No one can explain WHY cholesterol builds up in our arteries around the heart and not in other veins in the body – after all aren’t they all the same thing, just different sizes?
There is a growing body of evidence to suggest that cholesterol is actually a healing agent – cholesterol is building up at points in the arteries because they are DAMAGED.
Why are they damaged? What causes this damage in the arteries?
If cholesterol is viewed as a healing agent to heal the damage points in the arteries, then the risk levels associated with high total cholesterol levels seems to diminish, if not disappear.
There is also a growing body of evidence to suggest that LOW cholesterol levels in the body is a risk factor for cancers and other diseases since the body is depleted of cholesterol as a healing agent.
Interested in your views on this.
– David (last name unknown) Via the blog
Great questions, David. Let’s take them one at a time.
Since this answer involves the nitty gritty, and often convoluted, world of nutritional biochemistry, I will try my hardest to make it easy to follow.
Let’s start at the beginning.
You are right; cholesterol is absolutely necessary.
We need it for arterial protection as well as vitamin D synthesis and the production of hormones, including testosterone and estrogen.
However, cholesterol is not essential. If we were never to get it from our diet it wouldn’t be an issue because our body produces it.
Just like with vitamins and minerals, though, a certain amount is beneficial and health-promoting, but excess amounts are detrimental.
The large majority of cholesterol is produced in the liver.
Since cholesterol is not water soluble, it can not freely travel to other tissues through the blood.
Remember, cholesterol needs to be transported to other tissues so it can help repair membranes and aid in hormone production and vitamin D synthesis.
Instead, it has different “cars” to choose from.
These “cars” are called lipoproteins. As the name states, they are proteins that carry lipids (fats) inside of them.
The two most famous lipoproteins are HDL (high-density lipoprotein, commonly referred to as ‘ good cholesterol ’) and LDL (low-density lipoprotein, commonly referred to as ‘ bad cholesterol ’).
What determines whether a lipoprotein is high or low in density is the amount of cholesterol it contains in relation to its protein content.
Low-density lipoproteins carry lots of cholesterol.
As low-density lipoprotein travels through the blood, it looks for LDL receptors (since we are using the car analogy, think of LDL receptors as designated parking spaces or garages).
In the same way that you can’t park your car where you please, LDL receptors can’t drop off cholesterol wherever they please.
It just so happens that one of the main sites of LDL receptors – other than the liver — is coronary (”heart”) artery endothelial tissue.
Just like a parking garage has a “maximum capacity”, LDL receptors can only take up so much cholesterol.
Once LDL finds appropriate receptors, the liver knows to stop producing LDL.
Here’s another twist.
High intakes of saturated fat decrease the number of LDL receptors.
A lack of receptors consequently increases hepatic (liver) production of LDL.
In turn, more LDL floats around in the blood, having nowhere to go.
High amounts of LDL in the blood have a propensity to build up in the inner walls of damaged arteries that feed into the heart and brain.
Why do arteries get damaged in the first place?
That is something that isn’t entirely known, but the main theories are cigarette smoke, high blood pressure, and high triglyceride levels.
For some reason, coronary arteries are more susceptible to damage.
When there is damage to an artery wall, LDL deposits, coalesces into liquid droplets, and becomes oxidized.
Macrophages (a type of white blood cell) take in the cholesterol and form fatty streaks.
As time goes on, more LDL collects, and the area grows in size.
Smooth muscle cells begin slipping into the area, forming a cap over the deposited LDL. This cap is what we know as plaque (the yellow substance you see in the photo accompanying this post; notice how clogged that artery is!).
With time, the cholesterol crystallizes, calcium starts to deposit at the area, and the vessel becomes rigid, thereby blocking blood flow.
Here’s another twist.
HDL (“good cholesterol”) can also bind to these LDL receptors.
This is why increasing your HDL levels ( through exercise, consuming monounsaturated fats and soluble fiber, not smoking, and eliminating trans fat consumption ) is so crucial.
Not only does HDL transport excess cholesterol back to the liver for excretion (via bile acids), it also — and this is crucial — prevents macrophages from engulfing LDL and saves LDL from oxidation (and thereby reducing plaque formation).
Thus, if not genetically predisposed to high cholesterol (due to insensitive LDL receptors), the healthier your diet and lifestyle, the higher your HDL — and the more protection against plaque you have.
Research has provided strong evidence that weight loss itself increases HDL levels!