For several years, I have been following one of the strangest medical observations to emerge since the pandemic: long, white, fibrous structures being removed from the blood vessels of the deceased by embalmers.
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.
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.
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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