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.



  7 comments for “Atherosclerosis Basics Part I – Cause

  1. Helene
    February 27, 2015 at 3:58 am

    Excellent post. Thank you. Waiting for the follow-up one, then there will be a comment (challenging).

    • Helene
      February 27, 2015 at 6:24 am

      Excellent Post! Thank you. Waiting for the follow-up one – the most important. There will be comments.

  2. Sri
    March 7, 2015 at 2:12 am

    Was waiting for the Second Part to read this 🙂
    Thanks a lot

  3. carol
    January 27, 2016 at 7:03 am

    should i go my heart specialist if i have arterio
    sclorisous my doc said i have the disease
    he also said i cant drive

    • carol
      January 27, 2016 at 7:05 am

      my doc said i have arteriorsis doi get another opion from heart doc or a nerosurgeon

  4. Charles
    March 12, 2016 at 3:56 am

    The information is interesting & helpful.

    How do we reverse atherosclerosis?

  5. Evelyn Manteris
    November 6, 2016 at 9:54 pm

    Good information on learning what atherosclerosis is and how it affects a person. Is there any medication out there to stop the progression and/or reverse it? I understand eating healthy and exercising is important in helping to keep it at bay, but it was explained to me that it affects every vein in the body eventually leading to death. My spouse was diagnosed with it 2 1/2 years ago and under went 4 surgical procedures that all failed within 6 months or less and he was given a choice to go home and get his affairs in order because he had about one week before he would die or be transported to UVA Health Hospital in Charlottesville, VA for their assessment. After being off of blood thinners for 5 days they operated doing a double bypass on the left side of the heart. The right side also had a 95% blockage that was intermittent from one end to the other with an enlargement at the bottom of the right side of the heart. Three arteries on the back side were 100% blocked and the widow-maker was 95% blocked and the few stints that had been put in earlier were all calcified. He could feel every PVC his heart was producing from the lower left side of the heart that were unbearable. He was placed on a cholesterol medicine that had to be replaced with another one later and then removed from it. He was told that he was not a candidate for any of the other medications. He was told that he cannot undergo any other surgeries for the rest of his life that he might have after the double by-pass surgery. He stays fatigued, purple toenails and fingernails, gets winded easily, but not on oxygen. He suffers with muscle spasms, headaches, low back pain from 5 damaged discs and has Fibromyalgia. There is very little medicine that he takes, one adult aspirin per day, one Thyroid pill a day, vitamin C, & D and sees his cardiologist every 4 months for an EKG and check up. They did not give him more than one year to live after the surgery, but it has been two years as of March 2016. Is there anything new in the research that he could benefit from?

Leave a Reply

Your email address will not be published. Required fields are marked *