or some combination. Instead, that research sits quietly in the background, barely discussed.

That is not acceptable.

When someone dies after an unexplained cardiac arrest — particularly in this era — histology matters. The pattern of inflammation or scarring in the myocardium matters. Without it, we are left with assumptions dressed as conclusions.

Koizumi, Tomomi, and Masao Ono. "Cardiac Multiple Micro-Scars: An Autopsy Study." Case Reports 30.5 (2025): 103083.

Why This Matters Beyond One Case

The broader issue extends well beyond Princess Bha. Her case is important because it exposes a structural weakness in the current scientific posture.

We are living through a period in which infection, reinfection, immune dysregulation, vaccine exposure, endothelial injury, and inflammatory cardiac disease may all intersect. If our diagnostic process refuses to place all of those possibilities on the table, we will not understand what is happening.

The risk is not simply that one case may be misclassified. The risk is that a whole pattern may be missed.

When someone dies from sudden cardiac arrest in this era, families should be asking for histology where possible. They should be asking whether myocarditis was present, whether micro-scars were found, whether the pattern resembled infarction, immune injury, or something that does not fit any prior category. If the scientific establishment will not pursue those questions systematically, families may find themselves having to ask them alone.

That is a terrible position to be in. But it is where we are.

The Question I Am Left With

I do not claim to know what caused Princess Bha’s collapse. Mycoplasma myocarditis is possible. Vaccine-associated myocarditis is possible if the timing supports it. A mixed process is possible. A pre-existing vulnerability unmasked by infection is possible.

What I object to is the absence of visible diagnostic rigour.

I object to the idea that identifying Mycoplasma closes the question.

The right question is not, “Can Mycoplasma cause myocarditis?” It can. The right question is, “Was Mycoplasma the primary cause in this specific case, and what evidence excludes other plausible contributors?”

Until that is answered transparently, the case remains medically unresolved.

And that is the real problem. If we do not demand better answers now, we will spend the next decade slowly discovering what we should have investigated from the beginning.

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I understand why this feels charged. Once you create a clear diagnostic label, it changes how data flows, how research is funded, how care is organised, and yes, how liability might be assessed. But that is precisely why the code matters. Without it, we are choosing to keep these cases diffuse and harder to study.

A lesson from stomach ulcers

This reminds me strongly of the H. pylori story from thirty years ago. The medical consensus then held that stomach ulcers were caused by stress, diet, or excess acid. The idea that a bacterium could survive in the highly acidic stomach and drive chronic inflammation and ulceration was widely dismissed. Barry Marshall and Robin Warren faced significant pushback, and Marshall eventually drank a culture of the organism himself to prove the link. Once accepted, eradicating H. pylori with antibiotics transformed outcomes for ulcer patients and even reduced certain gastric cancers.

The parallel is not perfect, but the pattern is familiar: when a possible causal mechanism challenges existing assumptions or interests, the instinct can be to avoid creating the structures that would let us investigate it properly. An ICD code is one such structure. It is not proof of causation on its own, but it is the starting point for systematic observation.

The spectrum of people affected

In practice, the picture is more layered than headlines suggest. One group experienced clear problems in close temporal association with vaccination and have no other ready explanation. They tend to be the most vocal, because they have so often been dismissed or gaslit for years. A larger group developed new symptoms around the same period and now wonder whether there is a connection, especially as they hear similar stories. And there is the biggest group of all: people who simply do not feel right, with fatigue, unusual patterns of illness, or other changes, but who have never been encouraged to consider a possible link to vaccination.

For this last group in particular, I would not clinically leap to telling them their symptoms are vaccine-related without evidence or a way to test for it. That would risk creating anxiety without offering solutions. Yet without the research framework that better coding and tracking could support, we cannot develop those tests or identify the patterns that would let us help them. We stay stuck in anecdote and denial on both sides.

The arguments against the code

Some organisations, including the Alliance for Aging Research, have publicly urged the CDC’s ICD-10 committee not to create a specific code for adverse effects of COVID-19 vaccines. Their stated concerns are that it would skew thinking toward assuming harm, that causation in any individual case is often a diagnosis of exclusion and therefore unreliable, and that general codes for vaccine adverse events already exist and could be used where a link appears clear.

