A note on language. This essay engages a condition that mainstream cardiology describes in the vocabulary of lipid deposition, cholesterol infiltration, and genetic risk. Those terms appear here in quotation and attribution, within reference titles, and inside the names of official bodies. The author’s own analysis runs in a different register. Where mainstream cardiology sees an accumulating substance, this essay sees a repair process. Where it sees “bad cholesterol,” this essay sees red blood cells trapped in clots. The two registers do different work and the reader should feel the shifts between them.
This essay is a companion to “The Wrong Enemy: Blood Clots, Not Cholesterol,” which maps the full terrain of heart disease across history, politics, metabolism, stress, and treatment. The piece you are reading narrows the lens to one question that essay sketches but does not fully develop: what, physically, is an atherosclerotic plaque, and how is it built?
The vein that becomes an artery
A surgeon performing a coronary artery bypass graft strips a length of vein from the patient’s leg and sews it onto a coronary artery, bypassing a blockage. The vein served that leg for sixty years without a trace of atherosclerosis. Now it carries arterial pressure. It fills with plaque, sometimes severely, and sometimes within a few years.¹
The blood did not change. The LDL in that blood is the same LDL that passed through the vein every day of the patient’s life without harming it. What changed is the stress on the vessel wall.
A second oddity sits alongside this one. The pulmonary arteries, which carry blood from the right side of the heart through the lungs, almost never develop atherosclerosis. Neither do the pulmonary veins. The same blood circulates through them, with the same cholesterol, the same LDL, the same lipoproteins of every variety. Plaque almost never forms there.¹
If atherosclerosis were a disease of what circulates in the blood, the pulmonary arteries would be as diseased as the coronaries, and a vein grafted into arterial duty would stay as clean as the vein next to it in the thigh. Neither is true.
Mechanical stress on the arterial wall is the subject of this essay. Not what floats in the blood.
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Three figures the mainstream buried
Karl von Rokitansky (1804–1878). Viennese pathologist, prolific beyond belief, said to have performed or supervised tens of thousands of autopsies. He opened arteries for a living. In the 1840s he examined thousands of diseased arteries and saw the same thing again and again: fibrin, the sticky protein that binds blood clots, laid down in layers inside the plaques, in various stages of organization and repair. He proposed what he called the encrustation hypothesis: plaques are the remains of clots. He was describing what he found in the arteries of the dead, not theorizing beyond it.² His contemporary Rudolf Virchow pressed one question. If plaques form beneath the arterial lining, how does a blood clot get underneath that lining to begin with? Rokitansky had no answer. The answer was not available for another 140 years.
Elspeth Smith. Scottish pathologist at the University of Aberdeen. In a small-group teaching session there, she once told a room of fresh-faced medical students that LDL cannot cross the endothelium.³ For most of the students the sentence passed as a technical aside. For one of them, Malcolm Kendrick, it was the first visible crack in the façade of what they were being taught. Smith spent four decades documenting the role of the clotting system at every stage of plaque development, from initiation to growth to rupture. “After many years of neglect,” she wrote, “the role of thrombosis in myocardial infarction is being reassessed. It is increasingly clear that all aspects of the haemostatic system are involved: not only in the acute occlusive event, but also in all stages of atherosclerotic plaque development.”⁴ Her work was published, cited, and largely ignored by a research field with its attention fixed elsewhere.
Kilmer McCully (1933–2025). Harvard pathologist, trained at Massachusetts General Hospital. In 1968 he examined the arteries of two children who had died with severe arteriosclerosis. One was a boy who had died of stroke at age eight in 1933; the other was a two-month-old who had died of pneumonia. Both had the inherited condition homocystinuria, in which the amino acid homocysteine accumulates in the blood. Both children had severe arteriosclerosis throughout their bodies. In neither case did the plaques contain fat or cholesterol.⁵ The shared factor was elevated homocysteine. McCully proposed, in a paper published in 1969, that homocysteine damages the arterial wall and triggers the plaque-building process. By 1977 his laboratory at Massachusetts General had been taken from him. By 1979 his appointment was ended. He spent two years unemployed, then landed at the Veterans Administration hospital in Providence, Rhode Island, where he worked until his death in 2025.⁶
Three men, each describing a facet of the same thing. Rokitansky buried by a question he could not yet answer. Smith buried by indifference. McCully buried by career destruction.
