What is cholesterol anyway? And why are we worried about it? What does it do and why do we have it?When you hear doctors talking about watching your cholesterol, it’s because elevated levels of cholesterol, especially the bad types of cholesterol, have been positively correlated with increased risk of stroke and heart disease. Elevated cholesterol levels is associated with atherosclerosis, which is also called “hardening of the arteries”. What’s actually going on is plaque is getting deposited on artery walls, making the walls thicker and the arteries more narrow and less flexible. This causes an increase in blood pressure and can ultimately result a vessel blockage (like blocked heart arteries requiring a bypass or a stroke) or a rupture. One of the primary culprits here is low density lipoproteins (LDL). The LDL in your blood adheres to blood vessel walls and then becomes oxidized by a free radical. This triggers your immune system which sends white blood cells into the area, which coalesce on the LDL deposit and ‘eat’ the oxidized LDL. Your body then processes the ‘eaten’ LDL by pulling it out with high density lipoproteins (HDL), which you may have heard referred to as the “good cholesterol”. After it’s transported away, the your body takes the the broken down LDL and removes it. This is how it’s supposed to work.
What happens in atherosclerosis is that your body can’t keep up with the removal of oxidized LDL. This could be because you have too much of it, or not enough HDL, or some combination of the two. So the buildup, called plaque, on the blood vessel walls continues. The larger the buildup of plaque, the less flexible and more narrow the blood vessels gets.
There are two types of LDL that we know of so far. The larger type, LDL Type A (LDL-a) is much less likely to enter the vessel walls and become oxidized. The smaller type, LDL Type B (LDL-b) is much more likely because this type has a much greater ability to pass through the vessel’s wall.
Eating saturated fats increases large LDL (LDL-a). Small LDL (LDL-b) is increased when you eat excess carbohydrates which your body then processes into fat. There’s another molecule at play here called Lp(a). It’s a small molecule that’s similar to LDL-a. Your levels of Lp(a) are determined by your genetics. It’s typically higher in people of African descent (hence the predisposition toward high blood pressure) and can also be affected by liver disorders.
Researchers have yet to determine the purpose and function of Lp(a). It only shows up in Asian and African monkeys and in humans, which means it probably developed at some point not too long ago to counteract some environmental factor that might or might not still exist.
Someone with heart disease is four time more likely to have higher levels of Lp(a). Increased LDL-a without increased LDL-b has so far been shown to not increase the risk of heart disease. There does seem to be a correlation between high triglyceride levels and LDL-b, but it’s not fully understood yet.
The best way to lower LDL-b (the kind associated with heart disease risk) is to eat fewer simple carbohydrates (high glycemic index). Exercise has also been shown to both lower total LDL and to change the composition of LDL more towards the less harmful large LDL-a. Exercise also increases total HDL for most people, the ‘good cholesterol’ that removes oxidized LDL from your body.
There are several different cholesterol lowering drugs available today. Different drugs have different affects on your lipid profile; some effect the bad LDL more than others. The only thing proven to lower Lp(a) is niacin, but not everyone can tolerate it. If you’ve been diagnosed with high cholesterol and your doctor wants to treat you, ask for a more specific diagnostic test to make sure your treatment is matched to exactly what you you need.
Related reading: Framingham Heart Study