These points are not frivolous. Proving causation in medicine is frequently difficult, and we should be wary of labels that encourage premature conclusions. But if adverse events linked to these particular vaccines are more common or have distinct features compared with other vaccines, folding them into the broadest existing categories risks diluting the signal and slowing the very research that could clarify the picture. A dedicated code does not declare that every coded case was caused by the vaccine; it allows us to count and study them more precisely.

The legal dimension is also openly discussed. Once a specific code exists, it becomes easier to identify cohorts for potential claims, and that reality fuels resistance from various quarters. I understand the institutional anxiety. But avoiding classification out of fear of accountability does not protect patients. It simply leaves them without a recognised pathway to care or investigation.

Comments To The Proposed New Icd 10 Cm Code For Adverse Effect Of Covid 19 Vaccines Aar

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What we actually need

When I read the comments under discussions of this issue, the division is stark. Some express deep cynicism that anything meaningful will come from what they see as political theatre. Others share personal stories of family members who developed serious illness after vaccination and wonder about connections, while acknowledging that cancers and other conditions existed before the pandemic too. Both reactions point to the same underlying problem: we lack the structured tools to move beyond speculation.

What would genuine progress look like? It would mean treating this as a clinical and scientific question first. A specific ICD code would be one practical step toward better data collection. But the larger requirement is focused research into mechanisms—whether persistent viral proteins, immune dysregulation, or other pathways—and the development of diagnostic approaches that can help individual patients. That work has the potential to benefit not only those affected by these vaccines but also our understanding of other post-infectious or post-vaccination syndromes.

The H. pylori precedent shows what becomes possible once medicine stops resisting the evidence and starts building around it. We gained antibiotics that cure ulcers and prevent complications. Similar clarity here could open treatment avenues we are currently missing.

I keep returning to the patients who have been waiting five years. Many are not asking for political victories. They are asking to be seen clearly enough that medicine can actually help them. An ICD code will not solve everything on its own, but refusing even to create the category keeps us from taking the first necessary step. The science will only move forward when we give it the structures it needs.

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You may disagree with her. You may believe she was wrong. But when someone is willing to risk their reputation, their career, their finances, and ultimately their wellbeing to defend a position, I think we owe them the effort of understanding what they were trying to say.

That is why I have spent time learning about Christine Cotton.

I did not know her. I only became aware of her work after her death. Yet the more I read of her background and her arguments, the more she seemed to represent something larger than a dispute about vaccines. She represented a question science is increasingly struggling to answer.

What do we do with people who challenge the consensus?

Why Her Voice Carried Weight

Christine Cotton was not an influencer who had suddenly discovered an interest in vaccines.

She was a biostatistician with more than twenty-five years in pharmaceutical research. She had worked with major companies, reviewed clinical trials, and understood the regulatory process from the inside. She knew how studies were designed. She knew how data were analysed. She knew what regulators looked for, and what they were willing to accept.

That is what made her different. When she began questioning aspects of the Pfizer trial programme, she was not speaking as an outsider. She was speaking as someone who had spent a career evaluating exactly these kinds of studies.

That does not mean she was right. But it does mean her arguments deserved careful consideration.

The Debate Was Never Really About Process 2

Most discussions of Christine Cotton focus on the manufacturing differences between what she called Process 1 and Process 2.

In simple terms, her concern was that the vaccine eventually distributed to millions was made using a different large-scale production process from the material used in earlier development. She believed the bridging data between the two were insufficient. Regulators disagreed; they reviewed the comparability data and concluded the products were similar enough to proceed.

That disagreement matters, but I do not think it was the strongest part of her case. Many people fixed on Process 2 precisely because it is easy to explain. Her more substantial concerns were about trial methodology.

The Questions She Believed Needed Better Answers

Reading through her work, several themes recur.