1. What the word means
Athero comes from the Greek for gruel or porridge, describing the soft, pulpy core of some advanced plaques. Sclerosis is Greek for hardening. The disease was named for what pathologists found when they cut diseased arteries open: hardened vessels containing areas of soft, yellowish material.
Where it forms matters. Plaques develop in large and medium-sized arteries. They cluster at branch points, at bends, and where arteries narrow. They do not form in the small arterioles or in the capillaries. They do not form in veins. They almost never form anywhere in the pulmonary circulation.¹
The pattern is a map of mechanical stress. Branch points are where flow becomes turbulent. Bends are where shear forces concentrate. The locations where plaque forms are the locations where the arterial lining takes the hardest hit.
2. What is actually inside a plaque
A standard list of plaque components reads as follows: fibrin, platelets, red blood cells, white blood cells, smooth muscle cells, lipoprotein(a), collagen, calcium, and cholesterol crystals.⁷
Every item on that list, except smooth muscle cells and calcium, is also found in a blood clot.
The American Heart Association’s 1995 scientific statement, the Stary classification of atherosclerotic lesions, examined advanced plaques directly. The findings are startling to anyone taught that plaque is accumulated cholesterol:
“...38% of persons with advanced lesions had thrombi on the surface of the lesion. These thrombi ranged in size from minimal to grossly visible deposits, and some consisted of layers of different ages. Immunohistochemistry revealed wavy bandlike deposits related to fibrin within the advanced lesion of an additional 29% of persons. Because of their structure, these were thought to represent the remnants of old thrombi. Similar data were reported by other authors.”⁸
Thrombi of different ages. Fibrin bands within the plaque body. Visible layers suggesting repeated deposition over months and years. The AHA’s own document continues:
“The architecture of some multi-layered fibroatheromas could also be explained by repeated disruptions of the lesion surface, hematomas, and thrombotic deposits.”⁸
Fibrin cannot cross an intact arterial lining. Red blood cells cannot cross it. Platelets cannot cross it. The presence of all three in layered formations inside advanced plaques is only explicable if those components were there from the beginning, as components of blood clots that were subsequently covered over and incorporated into the artery wall.
Look at an advanced plaque in cross-section and the layers can be visible to the naked eye. Pathologists have compared them to tree rings.⁸
3. The question Virchow asked
Rokitansky’s problem was that nineteenth-century pathology had no concept of how new arterial lining is generated. The lining, called the endothelium, was understood as a passive layer of tiles. If plaques sit beneath the endothelium, and clots form on top of the endothelium, how does the clot get underneath? Rokitansky could not answer. Virchow pressed the point and the encrustation hypothesis fell into disuse.
The answer arrived in the 1990s with the identification of endothelial progenitor cells, bone marrow–derived precursors that circulate in the bloodstream and respond to breaches in the arterial lining by generating new endothelial cells on site.⁹ When a clot forms over a damaged patch of lining, these cells arrive and build a new endothelium directly on top of the clot. The clot is thereby drawn into the artery wall.
A 1968 study of pig aortas, funded by a tobacco company, had already documented the process without knowing what it was watching. The researchers stripped the endothelium from sections of the pig aorta, waited varying numbers of days, and killed the pigs to examine the damaged area. They described a blood clot forming over the damage, then shrinking, then becoming covered by “flattened cells with darkly staining elongated nuclei and spindle shaped cytoplasm lying on the surface of these thrombi.”¹⁰ They had watched new endothelium grow over the clot. They did not know what the cells were.
