Free The Great Cholesterol Myth by Jonny Bowden Page B

and other molecular junk that have caused the problem in the first place. (The word
macrophage
literally means “big eater.”)
    The macrophages are like sugar addicts at a pie-eating contest. They have no off button; they’ll keep eating, consuming oxidized LDL until they literally choke to death, leaving something called the
lipid core
of plaque. Once they reach a certain size they start to look like foam and actually become what pathologists call “foam cells,” living cells that will continue the work of the macrophages, fighting and consuming until the “invader” is gone.
    But it isn’t an invader that sets them off. It’s just plain old LDL experiencing chemical changes from sugar, starches, or oxidation and thus initiating an inflammatory process that can easily become an out-of-control “fire” within your arterial walls. As we’ve said, without inflammation, it’s pretty irrelevant what your cholesterol levels are.
    If inflammation isn’t halted and if macrophages continue to feast away until they bust, they’ll release a whole new set of toxins into the walls of the artery.
    “We can see this in surgery as a yellow streak inside the artery wall,” said Lundell, who has performed more than five thousand heart surgeries. “It is called the ‘fatty streak,’ and it is the beginning of significant heart disease.” 5
    The body tries to contain this fatty streak by building a wall to hold it in—scarring is an example. But the immune system is now on full alert; it sends more soldiers to the front, and they try valiantly to break down the wall (the scar tissue), and the cycle continues—more scarring, more soldiers. Over time, if the body’s immune system defenses are good enough, they will weaken the wall of the artery and literally “chew through” the scar tissue. A rupture will occur, resulting in more inflammation, and the potentially deadly cycle continues.
    Not good news.
    If the cycle is not stopped, the fatty streak grows into what’s known as plaque. (Plaque is basically a big old collection of foam cells.) Some foam cells will die, and they will release a whole bunch of the accumulated fats (lipids), which in turn develop into the aforementioned lipid core, a soft, yellowy substance that resembles melted butter (but isn’t nearly as good for you).
    Now if you stop the inflammation at this point in time, the artery heals itself with what’s called a
fibrous cap
. The fibrous cap is composed of fibrous scar tissue and will stay nice and stable. (Cardiologists like Steve call this “stable plaque.”) Of course, if there’s new inflammation, the cycle begins all over again.
    So the more inflammation continues, the more foam cells accumulate. This means more macrophages (Ms. Pac-Man), which in turn means more oozy, slimy
lipid core
. This lipid core gets into the bloodstream, where the blood immediately puts out a signal saying, “What the heck is this? Foreign object! Foreign object!” And a blood clot is formed in an attempt to keep this foreign, gooey substance from spreading.
    So the blood clot is actually a protective mechanism. It’s the blood’s—or the body’s, if you prefer—way of saying, “Let’s contain this threat and keep it from spreading!” But though this strategy makes sense, it has a big downside. That blood clot may block access to the heart muscle, preventing oxygen from getting through. Anytime you deprive cells of oxygen, the tissue they make begins to die.
    And when that tissue is the muscle of the heart, you’re looking at—you guessed it—a heart attack.
    So overall, LDL can be likened to trees in a forest. A forest that has tons of trees but gets plenty of rain isn’t likely to be the site of a wildfire, but a forest with far fewer trees can be a tinder box just waiting to ignite if all those trees are dried up (damaged) and there’s very little rainfall! Getting rid of the trees is surely
one
crude way to prevent forest fires, just as lowering