The first is follow-up duration. The point is straightforward: long-term safety cannot be known in the short term. During a pandemic, decisions have to be made before perfect information exists, and that is understandable. But honesty matters. There is a difference between saying “we know this is safe long term” and saying “we do not yet know the long-term outcomes, but the potential benefits justify proceeding.” Those are not the same statement.

Another concern was suspected but unconfirmed COVID cases. Cotton questioned whether large numbers of participants who developed symptoms had been fully accounted for in the efficacy calculations. She also raised questions about protocol deviations and overall trial conduct. Regulators reviewed these issues and remained satisfied; her position was that they warranted more scrutiny than they received.

Then there is the placebo crossover, which remains one of the most interesting issues for me. Once the vaccine showed early efficacy, participants in the placebo arm were offered vaccination. The ethical argument was obvious: if the vaccine worked, withholding it would be hard to justify. But the scientific consequence was equally obvious. You lose the ability to make long-term comparisons between vaccinated and unvaccinated groups.

That does not mean the decision was wrong. It means there was a trade-off. And I think it is fair to say so.

The Ventavia Question

Cotton also paid close attention to the Ventavia allegations, where a whistleblower claimed that some trial sites were not fully adhering to protocol.

Those sites were small relative to the overall study, and regulators concluded the broader findings remained valid. But Cotton’s concern reached beyond any single location. Her question was simple: if problems can occur at one site, how confident are we that similar issues were absent everywhere else?

That is not an unreasonable question. It is exactly the sort of question experienced auditors are trained to ask.

The Mistake Science Keeps Making

There is a broader lesson here. Science often treats disagreement as binary. Someone is either right or wrong. Trusted or discredited. Accepted or rejected.

Reality is rarely that clean. A person can be wrong about one part of a problem and correct about another. A critic can identify genuine weaknesses while still reaching conclusions others reject. The danger comes when we decide that one disputed point invalidates everything else they say. Apply that standard consistently, and very few experts survive it.

The pandemic taught us that scientific understanding evolves. Recommendations changed. Predictions changed. Policies changed. That is not failure; that is how science works. The problem is when we grant ourselves that flexibility and deny it to those who challenge us.

The Bigger Issue Nobody Can Ignore

The most striking thing I have observed recently is not the continuing argument about vaccines. It is the widening gap between scientific institutions and public trust.

I recently read the comments under a widely shared post claiming that COVID vaccines are among the safest medical interventions ever developed. The response was overwhelmingly negative. Whether those comments are scientifically justified is almost beside the point. The public believes something has gone wrong.

When millions of people feel unheard, ignored, or dismissed, trust begins to fracture. And trust is remarkably hard to rebuild once broken. That concerns me far more than any single disagreement over a clinical trial.

Remembering Christine Cotton

Christine Cotton’s final message was not really about statistics. It was about conviction. She believed she had found something important, and she believed it strongly enough to give years of her life to it despite enormous personal cost.

History will go on debating her conclusions. Regulators will go on defending theirs. Scientists will go on arguing the details. But something larger is worth holding onto.

Progress depends on people willing to ask uncomfortable questions. Sometimes those questions turn out to be wrong. Sometimes they reveal what everyone else missed. The difficulty is that we rarely know which is which at the time.

That is why voices like hers should not be ignored. Not because they are necessarily right, but because a healthy scientific culture has to be willing to listen.

It is June 2, 2026. By the time you read these lines, I will have left this world.

For those who do not know me, my name is Christine Cotton. I am what is known as a whistleblower. I worked for 25 years in the pharmaceutical industry in the management and analysis of clinical data. As a biostatistician, since December 2020, I have immersed myself in the documents of the COVID vaccine from the Pfizer laboratory. I have written numerous documents and done many broadcasts to share the real results. My conclusions are catastrophic, beyond the invalidity of the results due to errors or even manifest frauds. The Pfizer vaccine that the population received, that you may have received, is not the one from the clinical trial with the 95% efficacy announced by all the politicians, journalists, and TV doctors. You were administered a product for which there were absolutely no results, neither of efficacy nor of tolerance. This message is not intended to create sensationalism on social networks but to inform you of one of the biggest manipulations that humanity has ever known. All the evidence is in the latest version of my work, which I invite you to download and read. For the lazier ones and the very busy, the few pages of the conclusion and the links to the source documents will already enlighten you a great deal.