Rokitansky, had the answer been available to him, could have told Virchow that the clot does not form beneath the endothelium. The endothelium grows back over the top.
The implication is severe. Plaques do not form by LDL seeping through the lining. Plaques form at breaches in the lining, where clots arise, and the lining then regrows over the clot.
4. Where the cholesterol crystals come from
Pathologists examining plaques do find cholesterol crystals, often in abundance. The crystals look like sharp white needles under the microscope. Rudolf Virchow identified them in the 1850s and the mainstream explanation has run the same way ever since: the crystals must have come from LDL, which carries cholesterol in the blood.
They did not.
LDL carries cholesterol in the form of cholesterol esters, in which a cholesterol molecule is bonded to a fatty acid. Cholesterol crystals cannot form from cholesterol esters. To crystallize, cholesterol must be in its free, unesterified form.¹¹
Red blood cells provide it. The membrane of a red blood cell is roughly 40% lipid, and that lipid contains the highest concentration of free cholesterol of any tissue in the body outside the brain. When a red blood cell is incorporated into a clot and its membrane degrades, the free cholesterol is released, and that free cholesterol is what crystallizes within plaque.¹² ¹³
A 2012 paper in the Upsala Journal of Medical Sciences reported directly:
“...erythrocyte membranes were present in the necrotic core of advanced atherosclerotic plaques. Further studies have shown that erythrocyte membranes contribute to a significant increase of cholesterol accumulation in atherosclerotic plaques, since these membranes contain large amounts of cholesterol.”¹³
Cholesterol crystals in a plaque are a signature of trapped red blood cells, which is a signature of a clot. They are not a signature of LDL infiltration.
5. Plaques grow in episodes
The common mental picture of plaque buildup is gradual accumulation, like limescale in a kettle. The picture is wrong.
Plaques grow in discrete episodes. A patch of lining is damaged. A clot forms. New lining grows over the clot. The same patch is damaged again, in days or in weeks or in years. Another clot forms on top of the first. New lining grows over the second clot. The process repeats.
The AHA’s 1995 document described it directly:
“The fissure and hematomas that underlies thrombotic deposits in many cases may recur, and small thrombi reform many times. Repeated incorporation of small recurrent hematomas and thrombi into a lesion over months or years contributes to gradual narrowing of the arterial lumen.”⁸
A 2000 paper in the journal Atherosclerosis reinforced the point: “plaque rupture and subsequent healing is recognized to be a major cause of further rapid plaque progression.”¹⁴
What makes a plaque dangerous is the final event in this sequence. The repeating cycle of damage, clot, and healing eventually fails. A rupture of the plaque surface triggers a very large clot, big enough to block the entire artery. The downstream tissue dies. If the artery is a coronary, that tissue is heart muscle, and the event is called a heart attack. If the artery feeds the brain, the event is called a stroke.
The same process that builds the plaque is the process that eventually kills.
6. The measurement that should have ended the debate
If cholesterol in the blood were the cause of plaque in the arteries, then people with more cholesterol in their blood should have more plaque in their arteries. The question is testable. The test was performed, repeatedly, in the twentieth century. The method was simple: measure the blood cholesterol of a deceased person and measure the amount of atherosclerosis in their arteries at autopsy, then look for a correlation.
The results have been remarkably consistent.
Landé and Sperry (1936), examining a large series of autopsies: no correlation.¹⁵
Paterson and colleagues in Canada, tracking the blood cholesterol of veterans for years before they died and then examining their arteries: no correlation.¹⁶
Mathur and colleagues in Agra, India, studying 200 people who had died suddenly by accident: no correlation.¹⁷
Studies in Poland, Guatemala, and the United States: no correlation.¹⁸ ¹⁹ ²⁰
The Framingham autopsy study did find a correlation. The correlation coefficient was 0.36.²¹ A coefficient of 1.0 would indicate a perfect correlation; 0.0 would indicate none at all. A coefficient of 0.36 indicates a very weak relationship. The paper offered no diagrams, no individual data points, and did not discuss the number. Framingham was a federally funded study, politically significant, and its weak autopsy correlation did not interrupt the growth of the cholesterol hypothesis.
