COVID White Clots, Tissue Repair, and Rheumatoid Disease: Clues to Possible Medical Progress in the Face of the COVID Genocide

By Lewis Coleman, MD.

Dr. Coleman is one of the principals of the Three Sages substack.

Introduction

For me, there were important clues to future medical progress linked to the catastrophic COVID injections that were otherwise a black cloud of mass murder foisted upon the world by conspiratorial ruling elites and pharmaceutical companies gone insane.

The deadly and deceitful mRNA injections have reportedly been causing the formation of tough white protein strands bathed in amyloid protein in the small peripheral arteries of injection victims that apparently have been causing both sudden death in healthy young people and the lingering “Long COVID” syndrome. It immediately seemed obvious to me that these terrifying “white clots” must be composed of collagen, which is the main structural protein in the body. But what mechanisms are responsible for their unprecedented appearance in so many victims? Indeed, even most medical professionals seem unwilling even to ask the question.

Collagen is the body’s most common protein. It is white in color and composes tendons, ligaments, scars, and sclerosis (hardening of tissue). It is the tough protein which binds cells into specialized multicellular organs and tissues. It also binds calcium and carbon dioxide into hydroxyapatite, which is the substance of bone. Strangely, none of the physicians who have commented on these white clots found in association with the COVID “vax” has suggested that they might be composed of collagen, at least not to my knowledge. Perhaps this is because conventional medical theory cannot explain tissue maintenance and tissue repair; or perhaps they simply cannot imagine how collagen could form in blood circulation. However, the close association of the white clots with amyloid protein is compelling. Because amyloid protein occurs in many disease conditions, such as diabetes, any suggestion of its occurrence is an obvious red flag in any diagnosis.

Previously, in my book 50 Years Lost in Medical Advance: The Discovery of Hans Selye’s Stress Mechanism, published soon after the start of the COVID contagion, I had hypothesized that the source of the dangerous amyloid protein was “fibrin split products” that result from the disintegration of insoluble fibrin, the protein polymer that binds blood cells into viscoelastic clots. This fresh COVID evidence forced me to realize that my hypothesis was wrong. The good news was that this enabled me to formulate a simplified explanation of tissue maintenance, tissue repair, and chronic illness, including rheumatoid disease. My conclusions may be found in the articles cited in the footnotes to the present analysis presented here.

The following brief review of the mammalian stress mechanism, which was the focus of my book, is intended to refresh the memory of those who have already read the book but also to provide background information needed to understand my new hypothesis. Those who haven’t read the book may seek my previous articles published in Contentment Magazine or download copies of my published papers from my website at www.stressmechanism.com.

The Vascular Endothelium

In order to explicate this important topic, technical terminology and complex physiological concepts are necessary. The general reader is advised not to get “thrown” by these elements but rather to strive for an overview while appreciating the miraculous nature of the functioning of the human organism. After all, this is our home on planet earth, as long as we are here. We might as well try to understand it, even if it took an incredible level of superintelligence to create it. That is what medical research should be all about, not just generating profits for Big Pharma.

Central to our review is the critical role in the human body of the vascular endothelium. The vascular endothelium is a diaphanous layer of cells, only one cell thick, that lines the inner surface of all blood vessels and is the sole constituent of capillaries (the smallest blood vessels). It isolates blood enzymes from extravascular tissues, but it is “selectively permeable” so that it allows the passage of some blood enzymes and substances but not others. This explains how it regulates tissue maintenance. It produces numerous substances that enable the operation of the stress mechanism, including von Willebrand Factor, nitric oxide, fibronectin, vitronectin, ATIII, and Protein C. In organs, it is directly innervated by the autonomic nervous system, which regulates a “capillary gate” mechanism that governs hemodynamic physiology and organ activity. Obviously, the capillary gate must be working properly for the blood to deliver to cells substances they need and keep out those which are harmful.

The Enzymatic Interaction of Factors VII, VIII, IX, and X

The enzymatic interaction of factors VII, VIII, IX, and X is the “engine” of the stress mechanism. This interaction taking place deep within the human body’s chemical laboratory (and that of all mammals) generates the products of the stress mechanism; namely, thrombin, fibrinogen, soluble fibrin, insoluble fibrin, and collagen. Each of these products has its own pathways, serving various purposes and causing different symptoms and manifestations. Such variation partly explains the baffling nature of physiology and disease.

Blood Proteins

When I was in medical school, the fibrillar (string-like) blood proteins (fibrinogen, soluble fibrin, and insoluble fibrin) were indistinguishable from one another and were collectively called “fibrin.” It was crudely understood that their constantly fluctuating balance determined blood coagulability, but nobody knew how the mechanisms worked.

Their association with collagen was unknown. Since then, research technology has devised chemical and physical tests that distinguish these fibrillar proteins from one another and clarify their individual functions. They enable coagulation (clot formation), capillary hemostasis, blood flow regulation, organ regulation, cardiac output, cardiac efficiency, blood pressure, pulse rate, tissue maintenance, and tissue repair. When produced in excess they explain numerous disease manifestations, including tissue edema, organ disruption, blood hypercoagulability, heart attacks, strokes, fibrosis, sclerosis, scar formation, exudates, and pus. None of this was understood when I was in medical school.

Thrombin

I call thrombin the “Universal Enzyme of Energy Transformation.” It is the key enzyme in the process of blood clotting so necessary for human life. At normal levels, thrombin functions as it should; when elevated, strokes and other life-threatening conditions may occur. The enzymatic interaction of blood enzyme factors VII, VIII, IX, and X continuously regulates thrombin generation in all tissues throughout the body. Thrombin utilizes adenosine triphosphate (ATP) to energize, and therefore regulate, cell and extracellular enzyme activities throughout the body that repair tissues and regulate organs, including coagulation, mitosis, metabolism, inflammation, chemotaxis, cell hormone release, apoptosis, muscle contraction, and so forth. Thrombin activity requires Ca+, so the parathyroid glands maintain Ca+ levels within a narrow range to optimize thrombin activity. Thrombin also energizes the conversion of fibrinogen to soluble fibrin, as well as the conversion of soluble fibrin to insoluble fibrin and collagen.