I fell ill at the very moment I filed a complaint against the health authorities. For over a year, I have been suffering from excruciating pain starting from the lower back down to my legs, burning sensations in the skin, mainly in the legs and back. I have consulted general practitioners, neurologists, osteopaths, virologists, dermatologists, rheumatologists, psychiatrists, homeopaths... I have swallowed thousands of capsules of dietary supplements, anxiolytics, neuroleptics, painkillers prescribed by the pain center. I have even done bioresonance sessions and seen magnetizers, and this without any result.

I am at the end of what I can bear.

I ask forgiveness from those who love me, you who have followed me on social networks for 4 years, my friends, my parents, and above all to God or whatever his nature or name may be, to end my life—I, who have never ceased to protect it since childhood, whether plant, animal, or human life.

From the bottom of my heart, I thank those who have supported me, encouraged me, and all those who pray or have organized prayer groups. I am going to ask you to pray once more so that my soul may be in the light of the Creator as soon as possible.

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The researchers found that these patients did develop nasal antibodies after vaccination, and some could block the virus from binding ACE2, one of the key steps in infection. But the levels were far lower than in healthy controls.

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That detail takes us straight to the problem many people are now living with. They are not asking an abstract scientific question. They are asking, “Why do I keep getting sick?” Repeated respiratory infections, repeated COVID, longer recoveries, and strange symptoms that do not fit the old rules.

The paper matters because it reminds us that protection in the blood is not the same as protection at the border. And for a respiratory virus, the border is the mucosal lining.

The Nose Is Not a Side Issue

When a virus enters through the nose or mouth, it does not start by floating in the bloodstream. It starts by trying to break through the mucosal barrier and infect the cells lining the airway.

This is why mucus matters. When your nose runs with a cold, that is not just an inconvenience. It is defence. The body is trying to trap the virus, dilute it, and move it away before it can attach to cells.

But mucus is more than a mechanical barrier. Embedded in that layer is one of the most important tools we have against respiratory viruses: secretory IgA. It sits in the mucus and binds viruses before they can reach the cells underneath. If it works, the virus is trapped and cleared — coughed out, sneezed out, swallowed, or carried away by normal mucociliary clearance.

This is the first battle. Win it here, and the rest of the immune system may never need to fight.

The Border Patrol Problem

The analogy I keep returning to is border patrol.

Imagine a team is looking for one person, but they have only been trained to recognize a red jacket. If that person arrives in the red jacket, they are caught. But what if they change the jacket, add a hat, put on glasses, or alter their walk?

A poor border patrol misses them. A sophisticated one does not just look for the jacket. It reads height, build, gait, face shape, behaviour — multiple features at once. Even if one changes, the person is still recognized.

That is how broad immunity should work. A narrow response looks only for the red jacket. A broad response looks for the whole person.

This becomes critical with SARS-CoV-2 because the virus changes. If the immune system is trained too narrowly, especially around spike, then changes in spike can blunt recognition. The virus does not need to become invisible. It only needs to become different enough to slip past the first line of defence.

Why Spike Alone Was Never Enough

One of the central mistakes of the pandemic was assuming that a spike-focused systemic response could control a mucosal respiratory virus.

I am not saying injectable vaccines had no role. For high-risk people who had never met the virus, systemic vaccination made sense as a way to reduce severe disease. But if the goal was to reduce infection and transmission, the target should always have been the mucosal lining. That is where the virus enters, where early replication occurs, and where transmission begins.

The Koomen paper shows that vaccination can produce some nasal antibody response. It also exposes the weakness of assuming that a systemic injection automatically builds strong mucosal protection. In immunosuppressed transplant recipients the nasal response was clearly weaker, but the principle is broader: training the immune system in the bloodstream is not the same as training the border patrol at the surface.

That distinction should have been obvious from the beginning.

