Cholesterol and Vascular Disease: Part One – The History of Cholesterol

For over twenty years I have practiced and taught Cardiology. Starting in the invasive and hospital-based world (performing angioplasties, stents, atherctomies, lasers, and electrophysiologic procedures) and then segueing into prevention, cholesterol abnormalities, and cutting-edge non-invasive imaging of the carotid and coronary arteries, I have had the unique and great fortune to participate in exceptionally diverse aspects of cardiovascular health and illness. I have learned a great deal along the way and some of these experiences have been shared in articles and books I’ve written. Now I’d like to clarify one of the murkiest issues I’ve encountered in all my years of practice – the cholesterol conundrum. This post is the first of a series that will hopefully clarify the cholesterol debates that currently perplex numerous patients and physicians.

In the early 1900s a young medical student named Anitschkow made the initial association between cholesterol and vascular disease. He fed unsuspecting rabbits a high cholesterol diet. After they had enjoyed a number of tasty meals he sacrificed them in order to examine their aortas (the very large blood vessel that runs from our heart to our legs). What he found was revolutionary. The rabbits that consumed their normal low fat diets were just fine, but the cholesterol-fed rabbits had all developed severe plaques in their aortas. Of course none of the rabbits was lucky (they were all killed) but had they been allowed to live, the ones with normal diets would have done great, while those who had consumed large quantities of cholesterol would have suffered from heart attacks, strokes and premature death. Years went on and more and more scientists studied cholesterol and its effect on our bodies. In the 1940s, a technique called analytic ultracentrifugation was developed to study the fat within our blood. Scientists learned a great deal from this technology but one discovery stands out most for me. They learned that cholesterol does not float freely in our blood. It circulates instead securely contained within a variety of tiny particles called lipoproteins. These particles are used to shuttle cholesterol from one part of our body to another. Their job is to prohibit cholesterol from being exposed to contents in our blood stream – by protecting the cholesterol these particles prevent its crystallization, a phenomenon that if it occurred, would have devastating consequences.

The major lipoproteins – remember, these are the carriers of cholesterol – are called LDL, HDL, VLDL and Chylomicrons. Our livers make VLDL particles while our intestines make chylomicrons. LDL is the most atherogenic particle (causing plaque build-up), while HDL is an athero-protective particle (decreases plaque). The scientists and physicians of that time understood this and therefore wanted to establish a way to test patients and ultimately treat them for cholesterol disorders. They knew that counting the number of LDL lipoprotein particles would have been optimal, but the ultracentrifugation machines were too large and costly to place throughout the nation. They made a couple of assumptions and concluded that testing for the amount of cholesterol contained within all of our LDL particles could serve as an accurate surrogate marker for the number of LDL particles (LDL-P). They believed LDL-C (the amount of cholesterol within our LDL particles) would track beautifully with LDL-P. And so, LDL-C was dubbed the gold standard for cholesterol measurement and therapeutic interventions. Unfortunately the assumptions they made to dub LDL-C the gold standard by default were dead wrong.

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