If I want to know how much oil is in the engine of my car, I pull out the dipstick and take a look. It may register "full" or "add," telling me whether there's enough oil in the engine, or whether it's low and more needs to be added.
That's kind of what cholesterol does. Cholesterol serves as a "dipstick" to tell you what kinds of particles are in your bloodstream. While the dipstick in your engine is otherwise useless-it doesn't make the engine run better or faster-so it is with cholesterol. It is an indicator.
In the early days of trying to understand how and why heart disease develops, researchers learned that there were a variety of fat-transporting particles in the blood. Because there were both lipids (fats) and proteins in these particles, they were called "lipoproteins," or lipid-carrying proteins. Lipoproteins are complex particles, much smaller than a red blood cell but much larger than the cholesterol, proteins, triglycerides, phospholipids, and other components contained within.
Researchers distinguished these particles by density (in a centrifuge, which spins blood at high speed, separating the various components of blood by density). There were high-density lipoproteins (HDL), low-density lipoproteins (LDL), very low-density lipoproteins (VLDL), and intermediate-density lipoproteins (IDL). Measuring these various lipoproteins In the 1960s was not a practical reality outside of research laboratories. So an indirect method was developed: Measure the quantity of cholesterol in each fraction: the quantity of cholesterol in the high-density fraction, the quantity of cholesterol in the low-density fraction, and so on. It was crude, but it provided a rough indication of how much of each fraction there was in the blood. Even cruder, the cholesterol in the low-density fraction was the most cumbersome to measure, so it was not measured, but calculated:
(LDL cholesterol =
Total cholesterol - HDL cholesterol - triglycerides/5)
At a time when most physicians and the public had no idea what "cholesterol" was, nor barely understood nutrition nor the causes underlying heart disease, this simple, indirect approach served its purpose.
The technique of measuring cholesterol was introduced for widespread adaptation into the U.S. and rest of the world for discerning heart disease risk. For the initial two decades after its introduction, most attention was focused on measuring the total quantity of cholesterol that included all fractions, high-density on down. Over time, it became clear that the calculated LDL cholesterol fraction was a somewhat better predictor of heart disease risk, despite the fact that it was not even a measured value.
(Measuring cholesterol in lipoproteins did not, however, measure the cholesterol in the liver used to synthesize bile acids for digestion, or the cholesterol in female ovaries to manufacture estrogen, or the cholesterol in male testicles to manufacture testosterone. That cholesterol had nothing to do with heart disease or any other disease, but was just part of normal metabolism.)
So it happened that the world focused on cholesterol. But the notion that cholesterol was just a dipstick, an indicator, was lost and instead cholesterol became the target itself: reduce cholesterol intake from the diet, reduce total cholesterol content of the blood, etc. But this focus on cholesterol ignored the fact that much cholesterol, such as that in the high-density lipoprotein fraction, HDL, was necessary for life and health. In other words, cholesterol was not necessarily a bad thing.
In the 21st century, tests to measure lipoproteins directly are widely available. No longer do we need cholesterol as a crude and indirect dipstick for lipoproteins, nor do we need to calculate the low-density lipoprotein cholesterol, a value prone to wild inaccuracy. We can assess lipoproteins by size, density, the types of proteins contained, we can even count their number. We know, for instance, that particles in the low-density lipoprotein fraction vary in size, configuration, ability to adhere to the artery wall, potential for triggering inflammatory responses, oxidizability, and glycation (modification by blood glucose). We know that particles in the very low-density fraction increase dramatically with consumption of carbohydrates and become bloated with triglycerides, a fundamental phenomenon that triggers changes in the composition of other lipoproteins, enriching them with triglycerides, as well. We know that the size of the HDL particle is one aspect that determines whether it effectively provides protective functions or whether it does not. None of this involves cholesterol.
So understanding how heart disease is caused is largely about understanding how lipoproteins work in the bloodstream. It is not about cholesterol. In fact, we now no longer even need to talk about cholesterol if we can talk about lipoproteins.
Even the common statin cholesterol drugs do not really reduce LDL cholesterol. They reduce the number of low-density lipoprotein particles-there's a difference.
Recognizing that lipoproteins that circulate in your blood are the issue, not cholesterol, helps you and your doctor understand how to better gain control over risk for heart disease. More on that to come . . .
Published On: August 12, 2010