Koomen, Vera JCH, et al. "Kidney Transplant Recipients Develop Nasal Mucosal Antibodies to SARS‐CoV‐2 With ACE2‐Inhibiting Activity Following mRNA Vaccination." Transplant Infectious Disease (2026): e70230.

The Role of T Cells at the Mucosal Surface

Secretory IgA is only part of the story.

If the virus gets past IgA and infects a cell, the next defence is the T cell response. T cells do not chase free virus. They identify infected cells and destroy them. This matters because once inside, the virus turns that cell into a factory. A single infected cell can produce vast numbers of new particles. Destroy it early, and the infection is contained before it expands.

The way T cells recognize infected cells is remarkable. Viral proteins made inside the cell are processed and displayed on its surface as small fragments — almost like flags. The cell is announcing what is being built inside it.

A broadly trained immune system can read many of those flags. That includes spike, but not only spike: nucleocapsid, membrane and envelope proteins, ORF proteins, non-structural proteins. Natural infection exposes the immune system to a far wider range of viral material than a spike-only approach ever could.

The Difference Between Narrow and Broad Recognition

This is the part I think people need to grasp clearly.

If the immune system is trained mainly to recognize spike, its T cells and antibodies are watching for a limited set of signals. That does not mean there is no response. There is. The question is whether it is broad enough, especially at the mucosal surface, to detect infected cells quickly once the virus changes.

A broader response means multiple T cell populations can recognize multiple viral proteins. That leaves the virus fewer places to hide. Even if one part changes, the others remain visible.

This is why I keep returning to the border patrol. Look for one feature, and the virus has room to evade. Look for many, and it struggles to slip through.

This does not mean every naturally infected person has perfect immunity. They do not. It does not mean every vaccinated person has poor immunity. They do not. Biology is never that simple. But as a general principle, a broad mucosal response should be more resilient than a narrow, spike-dominant one.

Why People May Keep Getting Sick

This is where the discussion becomes uncomfortable.

If the mucosal barrier is weak, the virus crosses the border more easily. Once through, the body has to fight it internally — more inflammation, more tissue involvement, more immune activation, and potentially more cumulative damage.

People may say, “But I did not feel that sick.” That may be true. Yet milder symptoms do not mean a harmless infection. A virus can still drive inflammation, vascular effects, immune disruption and organ stress even when the acute illness seems mild.

This is why repeated infections matter. Each one is not an isolated event. It is another chance for the virus to interact with the immune system, the vasculature, the nervous system, the gut and the airways. If people are being infected again and again, the question is not only why the virus is still circulating. It is why the first line of defence keeps failing to stop it.

The Missed Opportunity

Looking back, the pandemic response should have separated two goals.

The first was reducing severe disease in high-risk people. For that, systemic immune training had a role. The second was reducing infection and transmission. For that, mucosal immunity should have been central.

We never made that distinction clearly enough. We acted as though a systemic vaccine strategy could solve a mucosal transmission problem — always a weak assumption. A more rational approach would have pursued mucosal vaccines far earlier and far harder, studying secretory IgA, nasal T cells, airway immunity, interferon responses and the biology of infection at the portal of entry.

Instead, the public conversation collapsed into antibody levels in the blood. That was never enough.

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Where We Go From Here

We now need honesty.

We need to stop treating repeated infections as normal background noise. We need to stop assuming that mild symptoms mean nothing important has happened. And we need to stop ignoring the mucosal immune system simply because it is harder to measure than serum antibodies.

The future has to be broader. That means looking at secretory IgA, mucosal T cells, gut-airway immunity, nasal nitric oxide, vitamin D status, sleep, metabolic health, chronic inflammation and repeated viral exposure. It means asking why some people are infected again and again while others stay resilient. Most of all, it means moving beyond spike as the whole story.

Spike matters. But it is not the whole virus. And the immune system, properly trained, was never built to watch for one flag. It is built to recognize patterns, multiple signals, and infected cells before the virus takes over.

That is the message I want people to understand. If we are going to explain why so many keep getting sick, we have to look at the border. We have to understand mucosal immunity. And we have to rebuild the kind of broad defence that does not just spot one red jacket, but recognizes the whole threat.

