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Over the last 50 years, the public has been subjected to a dizzying confusion of explanations of the role of cholesterol in cardiovascular disease. First we were told that our blood vessels were like pipes and cholesterol was like the calcium in hard water, causing clogs. Then we were told that, no, actually cholesterol only accumulates in arteries, not veins, and just in small segments of arteries a few millimeters (a fraction of an inch) long. We were told that cholesterol is bad and we need to get our total cholesterol levels down. Then we were told that cholesterol is actually good, HDL, or bad, LDL. We need more HDL and less LDL. Then it became common knowledge that not every kind of LDL cholesterol is harmful in our arteries, just the slightly less fluffy pieces of LDL called apo-A1. It was just these higher-low-density lipoprotein particles that are actually injurious to blood vessels, well, arteries, well, small segments of arteries under stress, when they are consumed by white blood cells, more specifically macrophages, and subjected to calcification.
What does all this mean in practical terms of staying healthy? It's probably a good idea to go back to the beginning.
"Cholesterol" Isn't the Enemy
Cholesterol is not toxic. It's essential to every cell in the human body. The body creates hormones by starting with cholesterol. Cholesterol is incorporated into the membrane lining every cell. The profound usefulness of cholesterol really is not hard to understand. The bloodstream consists mostly of plasma, which is mostly water. Cells would dissolve into the bloodstream if they didn't have a "raincoat." Cholesterol isn't soluble in water, so it can be used to protect cells from dissolution.
Because cholesterol isn't soluble in water, it can't circulate through the bloodstream without first being coated with something that is soluble in water. Cholesterol circulates through the bloodstream in a "balloon" of lipoprotein. Protein surrounds cholesterol and carries it where it needs to go. The glob of cholesterol can be large and light, surrounded by very low density lipoprotein (VLDL), or a little smaller, surrounded by low-density lipoprotien (LDL), or tight and compact, surrounded by high-density liproprotein (HDL). Each sphere of cholesterol matches to a different receptor on cell surfaces. It has a unique docking site. Receptors that capture VLDL don't capture LDL, and receptors that capture LDL don't capture HDL. Atherosclerosis involves "smaller LDL" called apo-A1. Other forms of cholesterol aren't involved in atherosclerosis (and more than just cholesterol is needed for atherosclerosis to occur).
When You Lower Your Cholesterol, Where Does It Go?
So, when you lower your cholesterol, it does not disappear. The body makes most of its own cholesterol. Only about 15 percent, at most, comes from food. "Extra calories" from carbohydrate and fat become the triglycerides that are the building blocks of cholesterol, which starts as VLDL cholesterol.
The statin drugs that every doctor prescribes to nearly every patient can actually increase the production of VLDL cholesterol, but they reduce the amount of LDL cholesterol in circulation in the bloodstream. That's usually a good thing, because both the larger and smaller pieces of LDL cholesterol become less numerous in most people. However, it's possible to have "normal" or "low" total LDL and too much apo-A1 LDL and still have elevated risk for atherosclerosis.