Atherosclerosis Basics Part I – Cause

Atherosclerosis or Hardening of the Arteries is Caused by Plaque Buildup. It Can Be Prevented and Reversed.


Atherosclerosis or hardening of the arteries is due to accumulation of plaque behind the artery walls. This can be prevented and reversed with lifestyle choices.  This post explains the cause of atherosclerosis. A future post will explain how to prevent and reverse it.

Atherosclerosis is the buildup of fatty material and other undesirable detritus inside the artery wall. It is an inevitable process, beginning in the womb. However, there are counter processes working to manage and reduce this load. Thus disease progression is a question of which wins the battle.

Because of this tipping point property, atherosclerosis can be attacked by reducing the processes that build it up, strengthening the processes that clear it, or preferably by both.

To fully understand what is going on, lets look at an artery. It has four layers. The inner layer, called the endothelium, is made up of a single layer of skin like cells. The endothelium is a very important layer, but it is a bit fragile. Next is a thin crosshatched elastic layer that is not made of cells, called the basement membrane. Next is a layer of muscle cells. What are muscle cells doing in an artery? They wrap around the ‘pipe’ and squeeze or relax to control the blood flow. (Veins have them too.) Finally there is a tough outer layer again made of connective tissue, a non-cellular material.


The inner layer, the endothelium, seals the artery pretty tightly. It prevents most things from leaking out of the artery. But you need to imagine the scale of things. Lets suppose atherosclerosis-cause-endotheliumyou were cellular sized and standing inside an artery. It would appear to be a large tunnel. You could easily make out the individual endothelial cells, being about your own size in your shrunken state. You would also be able to see that the cells are quite snug and tight up against one another. Lets suppose some LDL particles float by. This is the so-called bad cholesterol. There are a lot of these particles, but you will have to look closely to see them. If you took a copy of this post with you on your microscopic adventure, they would range in size from about this “o” to this “O” – really small compared to a cell.

Now take a close look and you will see some of the smaller “o” sized LDL particles are slipping behind the cell wall. The larger “O” sized ones tend not to do this, but the small ones can. This is bad news.

Let’s follow one of those small LDL particles and see what’s going on behind the endothelium inside the cell wall.

So far, our trapped LDL is not a problem. This is the body’s natural material and in of itself is not dangerous. Unfortunately some of this material is vulnerable. Fat and cholesterol in the LDL particle tend to get oxidized by local oxygen radicals. Oxidized LDL is toxic and can damage adjacent cells. The thin layer of endothelial cells are likely already damaged.

The damaged cells or threatened ones aren’t going to take this lying down. They secrete various signaling chemicals that call for help.

Circulating small leukocytes (white blood cells) respond to the cry for help, entering the area inside the artery wall, behind the endothelium. Once at the ‘scene of the crime’ they begin engulfing the oxidized junk and, if necessary, call for yet more leukocytes. Now as these cells engulf away, they get too large to get back out into the blood. They are stuck.atherosclerosis-cause-plaque They get in, but they don’t get back out. More rancid LDL piles up and more and more leukocytes get fatter and fatter, eventually forming a significant bulge in the artery. This is atherosclerosis. The lump of glop is called an atheroma.

The fattened up leukocytes now have a whitened fluffy appearance and are called foam cells. This situation can theoretically continue, causing more and more foam cells to form, and the lump in the artery wall to become thicker and thicker. However, the plot is about to take an interesting turn.

The Immune System Has One More Trick Up Its Sleeve

HDL particles soon make their appearance inside the artery wall. HDL particles are about half the size of the smallest LDL particles, the ones that invaded. The HDL particles are going to attempt to stabilize the growing mess. They offload the overloaded white cells by directly sucking the rancid fat material from the swollen cells into their own interior. They are going to swell up themselves, but not so much that they can’t escape back into the bloodstream. This calms things down.

The HDL particles are so versatile they seem like ‘junior’ cells. They aren’t at all. They are, however, very tiny.


The HDL along with the immune system is trying to repair the problem. It will easily be able to do this if there is plenty of HDL getting behind the artery wall, and the buildup of oxidized junk isn’t overwhelming.

Some people have slightly larger LDL particles which tend to not get behind the cell wall. These people don’t get atherosclerosis. Other people have smaller LDL particles. These people are at risk.

Now you might be genetically lucky and have the safe large size particles, or you might be unlucky and have the small one. But you don’t have to rely on luck, nor is there any guarantee you will keep the safe larger sizes.. You can control the size of your LDL particles, and by doing so can prevent or even reverse atherosclerosis. The next post on this topic, “Atherosclerosis Basics Part II – Prevention and Reversal”, will explain exactly how.


If the HDL cannot keep up, the atherosclerosis load increases and increases. The artery actually reshapes itself, bulging out to try to maintain the opening so that blood can flow.

Because of this re-shaping, a person can (and many do) have a very high atherosclerotic load without a rise in blood pressure. This is why a normal blood pressure doesn’t necessarily mean no heart disease. The opposite, though, is usually true.

The artery can’t reshape itself forever. As the plaque builds up, several things eventually go wrong. The arterial opening starts to get smaller.  Blood pressure is raised to try to compensate for this. Even so, there may not be enough blood. This situation is called ischemia. It may result in angina, a painful and dangerous heart condition.

A more serious problem is the integrity of the atheroma itself. As it grows, the endothelium separating it from the blood flow is largely destroyed. To try to seal the atheroma back up, the immune system forms a sort of scab, called a fibrous cap. This cap is flimsy, and can break, spewing all sorts of junk directly into the artery, where it immediately clots. This is the nightmare scenario. Now, something is loose in the artery that is going to get stuck somewhere as the artery narrows down to the capillaries. Once it clogs an artery, the down stream cells will be partially or totally cut off, resulting in a stroke, heart attack, or other such problem.

The swollen outer layer of the artery is also weakened and vulnerable. This is the spot where a hemorrhage or aneurism could occur.

Heart disease is unknown among hunter-gatherers.  Evidently, their arterial plaque buildup is more than compensated for by their circulating HDL. We can do this too. Stay tuned.



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