Orthodox Theory and Chronic Illnesses (Rheumatoid Diseases)

Orthodox medical theory regards chronic illnesses as baffling medical mysteries. These include diabetes, essential hypertension, rheumatoid arthritis, scleroderma, Sjogren’s disease, systemic lupus erythematosis, Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, and many others. These are categorized as “rheumatoid diseases,” and they inexorably worsen with time. They are often labeled “autoimmune disease,” as if the body were attacking itself. However, there is no evidence that the immune system causes harm of any sort.

Chronic illnesses cause painful, progressive, crippling inflammation, fibrosis, sclerosis (abnormal, harmful collagen deposition in tissues), and capillary destruction (accelerated capillary senescence). The research literature reveals that abnormal amyloid protein deposition is found in the afflicted tissues of all rheumatoid illnesses, but this is ignored in conventional medical theory, education, and practice. Detecting amyloid protein necessitates painful, expensive, invasive tissue biopsy, which is seldom performed, so that amyloidosis remains unsuspected and is seldom detected in clinical practice. This is a major failing of contemporary medical practice. Thus the sources of amyloid and its role in causing chronic illnesses remain mysterious.

As a generalization, orthodox medical practice offers no explanations or effective cures for either chronic illnesses or amyloidosis. So only symptoms are addressed. Symptomatic treatment mostly consists of toxic non-steroidal anti-inflammatory analgesics (NSAIDS) and toxic immune suppression medications that cause more harm than good.

Stress Theory, Tissue Maintenance, and Chronic Illness

Courtesy of evidence produced by the COVID contagion, stress theory confers a fresh explanation of chronic illnesses that clarifies the relationships of fibrillar (string-like) blood proteins, hemodynamic physiology, collagen generation, tissue maintenance, and tissue repair. The importance of this information, particularly in the face of a manmade worldwide health catastrophe, cannot be emphasized enough.

When I was in medical school, my stress theory lectures explained that “tissue maintenance” provides tissue strength by slowly replacing collagen and fibroblast mitosis (cell division) that replenishes aging tissue repair fibroblasts. Tissue strength declines with deteriorating tissue maintenance in old age. However, the details of this process remained unknown.

Likewise, the lectures explained that blood was an active, living substance that continued the process of clot formation even after it was removed from the body. However, whatever energized and enabled this activity remained a complete mystery. I remember thinking to myself, “How can we call ourselves doctors when we can’t even explain clot formation?” And, “I’ll bet I could figure that out, because it can’t be all that complicated!” But of course, I had plenty of other fish to fry and a living to earn as a practicing physician, so forgot all about this until many years later.

By the time I published my book on discovery of the stress mechanism, I was able to explain the nature of clot formation, atherosclerosis, and tissue repair, as well as the nature of surgical stress12, but I remained baffled by the unknown source of amyloid protein.13-15 I hypothesized that the most likely source of amyloid protein was “fibrin split products” resulting from the constant generation and disintegration of insoluble fibrin during capillary gate operation. I reasoned that these fibrillar protein fragments underwent “shape changes” to become amyloid protein. I now realize that this reasoning was wrong. The truth should have been obvious, but it didn’t dawn on me until the COVID “white clots” provided the compelling clue.

The COVID contagion began to spread while I was busy publishing my book, but the important evidence of the “white clots” didn’t appear until after my book was published, after the COVID injections were forced upon college students, teachers, medical workers, professional athletes, airline pilots, and even soldiers in the military services. Now, hundreds of healthy young people began to “die suddenly” soon after one or more mRNA COVID “immunizations,” aka “jabs”.

This was exceedingly unusual, and it caught my attention and inspired me to publish a paper explaining the COVID symptoms and strange deaths from the perspective of stress theory, because conventional medical theory couldn’t begin to explain these strange symptoms and deaths.10 Statistics soon confirmed that the “jabs” were causing the sudden deaths, while most deaths associated with ordinary pulmonary COVID were due to a combination of pre-existing illness, morbid obesity, and iatrogenic mechanical hyperventilation and failure to treat with ivermectin.16,17

Meanwhile, autopsies of the healthy young people who “died suddenly” revealed only that their hearts were strangely enlarged and distended, as if they were unable to expel their blood contents as they were dying.18,19 Based on these observations and evidence of abnormal blood coagulation, I attributed the sudden deaths to a hitherto unknown form of disseminated intravascular coagulation (DIC) which normally occurs only in critically ill patients dying from “multi-organ failure syndrome” and other forms of critical illness.10

I reasoned in accord with available evidence that the toxic contents of the “jabs” consisted of artificially weaponized coronavirus genetic material which attacked the vascular endothelium and caused it to release excessive quantities of von Willebrand Factor and tissue factor into blood circulation,. This would cause increasing blood hypercoagulability that remained free of symptoms until it became so severe that spontaneous DIC suddenly commenced throughout the body.10,20,21 Something like this occurs when overenthusiastic treatment with Epogen (artificial erythropoietin) elevates red cell mass to dangerous levels, whereupon spontaneous systemic clot formation suddenly begins. This also cannot be explained by conventional medical theory.22-24

However, my initial hypothesis was only partially correct. Soon after my paper was published, morticians began to report finding tough “white clots” in the small peripheral arteries of “jab” victims that were accompanied by abnormal red clots and saturated with amyloid protein. These unprecedented observations were overlooked during conventional autopsies, which examine only large proximal blood vessels near the heart for evidence of pulmonary embolus or heart attack that might explain the sudden deaths. Pathologists had never encountered these strange deaths and didn’t know what to look for, or where to look. They couldn’t understand the relationship of the distended hearts of the victims to their sudden deaths.