The 1959 Gore paper comparing aortic atherosclerosis in the United States, Japan, and Guatemala found something more striking. The Japanese subjects had the same degree of aortic atherosclerosis as the American subjects, despite a Japanese heart disease death rate one-sixth of the American rate.²² Plaque burden and heart attack rate were not tracking together.
A disease hypothesis that fails this test, repeatedly and across continents, is a hypothesis in trouble. The hypothesis was retained anyway. The reasons the hypothesis survived its own counter-evidence — Ancel Keys and the Seven Countries Study, the sugar industry’s role in redirecting blame, the statin trade and the institutional capture that followed — are mapped in “The Wrong Enemy.” That history is not repeated here.
7. The experiment that misled everyone
In 1913, the Russian pathologist Nikolai Anitschkow fed enormous quantities of cholesterol to rabbits. The rabbits developed thickened, cholesterol-laden lesions in their arteries. The experiment was taken as confirmation that dietary cholesterol causes arterial disease, and the finding anchored the cholesterol hypothesis for the next century.²³
Rabbits are herbivores. They do not naturally consume cholesterol, which is found only in animal tissue. Force-fed cholesterol at levels no rabbit would ever encounter in nature, the rabbits’ blood cholesterol rose to 10 to 20 times higher than the highest ever recorded in a human being. Cholesterol accumulated throughout the body: in the liver, in the kidneys, in the fur, in the eyes. The animals eventually died of emaciation. The lesions in their arteries did not resemble human atherosclerotic plaques. Different locations, different microscopic structure, no thrombus formation, no haemorrhage, no rupture.²⁴
When the same experiment was repeated on dogs, which are omnivores and metabolize cholesterol as humans do, the dogs regulated the intake and excreted the excess.²⁵ The dog comparison was a better model for humans. The dog comparison was ignored. The rabbit experiment had already fixed cholesterol as the suspect.
The rabbit has not been retired. More than a century after Anitschkow, the cholesterol-fed rabbit remains the archetypal animal model in atherosclerosis research, cited in textbooks and reproduced in laboratories as the canonical image of a cholesterol-caused arterial lesion. A herbivore poisoned with a substance it has no mechanism to process is still being used to illustrate what happens to humans who eat eggs.
8. Clots alone build plaques
The strongest test of whether plaques are built from clots is to examine arteries exposed to clots but not to the usual risk factors, and see whether plaques form.
The pulmonary circulation provides the test. Patients with chronic pulmonary thromboembolism have small clots repeatedly lodging in their pulmonary arteries. These arteries are otherwise immune to atherosclerosis. If plaques are built from clots, these patients should develop plaques in their pulmonary arteries.
They do.
A 2002 paper in Heart by Arbustini and colleagues examined the pulmonary arteries of patients with chronic thromboembolic pulmonary hypertension and compared them with patients with plexogenic pulmonary hypertension, in whom no chronic clots were present. The thromboembolic patients had plaques containing organizing thrombus, recent thrombotic material, calcifications, and cholesterol clefts. The plexogenic patients had fibrous thickening without the pultaceous (soft, lipid-containing) core. The authors wrote:
“Thromboembolic material is therefore sufficient on its own to induce plaque formation and influence its composition.”²⁶
They added that the coronary arteries of these same patients, examined by angiography and at surgery, were free of atherosclerosis. The patients were constitutionally resistant to coronary plaque. In their pulmonary arteries, where the clots were, the plaque developed anyway.
