What Is Atherosclerosis? An Essay on Healed Injury, Layered Clots, and the Repair That Medicine Refuses to See

[John Hilton]

What Is Atherosclerosis? An Essay on Healed Injury, Layered Clots, and the Repair That Medicine Refuses to See

https://www.unbekoming.com/p/what-is-atherosclerosis?

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.

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. 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. 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.

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.

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.

Cortisol and adrenaline. Chronic stress, through the HPA axis, elevates these hormones chronically. Both damage the endothelium and increase clot formation.

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.

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.

(I would venture to add that some vaccinations probably damage arteries, too.)