Upon learning of this new evidence, I suddenly realized that amyloid protein must be monomers of collagen, and that the white clots must be composed of collagen. This, in turn, provided me with fresh insight to the nature of tissue maintenance, tissue repair, and rheumatoid disease, all of which are closely associated.

Understanding all this necessitates the following review of fibrillar blood protein structures and functions. Please bear with me as we review these complex processes.

Fibrinogen

Fibrinogen is the source of fibrillar blood proteins. It is continuously produced by the liver and released into blood circulation. It cannot escape from blood into extravascular tissues due to its large size, and it has no direct effect on blood coagulation. It consists of three fibrillar, submicroscopic amino acid chains called alpha, beta, and gamma that are held together by “disulfide bonds.” Thrombin dissolves the disulfide bonds and releases these tiny amino acid (protein) chains into blood circulation. Thus freed, they are called “soluble fibrin.” You can again see from this process the crucial role played by thrombin in vascular physiology.

Soluble Fibrin

In blood, factor VIII adds “cross-links” of fibronectin, vitronectin, plasminogen, and gelsolin to alpha, beta, and gamma fibrillar subunits of soluble fibrin to produce insoluble fibrin monomers that polymerize into strands of insoluble fibrin. These reduce pulsatile blood turbulence below a critical threshold, whereupon they entangle blood cells into viscoelastic clots.15

The alpha, beta, and gamma subunits of soluble fibrin do not affect blood coagulability. They are so small that they can escape from blood into extravascular tissues via inflammatory gaps between the cells of the vascular endothelium, along with factors VII and X, where they serve as substrates for fibroblasts to produce amyloid monomers that polymerize into collagen. However, since factor VIII cannot penetrate the vascular endothelium due to its gigantic size, it isn’t present in extravascular tissues, so it cannot add cross-links of fibronectin, vitronectin, and plasminogen to the collagen structure. As a result, collagen is far stronger than insoluble fibrin.

Tissue Maintenance

When I was in medical school, my stress theory lectures explained how “tissue maintenance” consisted of slow “turnover” of collagen to sustain tissue strength, plus slow mitosis (cell division) of tissue fibroblasts that replace aging fibroblast cells. These are repair cells that are present in all tissues, but they look different depending on where they are found, as they are sub-specialized to fit the needs of their specific tissue.

In those days, of course, almost nothing was known about the individual properties of blood enzyme factors VII, VIII, IX, and X or how they enable tissue maintenance and tissue repair. These blood enzymes were categorized as “coagulation cascade enzymes” that interacted with one another in a sequential (“cascade”) manner to generate “insoluble fibrin” that somehow enabled clot formation. Nobody thought they had anything to do with tissue maintenance or tissue repair, except that viscoelastic clot formation to stem blood loss was recognized as the first step of tissue repair.

In extravascular tissues, where factor VIII is absent, the interaction of factors VII and X with soluble fibrin and fibroblasts produces amyloid monomer, which polymerizes into strands of collagen to enable tissue maintenance.

Soluble fibrin explains several disease manifestations when it is produced in excess. In eclampsia and other critical illnesses, it causes tissue edema that disrupts organs and damages tissues; it invades and bursts the liver;25 it forms “hyaline” casts in kidney glomeruli that disrupt renal function; it appears in urine as “albuminuria”; it collects in the lungs as “exudates” that disrupt gas exchange; and it promotes harmful amyloidosis, sclerosis, and fibrosis (collagen formation) in extravascular tissues, which destroys capillaries, undermines tissue oxygenation, and causes pulmonary sclerosis and rheumatoid disease.

We see here how many disease states are actually normal processes exaggerated by stimuli that result from hyperactivity. As we shall see later in this paper, this hyperactivity results from insults introduced from outside the human subject. Once set in motion, the disease states gradually become chronic so are increasingly difficult to arrest or reverse.

Insoluble Fibrin

In organ tissues, which are rich in autonomic innervation, sympathetic nervous activity releases von Willebrand Factor from the vascular endothelium into blood, which activates factor VIII that adds “cross links” of fibronectin, vitronectin, plasminogen, and gelsolin to fibrillar soluble fibrin and produce monomers of insoluble fibrin. The monomers polymerize into strands of insoluble fibrin that can be seen with a microscope. These strands are generated from the walls of capillaries, where they increase capillary flow resistance, which inhibits microvascular perfusion (“closes” the capillary gate), increases microvascular flow resistance, and reduces organ function.

Parasympathetic nervous activity releases nitric oxide (NO) from the vascular endothelium into blood. This activates plasminogen, which disintegrates the strands of insoluble fibrin, opens the capillary gate, reduces microvascular flow resistance, and increases organ perfusion and function. In the research literature, this is called “nitrergic neurogenic vasodilation” which reflects the alluring but false assumption that muscular arterial contraction and relaxation determines flow resistance. This “capillary gate mechanism” explains how autonomic nervous activity regulates organ perfusion, and thereby determines organ function.

Unlike soluble fibrin, insoluble fibrin cannot escape the intact vascular system. In the event of tissue injury, the damaged vascular endothelium directly exposes “tissue factor” in extravascular tissues to the enzymatic interaction of factors VII, VIII, IX, and X. This rapidly generates strands of insoluble fibrin that entangle platelets and blood cells to increase blood viscosity and coagulability. This process reduces pulsatile blood turbulence in the immediate vicinity of the injury which enables insoluble fibrin to entangle blood cells and bind them into viscoelastic clots and scabs.

Insoluble fibrin explains several effects:

1. Sympathetic nervous activity releases VWF from the vascular endothelium to activate factor VIII, which generates insoluble fibrin.

2. Factor VIII also generates thrombin, which activates TAFI (thrombin-activated fibrinolysis inhibitor) that stabilizes plasminogen and prevents the disintegration of insoluble fibrin.

