The Heart of the Matter (Part III)

The purpose of this post is to explain the process of atherosclerosis formation, or how plaque accumulates and hardens in the arteries resulting in terrible yet preventable things like high blood pressure, heart attacks, and strokes.

The traditional paradigm states that dietary saturated fat and cholesterol build up in the arteries over time to form arterial plaque. More recent research shows something different: arterial plaque is the result of arterial damage, inflammation, and oxidation.

It is important to know that the conventional view of cholesterol is negligent and oversimplified: they label HDL as the good cholesterol and LDL as the bad cholesterol. But there is more to the story: HDL stands for high density lipoprotein, and LDL stands for low density lipoprotein.  HDL and LDL are the proteins that carry cholesterol throughout the blood. We measure cholesterol by the amounts of these lipoproteins.

The key fact is that the smaller the lipoprotein, the more dangerous they are; smaller lipoproteins are significantly more likely to damage arterial walls than bigger lipoproteins.  More importantly, not all LDL poses a risk: it is the small, dense form of LDL cholesterol  that is most likely to injure the the arteries. An analogy from this post effectively gets the point across:

Think of it this way. Small, dense LDL are like BBs. Large, buoyant LDL are like beach balls. If you throw a beach ball at a window, nothing happens. But if you shoot that window with a BB gun, it breaks.

Knowing this, we can go through the basics of how atherosclerosis forms: 

1. The artery is injured.

2.  White blood cells (also called Leukocytes) rush to the scene and enter the arterial wall.

3.  They consume the offending LDL.

4. Depending on how much there is for the white blood cells to deal with, they become overtaxed with LDL cholesterol and become foam cells.

5. As these foam cells accumulate over time, they form fatty streaks.

6. In attempt to heal, smooth muscle cells cover the plaque resulting in a fibrous cap that is what clogs up the artery.

7. If the inflammation continues, the build-up progresses, and the fibrous caps become increasingly susceptible rupturing which in turn leads to blood clots or heart attacks.

To summarize, atherosclerosis begins when the artery is injured, and if the same factors that caused the initial injury persist, then the resulting, long-term inflammatory response to the injury causes a build-up of arterial plaque. Plaque cannot form unless there is a lesion/damaged spot. The American Heart Association, the government, reputable doctors, and skeptics alike are studying and documenting this.

Then what are these factors that cause the initial arterial injury? And what other factors increase the risk of  a continued inflammatory response?

Oxidation: One way to explain oxidation by starting out with its antithesis: antioxidants. Antioxidants are somewhat of a buzz word; we know they are good for preventing cancer. This is because they inhibit oxidation, a chemical reaction that can produce free radicals. Free radicals damage cells because they are missing electrons and try to take back electrons by attacking cells; antioxidants counteract this process. In short, oxidation causes cellular damage. And when the immune system senses damage, it produces an inflammatory response.

Cholesterol has been labeled as one of the main culprits in causing heart disease; however, cholesterol enables several essential functions that would require an entire other blog post to cover. It is true that there are dangerous forms of cholesterol:  as previously stated, the smaller and more dense the lipoprotein, the more likely it is to hurt the artery. Furthermore, the smaller the LDL, the more likely it is become oxidized. Oxidized LDL poses a significant threat to arterial walls.

So if you have high levels of small, dense, oxidized LDL looking for other cells to bully and steal electrons from, then you are in trouble, because that can cause an arterial injury.

So then what changes will decrease the your levels of small, dense, oxidized LDL?

  • Reduce your polyunsaturated fat (PUFA) intake. Unsaturated fat has a positive connotation in our culture (just like how cholesterol has a negative connotation). However not all unsaturated fats are the same: PUFAS are very prone to oxidation and consequently producing free radicals; monounsaturated fats are more stable. Unfortunately, PUFAs are ubiquitous and misconstrued as “heart healthy.” Avoid consuming processed foods, too many nuts, and soybean, canola, and corn oil.
  • Manage your blood glucose with a low-sugar diet. As I previously explained, high blood glucose levels and growing insulin resistance keep glucose in the bloodstream for longer. This increases the chances of glycation and Advanced Glycation End-products (AGEs): this is when a sugar molecule binds to a protein or fat molecule without an enzyme to digest that sugar. The result is an AGE which wreaks havoc by damaging cells and requiring the immune system to create an inflammatory response (which sounds an awful lot like oxidation and free radicals).
  • Eat healthy fats like butter, olive oil, and coconut oil. Gasp! Did I just say butter? But butter is a saturated fat. Yes, yes it is. And saturated fat rarely oxidizes. Furthermore, compared to grains, healthy fats are a superior source of energy because they do not elevate blood sugar levels or trigger an insulin response thus decreasing the risk of glycation and AGEs.
  • Don’t smoke, be completely sedentary, or eat trans fats and HFCS. These points are obvious and consequently do not merit elaboration.

There is plenty of evidence to support the connection between blood sugar, glycation, oxidation, and developing heart disease:

  • Oxidation and inflammation are observed as key players in arterial plaque accumulation.

In conclusion, heart disease is not as simple as this:

It is more accurately represented by this:

For more information, I recommend the following:

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3 responses to this post.

  1. This is an excellent post. Get’s the point across relative to cholesterol not being the simple bad guy, but still a possible player via oxidized LDL. Have you read “The Great Cholesterol Con” by Kendrick? Very funny book (surprising given the topic).

    I am adding your blog to my goggle reader subscription list.

    …Tim

    Reply

  2. Thank you Tim! I’ll have to check out “The Great Cholesterol Con.” I like your blog as well.

    Read you later!

    Reply

  3. […] It is possible to have low LDL cholesterol and still have heart disease; people with these symptoms have high triglycerides, high glucose levels, and high levels of C-Reactive Protein (inflammation). Sound familiar? […]

    Reply

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