Heart Disease Part 1: The Story of Cholesterol

We have all heard of cholesterol and what we’ve heard is that cholesterol is bad. Oh sorry, actually we are told there is a “bad cholesterol” and then there is a “good cholesterol.” So, one is good and one is bad. One gives us heart disease and one helps prevent it. But, is this actually true? Well, not exactly. The fact is, cholesterol itself isn’t really the cause of heart disease, though it tends to get the most attention. In this first article on heart disease, I’d like to clarify what cholesterol is, what it does and its role in heart disease.

Cholesterol is a type of lipid – known as a sterol – that is produced in our liver. It can also be found in the food we eat. Cholesterol has a number of important roles in our body. It is a component of cell membranes and is a precursor to bile acids that are used in the digestion of fats, several hormones and vitamin D. In fact, we really couldn’t live without cholesterol. Without it, we would be unable to make a number of vital hormones including aldosterone, testosterone, estrogen, progesterone and cortisol as well as vitamin D which is necessary for the proper absorption and utilization of calcium and is also involved in a number of other bodily processes including immune function. Clearly, cholesterol has many important functions.

In truth, there is no good or bad cholesterol. Cholesterol is just cholesterol. The good and bad idea refers to the packaging of cholesterol in the blood and where it’s going. You see, cholesterol, along with triglycerides, is packaged into little phospholipid and protein vehicles (particles) which are then distributed throughout the body. LDL is one type of vehicle, while HDL is another type. The names refer to the density of the vehicle. LDL is a low-density lipoprotein, while HDL is a high-density lipoprotein. The density changes based on the content of lipids versus proteins. LDL has more lipids, while HDL has relatively more proteins. LDL particles start out in the liver as VLDL particles (very low-density lipoproteins), but as they travel throughout the body dropping off supplies (triglycerides and cholesterol), their density increases and they become LDL particles. LDL particles are considered “bad” because they carry cholesterol to various parts of the body where they sometimes get stuck in our arteries (more on that later). HDL particles on the other hand, are also made in the liver. The major difference, however, is that they go out to pick up supplies from the rest of the body to bring them back to the liver. These particles are therefore considered “good” cholesterol.

This is the basic, simplified story of cholesterol – we eat it, we make it, we transport it and we make things from it. But how does cholesterol contribute to heart disease? I mentioned that LDL particles can get “stuck” in our arteries. While this is true, how this happens is somewhat complex and generally involves more than just the presence of LDL particles. One thing that will significantly increase this likelihood is oxidation. Oxidation occurs when a type of molecule known as a reactive oxygen species (ROS) (aka “free radical”) steals an electron from another molecule. When this happens to an LDL particle – or more specifically and most commonly to a polyunsaturated fat found within the LDL particle – you get an oxidized, and more reactive, LDL particle which is more likely to be “eaten” by a macrophage.

Macrophages are white blood cells that act, in part, as a clean-up crew in the body, searching for invaders and removing unwanted substances. When LDL particles become oxidized, they draw the attention of macrophages who then see them as an unwanted substance. When macrophages eat a lot of oxidized LDL they become what are known as foam cells and they send out a signal to the rest of the immune system to send in more troops to help clean up. This leads to an accumulation of foam cells just beneath the internal lining of the arteries – the endothelial cells – and eventually leads to the formation of a plaque.

From what I’ve discussed here, you may have recognized that LDL particles – especially oxidized LDL particles – are actually more to blame than cholesterol itself. The standard test for cholesterol measures the concentration of cholesterol found in LDL and HDL particles. This is called LDL-C and HDL-C. Research is finding, however, that measuring the LDL particle number (LDL-P) – meaning the number of LDL particles found in your blood – is actually a more relevant assessment for heart disease than the LDL cholesterol concentration. Often times, the cholesterol concentration is going to correlate with the LDL-P – meaning if your LDL-C is elevated, your LDL-P is usually elevated as well. This makes sense because if you have more cholesterol, you’ll need more vehicles to carry it around. This isn’t necessarily true in all instances, however, which is why the LDL particle number should be measured separately. I’ll discuss this more in the third article in this series when I discuss comprehensive testing for risk of heart disease.

In brief, this is how cholesterol, or rather, LDL particles contribute to heart disease, but it’s far from the full story. There are many other contributors to heart disease. Aside from what we’ve discussed here, a number of other factors are at play including endothelial dysfunction, oxidative stress and inflammation. But, we’ll save that for the next article.

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