3. Parasympathetic nervous activity releases nitric oxide (NO) from the vascular endothelium, which binds avidly to Ca+ and inhibits thrombin activity. This inhibits TAFI and accelerates the disintegration of insoluble fibrin into “fibrin split products” (also called “d-Dimer”), which reduces microvascular flow resistance and promotes organ perfusion, tissue oxygenation, organ protection, and organ function. In the research literature this is called “nitrergic neurogenic vasodilation,” but it has nothing to do with vascular muscle contraction or relaxation.

4. Insoluble fibrin is generated and disintegrated in capillaries in accord with autonomic balance to regulate capillary flow resistance (the capillary gate mechanism), which determines organ perfusion that regulates organ activity.14,26

5. Insoluble fibrin contains cross links of plasminogen that spontaneously disintegrate into plasmin unless it is continuously stabilized by “Thrombin Activated Fibrinolysis Inhibitor” (TAFI). Plasmin enzyme attacks the molecular structure of insoluble fibrin, causing it to disintegrate into “fibrin split products.”

6. Insoluble fibrin is generated in damaged tissues, where it binds platelets and red blood cells into a viscoelastic clot that substitutes for the damaged vascular endothelium, restores the barrier between the enzymes in flowing blood and tissue factor in extravascular tissues, and subsequently regulates the exposure of blood enzymes to tissue factor in the damaged tissues beneath its protective surface.1,27 The viscoelastic clot thus maintains thrombin generation within a narrow range to optimize cellular tissue repair activities in the damaged tissues beneath its protective surface, and prevents excessive thrombin generation that threatens to become malignant during the healing process.

7. Excessive insoluble fibrin generation in flowing blood can dangerously exaggerate blood coagulability. For example, cancer abnormally sheds both tissue factor and VWF into circulation, which exaggerates insoluble fibrin generation that increases blood coagulability and promotes infarction.28,29 This is called “Trousseau’s Syndrome,” and it explains why most cancer deaths are caused by heart attacks, strokes, and pulmonary embolus.

8. Insoluble fibrin forms tough scabs that protect damaged tissues that are exposed to air.

Figure 4. This photograph shows how strands of insoluble fibrin bind blood cells into a viscoelastic clot that substitutes for the vascular endothelium and regulates cellular tissue repair activities.

Collagen

Collagen is the “glue” that binds cells together to form complex multicellular structures. Tendons, ligaments, scars, and adhesions are composed of pure collagen. Abnormal collagen tissue deposits cause fibrosis and sclerosis. Like insoluble fibrin, collagen is composed of monomers made from the alpha, beta, and gamma subunits of soluble fibrin. These collagen monomers are amyloid protein. Like the insoluble fibrin monomers, amyloid monomers polymerize into strands; however, amyloid monomers are normally generated in extravascular tissues where factor VIII is absent, so they lack the cross-links of fibronectin, vitronectin, plasminogen, and gelsolin that are installed by factor VIII. Factors VII and X and soluble fibrin penetrate through the vascular endothelium, where they interact with tissue factor and fibroblasts to convert soluble fibrin into amyloid, which polymerizes into collagen. Collagen does not spontaneously self-destruct and is tougher, stronger, and more stable than insoluble fibrin because it lacks plasminogen cross links.

Rheumatoid Disease

We have now arrived at the point where normal processes turn into disease states. This is caused by chronic unremitting combinations of environmental stresses, or insults, such as pesticides, herbicides, and other environmental toxins, but also including emotional stresses from dysfunctional life situations, causing subclinical stress mechanism hyperactivity that increases the permeability of the vascular endothelium. These environmental insults also encompass stresses introduced into the body as “side-effects” of medications, interactions of prescription drugs, and substances contained in or produced within the body by the COVID “jab.”

This process of stress mechanism hyperactivity abnormally exaggerates the “penetration” of factors VII, X and soluble fibrin into extravascular tissues, which harmfully amplifies amyloid production and collagen polymerization in the extravascular tissues. This abnormal tissue repair hyperactivity produces painful inflammation, edema, fibrosis, sclerosis and capillary destruction in the afflicted tissues, which inexorably damages tissues and undermines their function. For example, diabetes causes fibrosis and sclerosis which causes the skin to appear dull and bluish and stiffens jaw muscles and tissues. This can dangerously frustrate endotracheal intubation. Similar fibrosis, sclerosis, inflammation, and capillary destruction explain the symptoms of rheumatoid arthritis, scleroderma, Sjogren’s Disease, Systemic Lupus Erythematosis, diabetes, hypertension, and other forms of rheumatoid disease.

Tissue hypoxia also promotes amyloid and collagen production.30-32 Collagen sclerosis and fibrosis accelerate capillary senescence and undermine oxygen delivery to cells and tissues. This accelerates collagen accumulation between and among heart muscle cells, which causes the heart walls to thicken with collagen that impairs cardiac contractility. As this pathological process progresses, the contractility of the failing heart declines, and the heart can no longer empty its contents effectively. The failing heart eventually “balloons” to larger diameter and becomes increasingly vulnerable to infarction, so that premature death ensues.

Proof of Concept

I have described a testable, heuristic hypothesis that explains chronic illness. I propose that the hypothesis be initially tested using an animal model treated with intravenous radioactive fibrinogen or soluble fibrin, to determine whether the radioactive soluble fibrin is incorporated into collagen in extravascular tissues.

I further propose that an animal model be treated with excessive intravenous quantities of tissue factor to see if this provokes the formation of collagen “white clots” surrounded by amyloid protein.

COVID, Collagen, Amyloid, White Clots, and Genocide

This takes us to the COVID “pandemic” and to the idea being put forth by many that it is a form of planned genocide.

