Over the past several years, I have been trying to understand a biological phenomenon that many people initially dismissed: the unusual white fibrous clots reported by embalmers across the world. These are not typical thrombi. They are pale, rubbery, and often extend for many inches through blood vessels. Their composition appears very different from the red fibrin-and-blood-cell clots we normally see in pathology. For a long time, these observations were simply labelled anecdotal — but a small number of researchers refused to ignore them.
Two individuals who have played an important role in bringing these findings forward are Bruce Rapley and Matt Shelton. Their efforts in documenting and helping coordinate analysis of these clot samples have been critical. Without that groundwork, none of the deeper biochemical investigations that followed would have been possible. What has emerged from those analyses is a potential mechanism that shifts our understanding of these clots entirely.
The Clue Hidden in Hemoglobin
One of the most striking findings from proteomic analysis of the clot material is the unusually high concentration of hemoglobin fragments. In some samples, hemoglobin accounted for a surprisingly large proportion of the total protein content within the clot. That observation immediately raised an important question for me: why is hemoglobin accumulating inside a clot structure? The answer, I believe, lies in a specific immune cell population that has been receiving increasing attention in the research literature.
The Role of THBS1+ Monocytes
Recent work has drawn my attention to a particular subset of monocytes — those expressing thrombospondin-1, or THBS1. This is a multifunctional glycoprotein involved in platelet activation, endothelial signalling, extracellular matrix remodelling, and immune modulation. But THBS1 also appears to be involved in haemoglobin and haem scavenging after red blood cell damage.
When red blood cells break down — a process called haemolysis — free haemoglobin becomes highly toxic to tissues. The body normally removes it rapidly through macrophages and associated clearance pathways. However, if haemolysis becomes excessive, or if those clearance pathways become dysregulated, free haemoglobin and haem fragments can accumulate in the circulation. And that changes the clotting environment dramatically.
Haemolysis: The Missing Piece
One of the most important observations in COVID research has been the appearance of immune-mediated haemolysis in some patients. A systematic review of 105 cases confirmed that COVID-19 can trigger autoimmune haemolytic anaemia, where antibodies target red blood cells and cause them to break apart prematurely. This destruction releases large quantities of free haemoglobin, haem iron, and membrane phospholipids — each of which is capable of promoting both inflammation and coagulation.
When THBS1-positive monocytes encounter this environment, they appear to participate in forming unusual fibrin-dominant clot structures. In other words, the white clots may be the downstream consequence of haemolysis combined with immune activation. That realisation, for me, was the moment the picture started to come together.
Where G6PD Deficiency Enters the Picture
If haemolysis is a major driver of this process, then one group of people immediately becomes relevant: individuals with glucose-6-phosphate dehydrogenase deficiency, or G6PD deficiency. G6PD is a critical enzyme that protects red blood cells from oxidative stress. Without adequate G6PD activity, red blood cells become extremely vulnerable to viral infections, systemic inflammation, certain medications, and oxidative metabolites. When oxidative stress rises, G6PD-deficient red cells rupture far more easily than normal cells. That creates exactly the biochemical environment needed for the THBS1 mechanism to activate.
The High-Risk Populations
Globally, over 400 million people carry G6PD deficiency, making it one of the most common enzyme deficiencies in the world. The prevalence is particularly high in Mediterranean, Middle Eastern, African, South Asian, and Southeast Asian populations, and in some regions it can reach 10–20% of the population. For most people with G6PD deficiency, this condition remains entirely silent until oxidative stress triggers haemolysis. A major systemic inflammatory illness — such as COVID — can be exactly that trigger. I think this is a factor that has been dramatically under-recognised.
Why This Matters for Embalmer Clots
If the THBS1-monocyte model is correct, then the unusual white clots reported by embalmers may represent the extreme end of a biological spectrum. The sequence I am proposing runs as follows. Viral infection or immune activation triggers oxidative stress. Susceptible red blood cells undergo haemolysis. Free haemoglobin accumulates in the circulation. THBS1-positive monocytes interact with the haemoglobin fragments. And unusual fibrin-dominant clot structures form. Individuals with G6PD deficiency would naturally sit at the highest-risk end of that pathway, because their red blood cells are inherently more fragile. This could help explain why the clotting patterns appear so variable between individuals — the variation may be driven, at least in part, by underlying differences in red cell resilience.
Why This Hypothesis Needs Urgent Investigation
What I am describing here is not a simple clotting disorder. It may represent a hybrid process involving immune activation, haemolysis, and abnormal fibrin structure formation. That possibility has enormous implications for understanding post-COVID vascular disease, unexplained thrombotic events, and persistent inflammatory syndromes. But hypotheses are only the starting point. The work now needs to move into properly designed studies examining THBS1 monocyte activity, haemoglobin fragmentation patterns, G6PD status in affected individuals, and detailed structural analysis of the clot material.
The Responsibility of Medicine
The work done so far by investigators — including those supported by the efforts of Bruce Rapley and Matt Shelton — has raised important questions. Those questions deserve answers. Medicine advances by investigating anomalies, not by ignoring them. And right now, the unusual white clots reported by embalmers may be one of the most important anomalies of the entire pandemic.
