Free The Great Cholesterol Myth by Jonny Bowden Page A

your heart.

WHEN LDL
REALLY
IS BAD FOR YOU: THE SMOKER’S PARADOX
    Here’s a riddle for you: Why is it that smokers with
normal
LDL (the so-called “bad” cholesterol) levels have a much higher risk of heart disease than non-smokers with elevated LDL levels?
    Sure, we all know how cigarette smoke damages the lungs, and that cigarette smoking significantly increases the odds of getting lung cancer. But, really, what’s the connection between smoking and heart disease, or, more specifically, between smoking and LDL cholesterol?
    Glad you asked.
    Besides the harsh smoke, cigarettes also graciously provide your body with myriad toxic chemicals, all at no extra charge, thank you very much. These chemicals and toxins both constrict the blood vessels and harm the arterial walls. Specifically, they cause your LDL to become oxidized—damaged by the free radicals that are found in abundance in cigarette smoke! (And, by the way, it’s not just cigarette smoke that can oxidize LDL. Heavy metals like mercury can do it, as can insecticides, radiation, and all manner of toxins in the environment, the air, and the food supply.)
    And listen carefully now: LDL is
never
a problem in the body
until
it becomes oxidized. Only oxidized LDL sticks to the arterial walls, contributing to plaque and causing further inflammation and injury. Non-oxidized LDL is pretty much harmless. It’s oxidation that actually initiates the process that culminates in atherosclerosis.
    So a smoker with a low amount of LDL,
most
of which has been damaged by oxidation, is at far greater risk for heart disease than a nonsmoker with a much
higher
level of LDL, only a tiny percentage of which has been damaged. It’s not the LDL that causes the problem—it’s
damaged
(oxidized) LDL.
    So LDL floats around in the bloodstream, delivering cholesterol to the cells that need it, and
some
of this LDL, the LDL that’s damaged by oxidation, infiltrates the endothelium. Once the endothelium becomes infiltrated with this damaged LDL, the process of inflammation begins in earnest.
    Remember our earlier discussion about harmless “bad” cholesterol (LDL pattern A) and dangerous “bad” cholesterol (LDL pattern B)? Well, one of the reasons why pattern B molecules (those BB gun–pellet types) are so bad is that they are the ones most likely to be damaged and most likely to be oxidized. On top of that, they’re small enough to penetrate the arterial walls in the first place. The smaller the particles (and pattern B particles are small indeed), the more inflammatory they are. Oxidized LDL is like “angry” LDL, and the smaller the particle, the angrier it is. So these nasty little damaged LDL particles stick to the endothelium and begin the process of inflammation. In the presence of oxidative damage—or in the presence of high blood sugar, which is such an important initiator of damage that we’ll examine it separately in chapter 4 —this LDL experiences chemical changes that the immune system perceives as dangerous.
    Once the immune system notices this damaged (oxidized) LDL, it sends in the heavy artillery. First,cells known as
monocytes
rush to the scene of the action, releasing chemicals called
cytokines
. Cytokines are essentially chemical messengers that help regulate the immune system response, but many of these cytokines are themselves highly inflammatory. In the presence of some of these cytokines, the lining of the blood vessels (the endothelium) secrete sticky little molecules called
adhesion molecules
that act like molecular glue, grabbing on to the monocytes that have rushed to the scene of the crime to help put out the fire. Heart surgeon Dwight Lundell, M.D., cleverly refers to this as the “Velcro effect.”
    Monocytes now convert into a type of cell we like to call “Little Ms. Pac-Man.” They’re technically called
macrophages
, and their job, much like Ms. Pac-Man in the video game, is to eat up the enemy, in this case the damaged LDL particles