We can start with the idea that in the annals of human history, mass murder at the whim of moral and mental midgets drunk with power and privilege is hardly new. Genghis Khan regarded people as useless and left mountains of skulls in the wake of his marauding armies. Julius Caesar slaughtered countless “enemies of Rome” for the sake of “glory.” Stalin starved millions of Ukrainian farmers. Mao’s “Great Leap Forward” led to the starvation of some 60 million Chinese. Pol Pot murdered countless Cambodians. And so it goes.

The COVID contagion may prove to be the most disastrous mass murder of all. It was unquestionably intended to serve as a method of genocide from the start. The ability to exaggerate the virulence of the ordinary coronavirus, which is but one of several viruses that cause the “common cold,” was reported in Scientific American in 2011.10,11,33 The devastating potential was immediately appreciated.20,21

The SARS, MERS, COVID, OMICRON, as well as mink contagions in the Netherlands and chicken contagions in China were all caused by weaponized, hyper-virulent versions of the coronavirus, again which normally causes the innocuous “common cold.” These were not “spontaneous mutations” as alleged by the Fauci fakir. They differed from one another only in the variation of their virulence. The “SARS” version was so virulent that it promptly killed its victims and couldn’t spread effectively. The “MERS” version that followed was less virulent but still too deadly to sustain itself in the wild. The COVID version was still less virulent, which enabled it to spread and shed its nasty effects (loss of hair, smell, and taste) effectively enough to frighten unsuspecting citizens to submit to far deadlier COVID “jabs” on penalty of loss of livelihood and other draconian measures.

There is no way that the COVID injections can be considered “vaccines.” All legitimate vaccines are prepared from purified viral and bacterial proteins. The immune mechanism cannot produce a protective immune reaction to either the DNA or RNA from the “jab,” both of which consist of nucleotides that are chemically distinct from proteins.

Instead of purified proteins, the fake COVID vaccines consist of weaponized mRNA that was mass-produced at negligible expense using modern enzyme technology that rapidly replicates small samples of weaponized coronavirus RNA produced in limitless quantities. This explains how the fake vaccines were prepared within weeks.

In contrast, legitimate vaccine preparation is a “trial and error” process that requires careful preparation of purified proteins from bacterial cell walls or viral capsids (the protein shell that encloses viral RNA), followed by years of careful animal testing before human safety trials can begin. There was no need for safety trials for the fake COVID mRNA “vaccine,” because it was never intended to function as a vaccine to begin with. It was always intended to function as a weapon of mass murder.

The COVID “jab” has already caused unprecedented declines in American life span for three years running, and the disaster is far from over. It has caused thousands of sudden, unexplained deaths in healthy young people and newborn babies, as well as miscarriages. It has damaged and likely destroyed the fertility of innumerable men and women, because the gonads are rich in tissue factor and are therefore “targets” of environmental stress. It has mimicked and exaggerated every known form of disease and left thousands of survivors crippled by the “Long COVID” syndrome. Many more will die prematurely from “turbo cancers,” chronic illnesses, and heart disease for years to come, even if future mischief is halted. To make matters worse, industrialized nations throughout the world were already facing catastrophic declines in fertility of the “best and brightest,” as economic prosperity inexorably discourages fertility.

The malicious intent of the COVID contagion is revealed by:

1. The omission of legally required safety testing

2. The absence of evidence that COVID represented a significant threat

3. Influencing Congress to pass laws protecting pharmaceutical companies from lawsuits.

4. Unconstitutional use of government to promote hysterical vaccination propaganda

5. Measures to force people to submit to the injections on penalty of loss of employment

6. Proof that pharmaceutical companies were fully aware of the deadly potential of the fake vaccines17

7. Continued promotion of the “jabs” despite overwhelming evidence of their excessive morbidity and mortality16

8. Statistical evidence that the COVID “jabs” cause of most of the deaths16

9. Promotion of COVID jabs for pregnant women and newborn babies

10. Unprecedented “white clots” found in the small peripheral arteries of healthy young victims killed by the “jabs”

11. Proof that pharmaceutical companies were fully aware of the dangers of the fake vaccines from the beginning17

The weaponized “novel” COVID mRNA material functions as a live virus. When confined to the lungs it is more virulent than the “normal” coronavirus, but it becomes far more dangerous when it is introduced into systemic circulation disguised as an “immunization.” Like all viruses, it attacks and hijacks the cells of the vascular endothelium and causes them to replicate viral particles that propagate throughout the body, disrupting the vascular endothelium and abnormally exaggerating its permeability. 10,11,33 The damaged vascular endothelium releases abnormal quantities of both tissue factor that activates factor VII and von Willebrand Factor that activates factor VIII. This causes chaotic stress mechanism hyperactivity, because some tissues are more permeable than Thus the COVID injections mimic every form of disease ever described. This also illustrates how the hyperactive stress mechanism alone can cause what appears to be numerous seemingly unrelated forms of disease.

Factor VIII hyperactivity promotes DIC—disseminated intravascular coagulation. Factor VII hyperactivity also promotes a disastrous level of amyloid production that polymerizes into collagen that forms tough, rubbery collagen “white clots.” These processes probably synergize each other, causing the sudden obstruction of small peripheral arteries by combinations of collagen “white clots” and abnormal “red clots” that disrupt oxygen transport and delivery and cause sudden, painless death in healthy young victims of the COVID “jabs.”

The reason that the abnormal collagen, amyloid, and red clots form in small peripheral arteries instead of large proximal arteries remains unclear, but the most likely explanation is the synergistic inhibition of pulsatile turbulence by these processes.