A 1955 paper by O’Neal and Thomas in Circulation, titled “The Role of Pulmonary Hypertension and Thromboembolism in the Production of Pulmonary Arteriosclerosis,” had found the same thing decades earlier. The authors studied children with congenital heart defects that threw clots from the heart into the lungs. These children were too young to have accumulated the risk factors medicine would later invoke, and they had developed full atherosclerotic plaques in their pulmonary arteries from the clots alone. The authors wrote that they “were able to demonstrate transition stages from clearly recognizable thrombi to arteriosclerotic lesions.”²⁷
The chain holds. Where clots repeatedly form, plaques develop. Where clots do not form, plaques do not develop. In a vessel bed famously resistant to atherosclerosis, the presence of chronic clots overrides that resistance.
9. What damages the lining
The remaining question is the only one left. If plaque is built from clots at sites of lining damage, what damages the lining?
The arterial lining is not a passive sheet of tiles. It is covered on the blood side by a layer called the glycocalyx, a fine mesh of sugars and proteins that keeps blood cells and clotting factors from touching the endothelial cells beneath.²⁸ The glycocalyx is where damage begins. Strip it away and the endothelial cells are exposed. Damage the endothelial cells and the tissue beneath is exposed, triggering clot formation.
The known insults are specific and well-documented.
Blood sugar spikes. A study published in Diabetes in 2006 directly measured what happens to the glycocalyx during a spike in blood glucose. The glycocalyx was stripped off, and fragments of it, including hyaluronan, could be measured floating in the bloodstream.²⁹ Any meal that spikes blood sugar does this. People who have been given the label diabetes do it chronically. People with the condition medicine calls prediabetes, often undiagnosed, do it chronically as well.
Sugar-damaged proteins. When excess sugar in the blood binds to proteins and fats, it damages them. The damaged molecules are called advanced glycation end products, or AGEs. Research has shown that AGEs can initiate and propagate atherosclerotic lesions independently of lipid status, meaning the damage is done directly, with no need for elevated cholesterol.³⁰
Homocysteine. The amino acid identified by McCully. Elevated homocysteine damages the lining directly. The B-complex nutrients folate, B6, and B12 are required for its metabolism, and intake of these through whole food is often inadequate on a modern processed diet. The fuller story of McCully’s discovery, its suppression, and the B-vitamin connection is told in “The Wrong Enemy.”
Smoking. The link between smoking and heart disease is one of the few that mainstream cardiology and this analysis agree on, and the mechanism is lining damage. Smoke damages the glycocalyx and the endothelium directly.
Heavy metals. Lead and cadmium, in particular, accumulate in the arterial wall and damage endothelial cells.³¹
Bacterial toxin. When bacterial fragments cross from the gut or the mouth into the bloodstream, as happens in leaky gut and in advanced gum disease, they trigger inflammation at the arterial lining. A 2018 study identified lipopolysaccharide, a bacterial toxin, embedded directly within atherosclerotic plaque.³²
Cortisol and adrenaline. Chronic stress, through the HPA axis, elevates these hormones chronically. Both damage the endothelium and increase clot formation.³³
Kidney disease. The condition medicine calls chronic kidney disease impairs nitric oxide synthesis, which is required to keep the endothelium healthy, and reduces the circulating supply of endothelial progenitor cells, which are needed to repair damage.³⁴
The list is not exhaustive, but the common thread is clear. These are insults that strip the glycocalyx, damage the endothelial cells, and either exceed the body’s capacity to repair the lining or exhaust the progenitor cell supply that performs the repair. Where the insult is intermittent, the lining heals and no plaque forms. Where the insult is chronic and the repair system is overwhelmed, the repair residue accumulates. That residue is what pathologists see on autopsy and name atherosclerosis.
The vein again
A vein in the leg, exposed for sixty years to the same blood as every other vessel in the body, does not develop plaque. Grafted onto a coronary artery and asked to carry arterial pressure, the same vein can fill with plaque within a few years.
Nothing in the blood changed. The oxygen tension did not change. The LDL did not change. The cholesterol did not change. The vein did not acquire a new disease.
