The Great Cholesterol Myth (7 page)

Mann also declared that NIH managers “used Madison Avenue hype to sell this failed trial in the way that media people sell an underarm deodorant!”
¹⁸

Michael Oliver, a highly respected British cardiologist, concurred. “The panel of jurists . . . was selected to include experts who would, predictably, say that . . . all levels of blood cholesterol in the United States are too high and should be lowered. Of course, this is exactly what was said.”
¹⁹

But the dissenting voices met with radio silence. With pompous certainty, the committee made clear in its final report that low-fat diets would afford significant protection against coronary heart disease for men, women, and children over two years old. “The evidence justifies . . . the reduction of calories from fat . . . to 30 percent, calories from saturated fat to 10 percent or less, and dietary cholesterol to no more than 250 to 300 mg daily,” it declared.
²⁰

As Dr. Phil might ask, “And how’s that workin’ for you?”

One study that attempted to answer this hypothetical question was the Women’s Health Initiative, the same program that has suggested that hormone therapy after menopause has more risks than benefits. This $415-million NIH study involved close to 49,000 people, aged fifty to seventy-nine, who were followed for eight years in an attempt to answer the question, “Does a low-fat diet reduce the risk of getting heart disease or cancer?”
²¹

They got their answer.

“The largest study ever to ask whether a low-fat diet reduces the risk of getting cancer or heart disease has found that the diet has no effect,” the
New York Times
reported in 2006.
²²

“These studies are revolutionary,” said Jules Hirsch, M.D., physician-in-chief emeritus at the Rockefeller University in New York City and an expert on how diets influence weight and health. The studies “should put a stop to this era of thinking that we have all the information we need to change the whole national diet and make everybody healthy.”
²³

Of course, none of these questionable findings stopped the cholesterol-lowering, fat-avoiding juggernaut that went into full swing in the late 1970s and continues, albeit bruised and battered, to this day. And we have to give the misguided researchers kudos for their motives—by reducing cholesterol levels, they sincerely believed they would be reducing heart disease. As Dwight Lundell, M.D., author of
The Cure for Heart Disease
, wryly put it, “They were taking the bull by the horn—but it was the wrong bull.”
²⁴

When we first met about this project, Steve brought to the meeting a series of papers by one of the most respected researchers in the world, Michel de Lorgeril, M.D., a French cardiologist and researcher at the prestigious National Centre for Scientific Research, the largest public organization for scientific research in France.

De Lorgeril has authored dozens of papers in peer-reviewed journals, and he was the lead researcher for the Lyon Diet Heart Study. The following quotation comes from his only book written in English, and it’s a perfect way to end this chapter:

“We can summarize . . . in one sentence:
Cholesterol is harmless
[italics ours]
!
”
²⁵

CHAPTER 3

SO IF CHOLESTEROL
ISN’T
THE CAUSE OF HEART DISEASE,
what is?

We know you don’t want to wait any longer, so here’s the short answer: The primary cause of heart disease is
inflammation
.

The subject of inflammation will be a running theme throughout this book for reasons that will soon be made clear, but the first thing you need to know about inflammation is this: It comes in two flavors. You’re probably already familiar with one of them, but it’s the one you’re
less
familiar with that’s at the core of heart disease.

Let us explain.

Almost all of us have experience with
acute
inflammation. It happens every time you stub your toe, bang your knee, or get a splinter in your finger. When you complain about your aching back, an abscess in your mouth, or a rash on your skin, that’s acute inflammation. It’s visible and uncomfortable, if not downright painful. The redness on your skin is a result of blood that’s rushed to the affected area. The swelling you experience is the result of an army of specialized cells (with names like
phagocytes
and
lymphocytes)
dispatched by the immune system to mend the injured area. (The job of these immune system cells is to surround the site of the injury and
neutralize nasty invaders such as microbes, preventing the spread of potential infection.) The swelling, redness, and soreness you experience as a result of acute inflammation are all natural accompaniments to the healing process.

So we all know about acute inflammation, most of us from personal experience. But the
other
flavor of inflammation,
chronic
inflammation, well, that’s a whole different ball game.

Acute inflammation hurts, but chronic inflammation kills.

