The Great Cholesterol Myth (9 page)

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 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 cholesterol indiscriminately
might
theoretically decrease the risk of a “fire” in your artery walls, but at what cost? Those trees serve a lot of ecological purposes, and removing them is not without consequences, both to the environment and to the landscape.

Wouldn’t it be better to reduce the conditions under which a fire is likely to break out? That way we could have all the wonderful benefits of trees with none of the side effects of a compromised ecology.

We hope we’ve convinced you that inflammation is at the core of heart disease, and that it’s inflammation—and its main initiator, oxidation—we need to be concerned about, not cholesterol.

But oxidation is only one of the conditions—albeit a very important one—that causes inflammation.

Another cause of inflammation is so important we’re giving it its own chapter. It’s something you eat every day and something you already know is bad for you, but only because of its well-documented role in diabetes and obesity. What you’re about to learn is the connection between this common food and heart disease.

By the time you finish the next chapter, you’ll be convinced—as we are—that this food is a far, far greater danger to your overall health, and specifically to your heart, than fat ever was.

We’re talking about sugar.

CHAPTER 4

FOR THOSE OF YOU WHO LIKE TO CUT RIGHT TO THE CHASE,
here’s this chapter’s take-home point: Sugar is a far greater danger to your heart than fat ever was.

The full story of sugar, and of its often ignored influence on heart disease, requires that we venture into a topic we like to call Endocrinology 101. We understand this sounds like something an evil high school biology teacher designed for the express purpose of making your life miserable, but we promise not to make your eyes glaze over. In fact, by the time you finish this chapter, you will know more than many doctors do about the common link among heart disease, diabetes, obesity, and hypertension—conditions that are not exactly of casual interest to most readers.

Once you understand the link that joins all of these modern degenerative diseases and its connection to heart disease, we believe you’ll come to the same conclusion we have: Our health gurus have tried and convicted the wrong man, your honor. Fat was innocent all the time.

It’s
sugar
that’s the true culprit in the American diet.

Our journey starts with one simple premise: Hormones control almost every metabolic event that goes on in your body, and
you
control some of the most critical hormones through your lifestyle. Food—along with several key lifestyle factors such as stress—is the drug that stimulates hormones, and those hormones direct the body to store or burn fat, just as they direct the body to perform a gazillion other metabolic operations.

“Food may be the most powerful drug you will ever encounter because it causes dramatic changes in your hormones that are hundreds of times more powerful than any pharmaceutical,” said Barry Sears, Ph.D. Hormones are the air traffic controllers that determine the fate of whatever flies in (or in our case, “slides” in through the gullet!).

This fact has been conveniently ignored by many mainstream dietitians and doctors whose standard message to overweight people at increased risk for heart disease is to simply reduce calories and saturated fat. But all calories are not created equal. Some foods significantly boost levels of a hormone that
stores
fat, while other foods do not—even when the calories are the same. Not coincidentally, that fat-storing hormone also has some serious consequences for the heart.

The name of that fat-storing hormone? Insulin.

Insulin, a hormone first discovered in 1921, is the star actor in our little hormonal play. It is an anabolic hormone, which means it is responsible for building things up—putting compounds like glucose (sugar and amino acids) inside storage units (such as cells). Its sister hormone, glucagon, is responsible for breaking things down—opening those storage units and releasing their contents as needed. Insulin is responsible for
saving
; glucagon is responsible for
spending
. Together their main job is to maintain blood sugar levels within the tightly regulated range it needs to be to keep your metabolic machinery running smoothly.

Insulin is at the hub of a significant number of diseases of civilization. When you control insulin, you reduce the risk for not only heart disease but also hypertension, diabetes, polycystic ovary syndrome, inflammatory diseases, and even, possibly, cancer.

Both insulin and glucagon are essential to health. Without insulin, blood sugar would skyrocket, and the result would be coma and death, the fate of virtually every type 1 diabetic in the early part of the twentieth century prior to the discovery of insulin. However, without glucagon, blood sugar would plummet, and the result would be brain dysfunction, coma, and death.

So the body knows what it’s doing. This little dance between the force that keeps blood sugar from soaring too
high
(insulin) and the forces that prevent it from going too
low
(glucagon, for one) is essential for survival. It’s interesting to note that although insulin is the only hormone responsible for preventing blood sugar from rising too high, there are several other hormones besides glucagon—cortisol, adrenaline, noradrenaline, and human growth hormone—that prevent it from going too low. You could say that insulin is such a powerful hormone that it needs five other hormones just to counterbalance its effects!

To see how insulin is
supposed
to work in the body, let’s take a look at a metabolism that hasn’t been “screwed up” yet by years of bad diet and sedentary living. Let’s look at the metabolism of a mythical five-year-old child who’s been living on an organic ranch, eating nothing but whole foods, breathing clean air, and getting a vigorous amount of exercise on a daily basis. (We know, we know—we haven’t seen too many of these kids, either, but let’s just postulate one for the sake of our discussion.)

The kid comes home from school and eats an apple. His blood sugar goes up slightly, as it always does when you eat food. The pancreas responds to this slight elevation in blood sugar by secreting a little shot of insulin, and insulin promptly goes to work rounding up the excess sugar in the kid’s bloodstream and escorting it over to the muscle cells. Which is just dandy, because this boy is now going to go out and play, or ride a bike, or work on the ranch, or do some other physical activity for which those muscle cells of his require fuel.

So far, so good.

The muscle cells welcome the extra sugar, which they use for fuel, and eventually blood sugar drops back down to normal and even goes down a bit further because the muscles are eating it right up. Now the boy gets hungry again, comes home, and eats supper. All is right with the world.

However, this ideal metabolism is not
your
metabolism.

Your metabolism looks like this: You wake up late, stress hormones coursing through your body. (These stress hormones are an important factor in heart disease, and we’ll discuss them at greater length later.) One of the things stress hormones do is send a primitive signal to the brain that it’s time to fuel up for an emergency. So you run out the door and stop at Starbucks for a sweetened latte and a “low-fat” bran muffin that contains a gazillion calories. Your blood sugar takes off like the
Challenger
. The pancreas says, “Uh-oh, better send in the big guns this time, the guy’s gone mad, there’s sugar all over the place!” And it produces a bucketful of insulin to try to start bailing all that sugar out of your bloodstream and get it to the muscle cells pronto!

Except the muscle cells aren’t having it.

“What do we need all this sugar for?” they ask. “This guy’s just going to sit around all day pushing a computer mouse, and when he goes home, he’s going to sit on the couch and play with the clicker.”

So the muscle cells begin to
resist
the effects of insulin. “We’re good,” they say, “go somewhere else.” Insulin now has no choice but to take its sugar pay-load to another location, and guess where it winds up?

Your fat cells, which happily welcome it in.

At first.

For a while, your pancreas can manage to keep up with the added demand for more and more insulin, and your muscle cells may still absorb enough sugar to keep you from becoming officially diabetic. But those elevated levels of insulin produced by excess sugar (in the diet and in the bloodstream) are not without serious consequences, including ones that directly affect the heart.

For a stunning example of this phenomenon, all we need do is look at the effect of insulin on blood pressure.