The cholesterol conundrum

The tricky balance between “good” and “bad” lipids

Melissa Marino, Ph.D.
Published: October, 2007

Computer illustration of low-density (LDL, right) and high-density (HDL, left) lipoproteins
Hybrid medical animation / Photo Researchers, Inc.
Cholesterol—that sticky, waxy, fat-like substance that clogs our arteries—has gotten a bad rap that is only partially deserved.

It’s a crucial component of our cell membranes. It helps prevent the diffusion of small water-soluble molecules into the cell, and keeps membranes fluid enough to maintain their firm, but pliable, consistency.

A sterol molecule, cholesterol also is the precursor for steroid hormones like estrogen, testosterone and cortisol, which are important for reproduction, metabolism, immune function and stress responses.

What gives cholesterol either a “bad” or “good” reputation is the company it keeps—the lipoproteins that transport it through the body.

Lipoproteins are made by both the intestine and the liver and contain cholesterol, triglycerides and proteins. Triglycerides are the primary means by which the body transports and stores fatty acids, the basic unit of fat that our cells burn for energy.

High-density lipoprotein (HDL) is considered to be “good,” because it carts excess cholesterol off to the liver, where it is excreted in bile. Low-density lipoprotein (LDL), on the other hand, contributes to atherosclerosis.

LDL begins as a very low density lipoprotein (VLDL) produced in the liver. VLDL can be broken down in the bloodstream into fatty acids to provide an immediate source of fuel, and it also transports triglycerides to fat cells for later use.

In either case, after giving up its cargo of fat, VLDL becomes LDL, which then transports cholesterol to peripheral tissues. In some tissues like the skin, accumulation of cholesterol is inconsequential. The problem starts when cholesterol builds up along artery walls.

“For the same reason you don’t want too much calcium in your water, you don’t want too much LDL in your plasma—because your pipes will get encrusted,” says Sergio Fazio, M.D., Ph.D., who co-directs the Atherosclerosis Research Unit at Vanderbilt University Medical Center with MacRae F. Linton, M.D.

The artery wall doesn’t like the accumulation of cholesterol, and recruits cells from the blood, mainly macrophages, to try to clean it up. These macrophages become engorged with cholesterol, and are known as “foam cells” due to their bubbly appearance.

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