Treatments for Pulmonary COVID

Public alarm over the disastrous effects of the COVID “jabs” calls for an immediate worldwide search for possible antidotes. Staring with the infection itself we know that regular use of Vitamin D3 can prevent or mitigate the severity of contagious COVID. Ivermectin can cure it. In-hospital mechanical hyperventilation hastens the death of these victims.34

Contrary to government “protocols,” if COVID pneumonia necessitates hospitalization, it should be managed as follows:

1. Elective endotracheal intubation to protect medical staff from the contagion, provide respiratory support when needed, and enable measurement of inhaled and exhaled gas mixtures

2. Intravenous narcotics to control harmful nociception and maintain exhaled CO2 concentrations in the range of 50-100 torr to optimize cardiorespiratory function and tissue oxygenation

3. Maintain transcutaneous oxygen levels in the range of 60-100 torr using synthetic opioid supplementation

4. Allow patients to breathe spontaneously whenever possible

5. Intravenous magnesium sulphate using eclampsia protocols should simultaneously paralyze the viral mRNA and stabilize the permeability of the vascular endothelium

6. Avoid mechanical hyperventilation, which confers no benefits and is inherently harmful, depleting body reserves of carbon dioxide and undermining cardiorespiratory function and tissue oxygenation. (Most of the deaths of hospitalized COVID victims were caused by mechanical hyperventilation.)

7. Control fear and anxiety using ½ MAC general anesthesia

8. Supplemental treatment with Ivermectin and vitamin D

9. Antibiotics as necessary to control bacterial infestation

These measures should hasten recovery and minimize pulmonary sclerosis in survivors. Of course none of these measures should be undertaken without the authorized approval and cooperation of your designated medical practitioner.

Treatments for Rheumatoid Disease

The stress mechanism as described above also leads to the suggestion that an effective treatment for rheumatoid disease is chelation therapy. Also, sleeping in a tent where atmospheric air is enriched with carbon dioxide may also ameliorate rheumatoid disease by promoting tissue oxygenation that inhibits abnormal collagen production. Rest in conditions removed from environmental insults also gives the body a better chance to activate its innate healing capabilities.

Treatment for Sudden Cardiac Arrest in the Field after COVID “Jabs”

Many victims of the COVID injections “die suddenly” and unexpectedly in circumstances where nobody is available to resuscitate them; thus they do not survive. However, the lucky few who collapse in circumstances where someone is available to administer CPR, especially when automated defibrillation devices are available, have a chance. The drug streptokinase would probably be effective if it were available, but it is presently banished from North America by the dubious action of the federal Food and Drug Administration. TPA or chelation therapy would likely help, but these are not conventional CPR treatments. Breathing carbogen should also be helpful, but its therapeutic properties presently remain forgotten.34 Antidotes to the deleterious effects of the COVID “jab” are practically non-existent, and the government is taking no steps to research or implement any. Part of the problem is that the government refuses to acknowledge that these deleterious effects even exist, except in “rare” cases that don’t requires any special attention. This failure is also part of the murderous effects of the COVID pandemic.

Treatments for COVID injections and “Long COVID”

The stress mechanism indicates that the victims of COVID injections who suffer “Long COVID” are fortunate to be alive, but they suffer from residual damage to their arterial tree that undermines tissue oxygenation. This explains why they suffer chronic weakness, fatigue, and stubborn bacterial infections.

Stress theory indicates that the most effective treatment for “Long COVID” would be chelation therapy with EDTA, which binds avidly to Ca+ and inhibits thrombin generation. This should simultaneously paralyze the lingering mRNA, mitigate harmful stress mechanism hyperactivity, minimize the inflammation and excessive permeability of the vascular endothelium, reduce blood coagulability, promote the disintegration of abnormal blood clots, open the capillary gate, and improve tissue perfusion. Alternatively, intravenous magnesium sulphate or trisodium citrate should be comparably beneficial. All these chemicals are powerful anticoagulants with extensive safety records for human treatment. Unfortunately, effective use of chelation therapy is almost non-existent. Even the process of finding a qualified, licensed practitioner may be a daunting task beyond the ability of most patients to navigate. And chelation may not be covered by health insurance. Thus the ability of the nation’s health care system to ameliorate the adverse effects of the “jab” is tragically deficient.

The Nature of Chronic Illness

The clues provided by the COVID contagion confer a fresh explanation of chronic disease. To summarize, subclinical stress mechanism hyperactivity causes mild systemic inflammation which exaggerates the permeability of the vascular endothelium that allows excessive entry of factors VII, X and soluble fibrin into extravascular tissues. This abnormally exaggerates amyloid and collagen production that causes progressive, debilitating fibrosis and sclerosis as well as painful inflammation and accelerated capillary senescence.

Treatments for Chronic Illness

As indicated above, stress theory indicates that chelation therapy is the best prospective treatment for rheumatoid disease. Sleeping in a tent with CO2 enriched atmospheric air should also be therapeutic, because it opens the capillary gate, improves tissue perfusion and oxygenation, promotes angiogenesis (capillary proliferation) and prevents tissue hypoxia that promotes harmful fibroblast collagen production. But again, such treatments, while perfectly legal, are virtually impossible for most of today’s patients to obtain without extraordinary exertion, expense, and ferreting out of competent medical personnel.

It is obvious, however, that safe antidotes for tissue factor, the final culprit in dysfunctional systemic circulation, would be a boon for the treatment of all forms of disease, and there is solid evidence of its potential utility.35 Drug companies have inexplicably ignored this opportunity for profitable pharmaceutical development. In theory, such a treatment could provide a reliable cure for cancer and could quickly control all forms of critical illness when combined with general anesthesia, hypercarbia, and supervised narcotic supplementation. All this points to an urgent call for more research and development in the concepts I have presented. Unfortunately, this call cannot be answered by a health care system captured by Big Pharma for profit extraction and crippled by government regulatory capture.

Conclusion

The COVID conspiracy will surely be remembered as the “Crime of the 21st Century.” The disaster is far from over, and it may yet become the worst example of mass murder in recorded history. Unless the atrocities are halted immediately and stress theory is harnessed to produce effective cures, the lingering deaths from miscarriages, infertility, turbo cancers, heart disease, and crippling “Long COVID” will continue for years to come and will exacerbate the natural decline in fertility that accompanies economic success among developed economies.