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Those things matter. Lyme is caused by Borrelia bacteria carried by infected ticks, usually picked up in wooded or grassy areas. Remove the tick early and the risk falls. If infection takes hold, it can produce the classic bullseye rash, fever, fatigue, muscle and joint pain, neurological symptoms, and sometimes cardiac involvement.

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But that is only the first layer.

The deeper question is why so many people now describe chronic inflammatory symptoms after COVID — and why some of those symptoms look so much like Lyme, Epstein-Barr reactivation, shingles, autoimmune flares, and other conditions that had previously gone quiet.

That is the pattern I want to focus on.

The Vaccine Tells Us Something Important

Pfizer and Valneva have been developing a new Lyme vaccine. The recent phase three results suggested around 73% efficacy after four doses, which sounds encouraging. But the detail matters.

This is not an mRNA vaccine. It is a protein-based vaccine targeting a bacterial surface protein called OspA, and the strategy is very different from how most people imagine vaccines working.

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The public is tired of COVID. The media is tired of COVID. Even much of the scientific community seems tired of it. The keyword data says the same thing: people are no longer searching for it with any urgency. COVID has become a word most people would rather not hear.

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But that is exactly what concerns me.

When I look at the data after the pandemic, I do not see reassurance. I see signals. I see patterns across age groups that do not look random. Liver disease rising. Hypertensive heart and renal disease appearing more prominently. Myocarditis signals in older cohorts. Abnormal patterns affecting different organs in ways that still need explanation.

The danger is not simply that COVID is still circulating. The danger is that we may be looking for the wrong disease.

Same Virus, Different Disease

One of the simplest ways I explain this is with varicella zoster virus.

Most people know it as the virus that causes chickenpox. In children, it presents with fever, an itchy rash, and spots across the body. That is the disease everyone recognises.

But later in life, the same virus can reactivate and cause shingles. This looks completely different: localised, painful, nerve-related, appearing in an entirely different clinical pattern. If we did not already know the biology, most people would assume chickenpox and shingles were two separate diseases.

That is the point I think we are missing with SARS-CoV-2.

The disease we saw early in the pandemic was acute COVID-19, dominated by respiratory compromise, pneumonia, inflammation, clotting, and hospitalisation. That presentation caught the world’s attention because it was visible, dramatic, and frightening.

But what if the later phase does not look like that? What if reinfection, repeated exposure, prior immune priming, and persistent spike-related immune activation produce a very different disease picture?

That is where I believe we are now.

Why Reinfection May Look Different

I do not expect the next phase of COVID harm to look like 2020.

This is where I differ from others who are still waiting for a dramatic new variant to reproduce the severe respiratory collapse we saw early on. I think a highly immune-evasive version of the virus may already be here. It simply may not be presenting in the way people expect.

Instead of one obvious respiratory illness, we may be seeing a mosaic. One person develops blood pressure instability. Another develops kidney dysfunction. Another has persistent gut symptoms. Another has palpitations, myocarditis, neurological symptoms, brain fog, fatigue, or vascular problems.

At face value, these look like separate diseases.

But I keep asking the same question: could they be different manifestations of the same underlying immune problem?

The Group I Worry About Most

The key question is not simply whether someone has been vaccinated or unvaccinated. That framing is too crude.

The better question is this: who is at risk of a hyperimmune response when they are re-exposed to spike protein?

The first group I worry about is people who had moderate to severe COVID-19. If someone was hospitalised, required oxygen, or mounted a major inflammatory response during their first infection, that tells me something. Their immune system did not merely encounter the virus. It reacted intensely. That kind of response may leave the system primed.

This is why I always believed we should have been cautious about vaccinating people shortly after moderate or severe COVID. My concern was not ideological. It was immunological. If the spike protein was central to the immune activation, why would we assume that repeated spike exposure in an already primed immune system was risk-free?

The second group is what I would call vaccine hyper-responders. Not everyone who was vaccinated, but the people who had strong systemic reactions: prolonged lymph node swelling, hypermetabolic lymphadenopathy, persistent immune symptoms, or inflammation well outside the normal time frame. That suggests the systemic immune system was strongly activated.