What changed is the mechanical stress on the vessel wall. The vein, built for low-pressure drainage, is now being pulsed at systolic pressure. The glycocalyx and endothelium of a vein are not designed for that stress and begin to fail. Microscopic damage sites appear. Clots form over them. New lining grows over the clots. The next pulse creates the next damage. Clot layers on clot layers. Plaque.
A disease framework that identifies atherosclerosis as a condition of what circulates in the blood cannot accommodate this fact. A framework that identifies atherosclerosis as the residue of repeated damage can. The vein graft is a controlled experiment that the body performs on itself.
A reader who accepts this has to accept several things along with it. The cholesterol number on a routine blood panel is not the thing that matters. The statin a doctor is prescribing is addressing a measurement rather than a mechanism. The question “am I at risk” has to be asked in a different language than it has been asked in for seventy years, and the tests that answer it are not the tests ordered by default. These are not small adjustments. They are a different map, with the roads leading to different places. The reader is free to put the map down. The arteries will build what they build either way.
What to do with this
What follows is information, not medical advice. Nobody should alter or discontinue a prescribed medication without consulting their physician.
This essay does not engage two bodies of trial evidence that a sophisticated reader will raise. The B-vitamin trials (HOPE-2, NORVIT, VISP) lowered homocysteine with synthetic folic acid and did not reduce cardiac events; the question of whether that result bears on McCully’s thesis, or on the difference between whole-food folate and synthetic folic acid, deserves its own treatment. The PCSK9 outcome trials (FOURIER, ODYSSEY) showed small absolute reductions in events from LDL lowering, alongside their own mortality signals; the question of what those trials actually measured deserves its own treatment too. Both are owed essays of their own.
The pathology above identifies what damages the arterial lining. Avoid or reduce what strips the glycocalyx and damages the endothelium: blood sugar spikes from processed carbohydrates, industrial seed oils, periodontal infection and dysbiotic gut bacteria, smoking, chronic unmanaged stress, and environmental lead and cadmium. Do the inverse: steady blood sugar through whole foods, adequate high-quality animal protein to supply the amino acids from which the glycocalyx is rebuilt,³⁵ serious treatment of oral and gut problems, enough sleep for the HPA axis to reset, and movement that encourages circulation. The fuller prevention protocol, including specific nutrients and therapeutic interventions, is in “The Wrong Enemy.”
The tests that track these processes are different from the tests mainstream cardiology relies on. If a reader can ask a doctor for one test first, a coronary artery calcium score images the plaque burden directly, which total cholesterol and LDL do not. Fasting insulin and HbA1c capture the state of glucose regulation that total cholesterol ignores. Homocysteine measures the amino acid McCully identified. hs-CRP measures the inflammatory state. Lipoprotein(a) measures a particle genuinely bound up in clot formation. These tests exist. They are usually not ordered by default.
A reader convinced by the analysis above has one question left: what to tell a doctor. The honest answer is that most doctors are trained within the framework this essay rejects and will respond accordingly. Reading the sources listed in the references is the best preparation for that conversation.
How to Explain It to a Six-Year-Old
Imagine you scrape your knee. A scab forms. Underneath the scab, new skin grows. When the new skin is ready, the scab falls off, and your knee looks almost like it did before.
Now imagine the scab forms inside a tube that carries water, like a garden hose. If the scab fell off inside the tube, it would float along until the tube got narrow somewhere, and then it would get stuck. If it got stuck in the wrong place, like the pipe to your heart or your brain, that would be very bad.
So inside a blood vessel, the scab is not allowed to fall off. Instead, your body grows new skin on top of the scab, which pulls the scab into the wall of the tube. The scab is tucked away inside the wall where it cannot float off and cause trouble.
That works beautifully, as long as it only happens once.
But what if the same spot inside the tube gets scraped again? A new scab forms, in the same place. New skin grows over the top of that one too. Now you have two layers of tucked-away scab inside the wall. Scrape it again, and there are three layers. Then four. Then five.