What sort of punishment is adequate for the deceitful few who have caused so much harm to so many and threatened the very survival of civilization? At the very least, there should be something like the Nuremberg trials to evaluate the evidence and impose adequate justice, if only to discourage similar criminality in the future. Unfortunately, none of this is likely, because these master criminals control the governments of the world and their police and military. God help us all.

Meanwhile, stress theory promises the development of treatments that can neutralize similar mischief in the future and introduce a new era of human existence that can gradually become free from the eternal curse of chronic disease and premature death. Perhaps the COVID disaster will help to pave the way to necessary reforms and mitigate such mayhem in the future.

1 Coleman, L. S. Stress repair mechanism activity explains inflammation and apoptosis. Advances in Bioscience and Biotechnology 3, 459-503 (2012). https://doi.org/10.4236/abb.2012.324065 http://www.scirp.org/journal/PaperInformation.aspx?paperID=21883

2 Coleman, L. S. How Emotional Stress Can Kill You. Contentment Magazine Winter 2021-2022 (2021-2022 Winter). <https://www.stress.org/how-emotional-stress-can-kill-you>.

3 Coleman, L. S. Oxygen Transport and Delivery,

4 Coleman, L. S. sleep, Anesthesia, and the Fight or Flight Mechanism. Contentment Magazine 2022, This is an article from the Winter 2022 issue of Contentment Magazine (2022). <https://www.stress.org/sleep-anesthesia-and-the-fight-or-flight-mechanism>.

5 Coleman, L. S. The Three Activation Pathways of the Stress Mechanism. Contentment Magazine 2022 (2022). <https://www.stress.org/the-three-activation-pathways-of-the-stress-mechanism>.

6 Coleman, L. S. The Great Medical Hoax of the 20th Century, https://www.amazon.com/Great-Medical-Hoax-20th-Century/dp/B09X4BCTWG/ref=sr_1_1?crid=8A8KBG2F26D7&keywords=the+great+medical+hoax+of+the+20th+Century&qid=1659205157&sprefix=the+great+medical+hoax+of+the+20th+century%2Caps%2C153&sr=8-1

7 Coleman, L. S. Lewis Coleman’s Landmark Discovery in the Science of Stress. Contentment Magazine (2022). <https://www.stress.org/wp-content/themes/Avada-child/lib/3d-flip-book/3d-flip-book/?mag_id=46464&token=49661>.

8 Coleman, L. S. The Mammalian Stress Mechanism. Contentment Magazine Spring 2022 (2022 Spring). <https://www.stress.org/wp-content/themes/Avada-child/lib/3d-flip-book/3d-flip-book/?mag_id=50392&token=36882>.

9 Coleman, L. S. CO2, A Powerful Tool to Reverse the Ravages of Stress. Contentment Magazine Summer 2022 (2022 Summer). <https://stressorg-magazines.s3.amazonaws.com/contentment/2022/Contentment-Summer-2022-2.pdf>.

10 Coleman, L. S. The Mammalian Stress Mechanism Explains COVID, Long COVID, and Sudden Death. Science Set Journal of Cardiology Research (2023). https://www.mkscienceset.com/articles_file/937-_article1692189623.pdf

11 Coleman, L. S. COVID and the Immune Mechanism. Contentment Magazine 2023 (2023). <https://www.stress.org/covid-and-the-immune-mechanism>.

12 Coleman, L. S. A testable hypothesis that may explain the morbidity and mortality caused by surgical stress. Anesth Analg 103, 1589; author reply 1589-1590 (2006). https://journals.lww.com/anesthesia-analgesia/Fulltext/2006/12000/A_Testable_Hypothesis_That_May_Explain_the.68.aspx

13 Coleman, L. S. An Improved Explanation of Atherosclerosis. PLoS Medicine 2(4):e98 (2005). http://medicine.plosjournals.org/perlserv/?request=read-response&doi=10.1371/journal.pmed.0020098

14 Coleman, L. S. A capillary hemostasis mechanism regulated by sympathetic tone and activity via factor VIII or von Willebrand's factor may function as a "capillary gate" and may explain angiodysplasia, angioneurotic edema, and variations in systemic vascular resistance. Med Hypotheses (2005). http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16338094

15 Coleman, L. S. Insoluble fibrin may reduce turbulence and bind blood components into clots. Med Hypotheses 65, 820-821 (2005). http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15993007

16 Dowd, E. Cause Unknown: The Epidemic of Sudden Deaths in 2021 and 2022. 216 (Skyhorse, 2022, December 13) https://www.amazon.com/Cause-Epidemic-Sudden-Childrens-Defense/dp/1510776397/ref=tmm_hrd_swatch_0?_encoding=UTF8&qid=1679166465&sr=8-1

https://articles.mercola.com/sites/articles/archive/2023/03/18/epidemic-sudden-deaths-finally-made-news.aspx?ui=063ac0a92006e5012244a16187dd09023089107133e97a24b565285d1ef47e90&sd=20220103&cid_source=dnl&cid_medium=email&cid_content=art1HL&cid=20230318&cid=DM1365600&bid=1748791226.

