Cholesterol -The Good, the Bad and the Ugly (Friend or foe?)
Over the years, cholesterol has earned such a bad rep that it is almost impossible to believe our body actually needs it. Yes, WE NEED CHOLESTEROL and without it we will cease to exist. It is a waxy, fat-like substance present in every cell of the body where it is used in making cell membranes, important hormones such as progesterone, estrogen, testosterone and cortisone, Vitamin D and bile acids required for digestion of fats. And believe it or not, our brain is the most cholesterol rich organ in the body with approximately 25% of the total cholesterol in the body being located in this vital organ.
Now, blood being mostly water doesn’t effectively mix with fat molecules such as cholesterol. As such, cholesterol doesn’t travel freely in the bloodstream. Instead, it travels around in small packets of proteins, known as lipoproteins. Lipoproteins contain proteins (apolipoproteins), phospholipids, triglycerides and cholesterol, but in varying amounts. Traditionally, we usually talk about two types of lipoproteins that are involved in moving cholesterol and other fats (lipids) around the body:
- Low-density lipoprotein (LDL): It carries cholesterol from the liver, where it is synthesized, to the cells where it is separated from low density lipoprotein and used for many functions. It is also called “bad cholesterol”
- High-density lipoprotein (HDL): It transports excess or unutilized LDL cholesterol from tissues and arteries back to the liver, where it is broken down into bile acids. It is also called “good cholesterol” as it is helping to eliminate excess cholesterol.
- First, LDL and HDL are lipoproteins – that is, fats combined with proteins – and not simply cholesterol.
- Second, lipoproteins mainly contain protein, triglycerides and cholesterol, but in varying amounts. And that leads us to another type of lipoproteins that are not usually highlighted during our heart-to-heart (pun intended) conversation with doctors on our high cholesterol levels. Enter VLDL: Very Low Density Lipoprotein that mainly carries triglycerides to the body tissues.
Did you know that LDL cholesterol is not the bad guy here? It is because plaque is bad but cholesterol is not the reason why plaque is there in the first place. It is just a by-product when our body’s immune system responds to any arterial damage or inflammation. Wow! But also keeping fair to the traditional thought process, LDL particles do contribute to the plaque build-up, but not just because of LDL cholesterol, and rather due to Lp (a), which is a sticky form of LDL cholesterol and promotes plaque formation.
A lesson in heart health: Atherosclerosis or Plaque – What is it actually?
Whatever plaque may be, we can’t get away by simply labelling it as ‘build-up’ of fat in our arteries!! Plaque happens when our body is trying to patch up or fix damage to our arteries.
We all have heard that fatty foods, especially those rich in cholesterol, cause arterial fat deposits or plaque. Something like what happens to a drain pipe under the sink when it gets clogged with the grease over time? But this analogy could only work if our arteries would simply function like plumbing in our kitchen sink. They don’t.
To understand this clearly, let’s take an example. What happens when you get a deep cut in the skin? The skin heals itself by first forming a clot that makes a scab. When the skin underneath heals, the scab falls away. A similar process occurs when the arterial wall is damaged or inflamed, which does occur on a day to day basis: except that now this scab will be called plaque. Let’s see.
- Damaged arteries trigger the body to kick start its immune system – releasing white blood cells, fibrins, cholesterol and other anti-inflammatory chemicals to rush to the site of injury. All these together form a clot or patch over the damaged artery wall. Cholesterol? Yes! Our body releases cholesterol, as it is a natural anti-oxidant and anti-inflammatory – an important part of the body’s defence mechanism. It is also required to make new healthy cells to replace the damaged or dead cells at the site of injury.
- Now, the body can’t risk this clot or scab to break away and float around freely in the bloodstream. If it were to fall off the arterial wall, it would restrict the blood flow to vital organs such as the heart and the brain – causing a heart attack or a stroke.
- Instead the clot is drawn into the arterial wall and is deposited there. Over time, this accumulation gives rise to plaque.
Instead of identifying the root cause of arterial damage and making arteries stronger, we blame the patch up for the weakness of arteries and the resulting collapse. Sounds ridiculous? But that’s exactly how we are convinced to look at the cholesterol issue. Terming LDL as bad cholesterol is misleading. High LDL levels means there may be pro-inflammatory reactions and LDL is only carrying cholesterol to these sites to do what it is supposed to do: repair the cellular damage as well as to prevent the formation of pro-inflammatory lipids that generates free radicals. To know more about the ant-inflammatory benefits of cholesterol, you can read this article.
Yes, it is true that plaque can indeed constrict the blood vessels and increase the chances of risk factors associated with cardiovascular diseases such as high blood pressure and heart attacks. Plaque is bad, but cholesterol is NOT the reason why plaque is there in the first place.
Let us, however, play fair to the current dogma of conventional medical claims. A small sticky part of low density lipoprotein, called Lp (a) does contribute to the plaque build-up. It is very sticky and gets attracted to the damaged arterial walls forming clots (that is, plaque that may become dangerous). LDL particles come in various sizes, and large ones are not a problem. Only smaller, denser LDL particles such as Lp (a) can cause problems. It is because they are able to squeeze through the arterial lining where, if they are oxidized, can cause damage and inflammation.
But, the picture is still not complete. There are some pieces of the puzzle still left. For example, what if there are other important materials that can be called upon by the body to repair the vascular damage? What if the body doesn’t have to use Lp (a) that leaves behind residual sticky trappings that promotes plaque formation?
Intrigued? Watch out for Part 2 in this series.