After many years of scraping the same spot and tucking away the scabs, there is a lump inside the wall of the tube. The lump is made of all the old scabs piled up. The tube is narrower there now, because the wall has gotten thicker.
That lump is called a plaque. Doctors used to think the lump was fat that leaked in from the blood. It is not. It is scabs. It is what the body built to patch the wall every time something scraped it.
The question that matters is not what the scabs are made of. The question is what keeps scraping the same spot.
In Print
The Unbekoming library is available in paperback, printed to order through Lulu and shipped worldwide. The shelf begins with the paradigm question underneath everything else — No Virus, the isolation problem, the collapse of virology’s foundational claims, and a disease-by-disease reappraisal — and moves through the suppressed compounds mainstream medicine set aside: The DMSO Book, Chlorine Dioxide: The Forbidden Remedy, The Iodine Book, and The Hydrogen Peroxide Book. Two more recover what’s still on the kitchen shelf: Baking Soda and The Castor Oil Book. Two more recover the minerals modern soil, water, and processing quietly stripped from the diet: The Magnesium Handbook and The Boron Book. Sitting alongside these is No Contagion, co-authored with Jamie Andrews — the case against germ theory itself, catalogued through 258 failed contagion experiments.
The critique books cover what medicine, dentistry, psychiatry, and veterinary practice have become. The Unvaccinated treats the completely unvaccinated as a comparison group across twenty chapters and five appendices. Medicalized Motherhood follows a woman through 123 documented interventions from teenage pill to postpartum discharge. Drilling for Profit treats cavities, gum disease, and crooked teeth as the dietary problem they are. What Your Vet Can’t Tell You applies the same critique to pets. Escape from Psychiatry documents the fabrication of the DSM and the specific damage of every major psychiatric drug class. The Vitamin K Injection covers what happens in the first hours of a newborn’s life.
The full shelf is at lulu.com/spotlight/unbekoming. A physical book reaches the person a Substack post never will — the skeptical relative, the friend who won’t click a link but might open a book, the visitor whose eye lands on a coffee table. Buy one to keep, and one to give away.
References
Kendrick, M. (2021). The Clot Thickens: The Enduring Mystery of Heart Disease. Columbus Publishing, chapters 2–3. On the absence of plaque in veins and the pulmonary circulation, and on vein grafts as coronary bypass grafts.
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Kendrick, M. (2021). The Clot Thickens, chapter 2. Kendrick recounts Smith’s teaching remark that LDL cannot cross the endothelium during a small-group session at Aberdeen University, which he identifies as his first exposure to a crack in conventional cardiovascular thinking.
Smith, E. B. and Thompson, W. D. (1994). “Fibrin as a factor in atherogenesis.” Thrombosis Research 73(1): 1–19. https://www.sciencedirect.com/science/article/pii/0049384894900493
McCully, K. S. (1969). “Vascular pathology of homocysteinemia: implications for the pathogenesis of arteriosclerosis.” American Journal of Pathology 56(1): 111–128.
McCully, K. S. and McCully, M. (1999). The Heart Revolution: The Extraordinary Discovery That Finally Laid the Cholesterol Myth to Rest. HarperPerennial, foreword and pages 7–10.
Kendrick, M. (2021). The Clot Thickens, chapter 2, on plaque composition.
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Kendrick, M. (2021). The Clot Thickens, chapter 2, on cholesterol esters versus free cholesterol.
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Paterson, J. C., Armstrong, R., and Armstrong, E. C. (1963). “Serum lipid levels and the severity of coronary and cerebral atherosclerosis in adequately nourished men, 60 to 69 years of age.” Circulation 27: 229–236.
Mathur, K. S., Patney, N. L., Kumar, V., and Sharma, R. D. (1961). “Serum cholesterol and atherosclerosis in man.” Circulation 23: 847–852.
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Again Unbekoming, thank you for sharing your knowledge
I became aware of the endothelium while researching the covid issue and countermeasures. The worldwide clinical trial continues. I doubt we will ever know the results and mechanisms.