The third group is people with poor mucosal protection: the ones who keep getting reinfected. Their upper airway defences are not holding the virus at the surface. That matters, because the most important boundary in this entire discussion is the mucosal barrier.

The Castle Wall

I use the analogy of a castle because it makes the immunology easier to understand.

Strong mucosal immunity is a well-defended castle wall. There is a moat, a strong gate, and guards on the outside. The attackers may arrive, but they cannot easily get in. That is what the nose, throat, tonsils, adenoids, and airway lining are meant to do. They are not passive surfaces. They are active immune barriers.

If SARS-CoV-2 stays at the mucosal surface, the risk is much lower. The battle stays outside the castle.

But if mucosal immunity is weak, the situation changes. Now the virus gets through the gate. It enters the bloodstream, the lymphatics, and deeper tissues. The immune system is no longer fighting outside the walls. It is fighting inside the city. That is where damage occurs.

And it is not simply the virus. It is the immune response to infected cells, persistent antigen, immune complexes, macrophage activation, endothelial injury, clotting, and autoimmune-like responses.

This is the part many people still do not grasp. A strong systemic immune response sounds good, but if the virus is already inside the body, that same response may cause collateral damage.

The Critical Distinction

This is why I keep saying the same thing: the issue is not vaccination status alone. The issue is whether spike exposure is triggering systemic immune activation.

If someone has strong mucosal immunity, even prior immune priming may not matter much, because the virus never gets inside. But if the virus breaks through the mucosal barrier, everything changes.

People often know when this happens. The illness feels different. It lasts longer. There are more systemic symptoms. Blood pressure becomes unstable. Gut symptoms flare. Palpitations occur. Fatigue is deeper. Recovery is slower.

That tells me the virus may not have stayed at the wall. It may have entered the castle.

Why the Dashboards Matter

When I look at the post-pandemic dashboards, I am not seeing isolated noise. I am seeing patterns that could fit with systemic immune injury.

In middle-aged groups, blood pressure and kidney-related signals matter. In older groups, myocarditis signals matter. Liver abnormalities matter. Mineral metabolism disorders matter. None of this is the old picture of COVID as simply a respiratory disease.

This is why the chickenpox and shingles analogy is so important. The same virus can produce different manifestations depending on timing, immune context, tissue vulnerability, and patterns of reactivation or re-exposure.

So if we are only looking for severe respiratory COVID, we may miss the disease that is actually emerging.

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Why Nobody Wants to Look

The public wants to move on. I understand that. People are tired. They do not want more fear, more restrictions, or another lecture about COVID.

But science does not work by emotional exhaustion.

The scientific community also seems reluctant to return to this territory. If we seriously examine ongoing COVID pathology, we may also have to re-examine pandemic decisions, vaccine strategy, public health messaging, and the assumption that repeated infections are harmless.

That is uncomfortable. But ignoring uncomfortable pathology does not make it disappear.

The Point I Want People To Understand

I am not saying everyone is at equal risk. That would be wrong.

I am saying the people I worry about most are those with prior immune priming and weak mucosal defence: people who had severe COVID, people who had unusually strong immune responses after vaccination, and people who repeatedly fail to contain reinfection at the mucosal surface.

The real question is not, “Have I had COVID before?”

The better question is, “When I am exposed again, does my immune system keep the battle outside the castle, or does the virus get inside and trigger a systemic response?”

That is the framework I think the public needs.

Where We Go From Here

We need to stop pretending COVID is over simply because the acute hospital crisis has changed shape. The disease may have changed its presentation.

The question now is whether ongoing circulation is creating a slow, broad, multi-system burden that we are failing to name, because we are still looking for the old version of the disease.

I do not think we can afford that mistake.

We need better surveillance. We need better immune phenotyping. We need to understand mucosal immunity, reinfection risk, spike persistence, macrophage activation, and why some people develop systemic consequences while others do not.

Because if this model is correct, the problem is not behind us.

It is evolving in front of us.

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