17 Wolf, N. The Pfizer Papers. (War Room Books)

18 Gill, J. R., Tashjian, R. & Duncanson, E. Autopsy Histopathologic Cardiac Findings in 2 Adolescents Following the Second COVID-19 Vaccine Dose. Arch Pathol Lab Med 146, 925-929 (2022). https://doi.org/10.5858/arpa.2021-0435-SA https://www.ncbi.nlm.nih.gov/pubmed/35157759

19 Hulscher, N. a. A., Paul E and Gessling, Heather and Hodkinson, Roger and Risch, Harvey and Trozzi, Mark and McCullough, Peter A. A Systematic Review of Autopsy Findings in Death after COVID-19 vaccination. Lancet “This pre-print has been removed by Preprints with The Lancet because the study’s conclusions are not supported by the study methodology” (2023). https://www.youtube.com/redirect?event=video_description&redir_token=QUFFLUhqbmx5NG5PMHk2eVItS2hfSDJhRlF6ZUFfTWNhd3xBQ3Jtc0tuWjN4N21HT0RrT1A2QTBCaWhGUmRJNVlkNUJ1cy1YTWp1MlBiUGhrRmNSYkVqd3JKUkRid0NsNVg3eGhGNTlvY2xOeTBqaTk0MVluQWIxUWpHM043ek90dFJkVV9Cc21rTzNIZGZuTjR6RGZXbUdObw&q=https%3A%2F%2Fphilipmcmillan.substack.com%2Fp%2Fcovid-vaccine-implicated-in-most%3Fsd%3Dpf&v=o7s-SJUqgAE

20 Interlandi, J. Contagion: Controversy Erupts over Man-Made Pandemic Avian Flu Virus, <https://www.scientificamerican.com/article/contagion-controversy-erupts/> (2011).

21 Interlandi, J. A man-made contagion, <https://www.ncbi.nlm.nih.gov/pubmed/22295668> (2012).

22 Hoffman, R. S., Cobrin, G., Nelson, L. S. & Howland, M. A. Erythropoietin overdose treated with emergent erythropheresis. Vet Hum Toxicol 44, 157-159 (2002). https://www.ncbi.nlm.nih.gov/pubmed/12046968

23 Malyszko, J., Suchowierska, E., Malyszko, J. S. & Mysliwiec, M. A comprehensive study on hemostasis in CAPD patients treated with erythropoietin. Perit Dial Int 22, 582-592 (2002). http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12455569

24 Information for Epogen/Procrit (Epoetin alfa). (2017). <https://www.fda.gov/drugs/postmarket-drug-safety-information-patients-and-providers/information-epogenprocrit-epoetin-alfa>.

25 Rath, W., Faridi, A. & Dudenhausen, J. W. HELLP syndrome. J Perinat Med 28, 249-260 (2000). http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11031696

26 Coleman, L. A Testable Stress Mechanism Explains Both Unified Stress Theory and Capillary Gate Theory. FDA Anesthesia & Life Support Drugs Advisory Committee pp239-243 3/29/07 (2007).

27 Coleman, L. S. A Stress Repair Mechanism that Maintains Vertebrate Structure during Stress. Cardiovasc Hematol Disord Drug Targets (2010).

28 Wang, X., Zhang, X., Zhang, C., Qi, L. & Liu, J. Plasma von Willebrand factor levels in patients with cancer: A meta‑analysis. Oncol Lett 28, 399 (2024). https://doi.org/10.3892/ol.2024.14532 https://www.ncbi.nlm.nih.gov/pubmed/38979552

29 Kasthuri, R. S., Taubman, M. B. & Mackman, N. Role of tissue factor in cancer. J Clin Oncol 27, 4834-4838 (2009). https://doi.org/10.1200/JCO.2009.22.6324 https://www.ncbi.nlm.nih.gov/pubmed/19738116

30 Genovese, A., Chiariello, M., Latte, S., DeAlfieri, W. & Condorelli, M. Bilateral ventricular hypertrophy in rats exposed to acute or chronic hypobaric hypoxia. Respiration 44, 289-293 (1983). http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=6224280

31 Genovese, A., De Alfieri, W., Latte, S., Chiariello, M. & Condorelli, M. Regression of myocardial hypertrophy in the rat following removal of acute or chronic hypobaric hypoxia. Eur Heart J 3 Suppl A, 161-164 (1982). http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=6210541

32 Genovese, A., Latte, S., Bozzaotre, M. & Chiariello, M. Response of the left ventricular connective tissue to hypoxia. Res Exp Med (Berl) 183, 111-115 (1983). http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=6658198

33 Coleman, L. S. Are the COVID mRNA Vaccination Injections Thinly-Disguised Genocide? VT Uncensored Foreign Policy (2024, February 26). <https://www.vtforeignpolicy.com/2024/02/are-the-covid-mrna-vaccination-injections-thinly-disguised-genocide/#comment-10318>.

34 Coleman, L. S. Four Forgotten Giants of Anesthesia History. Journal of Anesthesia and Surgery 3, 1-17 (2015). <http://www.ommegaonline.org/article-details/Four-Forgotten-Giants-of-Anesthesia-History/468>.

35 Welty-Wolf, K. E. et al. Coagulation blockade prevents sepsis-induced respiratory and renal failure in baboons. American journal of respiratory and critical care medicine 164, 1988-1996 (2001). http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11734456

Dr. Lewis S. Coleman is Chair of the Science and Education Board of the American Institute of Stress. He is a board-certified anesthesiologist who completed his BS degree in biology at the Ohio State University, obtained his MD degree from New York Medical College, and completed his surgical internship and anesthesiology residency at UCLA, followed by 40 years in private practice. Coleman’s basic sciences instruction at NYMC miraculously coincided with the two-year sojourn of Dr. Johannes Rhodin, who was retained by the school to reform its curriculum. Dr. Rhodin was a famous researcher and expert on the stress theory of Dr. Hans Selye. His lectures devastated the dogma of classical physiology and convinced Coleman that stress theory represented the future of medicine. Many years later, these lectures enabled Coleman to identify Selye’s long-sought Mammalian Stress Mechanism. This promises to revolutionize medicine and provide a new era of health, longevity, and freedom from the eternal scourge of disease and premature death. Coleman sets forth his ideas in his important new book, 50 Years Lost in Medical Advance: The Discovery of Hans Selye’s Stress Mechanism.

Dr. Coleman is a principal with the Three Sages Substack. This article was edited for publication by Richard C. Cook, author of Our Country, Then and Now.