Chronic inflammation flies beneath the pain radar. Much like high blood pressure, it has no obvious symptoms. Yet chronic inflammation is a significant component of virtually every single degenerative condition, including Alzheimer’s, diabetes, obesity, arthritis, cancer, neurodegenerative diseases, chronic lower respiratory disease, influenza and pneumonia, chronic liver and kidney diseases, and, most especially, heart disease.

When chronic inflammation exists unchecked in the cardiovascular system, it usually spells big trouble for the heart.

And inflammation is rarely a local phenomenon. For instance, women with rheumatoid arthritis, a highly inflammatory condition that primarily affects the joints, wind up having double the risk of a heart attack when compared to women without it. Microbes that cause problems in one part of the body can easily migrate to other areas and cause inflammatory damage there. An infection that starts in the gums, for example, can easily leak bacteria into the bloodstream, bacteria that may then find fertile ground in a weakened arterial wall and fan the fires of inflammation there.

So how exactly does inflammation happen, and, more importantly, what can we do about it?

In
The Most Effective Ways to Live Longer
, Dr. Jonny introduced the concept of the “Four Horsemen of Aging.” These Four Horsemen all contribute mightily to heart disease, and we’ll go over all of them in the pages that follow. For those of you who just have to know
right now
what they are, here’s the list: oxidation, inflammation, sugar, and stress. In this chapter, we’ll concentrate on the first two.

One of the prime initiators of inflammation is
oxidation
. If you’ve ever seen rust on metal, you’re familiar with oxidation (also known as
oxidative damage
), even if you didn’t know the technical name for it. You’re also familiar with oxidation if you’ve ever left apple slices out on a picnic table where they were exposed to the air. They turned brown, didn’t they?
That’s
oxidative damage.

For those of you who don’t remember high school chemistry (or would understandably prefer to forget it), electrons travel in pairs and orbit around atoms. Every so often one of those electrons gets “loose,” and pandemonium ensues. The unpaired electron—known as a
free radical
—starts running around like a headless chicken trying to find its head. Free radicals are like college sophomores on spring break—temporarily free from the constraints of dormitory living, they basically go nuts and will “mate” with anyone! Free radicals “hit” on existing, stable pairs of electrons thousands of times a day, trying to find an electron they can pair-bond with and meanwhile, inflicting enormous damage upon your cells and DNA.

The free radicals that come from oxygen (known, not surprisingly, as
oxygen free radicals)
are the most deadly and damaging. (Now you know what the term “
anti
oxidants” means—it’s a class of substances, including certain vitamins, minerals, and many plant chemicals, that helps neutralize free radicals, soaking them up like little sponges, thus limiting the damage they can do to your body. The reason cut apple slices don’t turn brown so quickly when you squirt lemon juice on them is because lemon juice contains a fair amount of vitamin C, a powerful antioxidant.)

Free radicals are so important that in the mid-1950s a scientist named Denham Harman, M.D., Ph.D., put forth a theory called the Free Radical Theory of
Aging that remains popular to this day.
²
In it he basically proposes that aging is a kind of “rusting from within,” largely due to the damage caused by oxygen free radicals.

Okay, hold that thought. We’re going to come back to it. But before we go any further, let’s look at the arteries, or more specifically the arterial walls, because that’s where the damage starts.

The arterial walls are anything but hard and firm. They’re composed of smooth muscle that expands and contracts like a mini accordion; they respond to the rhythm of the heart and accommodate the pulsing of the blood. These arteries—far from being a static system of tubes and pipes—are a living, breathing,
very
dynamic organ. And the innermost layer of the artery walls—the “interface,” if you will, between the blood inside the arteries and the walls that contain it—is a central player in our little drama. This layer is called the
endothelium
—and it’s the starting point for the damage that can ultimately lead to a heart attack.

Big word, endothelium, yes, not often bandied about in cocktail party chatter about heart disease, but it’s one of the most important places in the arteries for
you to know about because
that’s
where the damage to your arteries starts. The endothelium is only one cell thick, but it’s where a tremendous amount of biochemical activity takes place. There’s even a name for the pathological state in which damage to that innermost layer exists—it’s called
endothelial dysfunction
, and it’s a key event in the development of heart disease.

Okay, we’ve introduced two important concepts here—oxidative damage and inflammation—and one important structure—the endothelium. Now we need to take a look at what cholesterol is and see how it fits into the whole picture. Once we do, we will return to the interaction among oxidation, inflammation, and the arterial walls.