PreventandReverseHeartDisease

I chose that particular target threshold for a number of reasons. For one, there was the clarion example of those parts of the world where cardiovascular disease is nearly nonexistent: in those areas, cholesterol levels are consistently below 150 mg/dL.¹ Cornell University professor emeritus Colin Campbell, an expert in biochemistry and nutrition, was the director of a twenty-year project that involved Cornell, Oxford University, and the Chinese Academy of Preventive Medicine—one of the most comprehensive studies of nutrition ever.² Among other things, the project found that the normal range of cholesterol among residents of rural China, where coronary artery disease is rarely seen, falls between 90 and 150 mg/dL. (Comparing those levels with levels in the United Kingdom, where cholesterol levels are far closer to those in the United States, Sir Richard Peto, an Oxford epidemiologist who worked with Dr. Campbell, couldn’t resist commenting that when it comes to cholesterol, “There is no such thing as a normal Englishman.”)

But there was also a growing body of work by physicians and scientists at home that underscored the evidence from abroad. Perhaps the most important was the Framingham Heart Study, the fifty-year project—run by the National Heart, Lung and Blood Institute, Boston University, and other academic collaborators—that has collected and analyzed medical data from several generations of residents of Framingham, Massachusetts. Dr. William Castelli, former director of the study, put it quite baldly: over all those years, no one in Framingham who maintained a cholesterol level lower than 150 mg/dL has had a heart attack.³

Cholesterol is a white, waxy substance that is not found in plants—only in animals. It is an essential component of the membrane that coats all our cells, and it is the basic ingredient of sex hormones. Our bodies need cholesterol, and they manufacture it on their own. We do not need to eat it. But we do, when we consume meat, poultry, fish, and other animal-based foods, such as dairy products and eggs. In doing so, we take on excess amounts of the substance. What’s more, eating fat causes the body itself to manufacture excessive amounts of cholesterol, which explains why vegetarians who eat oil, butter, cheese, milk, ice cream, glazed doughnuts, and French pastry develop coronary disease despite their avoidance of meat.

Medicine subdivides cholesterol into two types. High-density lipoprotein, or HDL, is sometimes known as “good” cholesterol. Medical experts do not know precisely how, but it seems to offer some protection against heart attacks—by collecting excess cholesterol and carrying it away from the arteries to the liver, which can break it down and dispose of it. As total blood cholesterol rises, you need more and more of the HDL cholesterol to protect you against heart disease.

Low-density lipoprotein, or LDL, is “bad” cholesterol. When too much of it is present in the bloodstream, it tends to build up along artery walls, helping to form the plaques that narrow blood vessels and ultimately may clog them altogether.

The coronary arteries are the blood vessels that supply oxygen and nutrients to the muscle of the heart. They get their name from the Latin word for “crown” because they encircle the heart almost like a royal headpiece. They are relatively small, but exceedingly important: without the nourishment they bring to the incredibly efficient pump they serve, the heart becomes injured, begins to fail, and may die.

The innermost lining of all blood and lymph vessels and the heart is called the endothelium. Far more than a simple membrane, the endothelium is actually the body’s single largest endocrine organ. If all the endothelial cells in your body were laid out flat, one cell thick, they would cover an area equal to two tennis courts.

Healthy arteries are strong and elastic, their linings smooth and unobstructed, allowing a free flow of blood. But when the levels of fats in the bloodstream become elevated, everything begins to change. Gradually, the endothelium, the white blood cells, and the platelets, the blood cells that cause clotting, all become sticky. Eventually, a white blood cell adheres to and eventually penetrates the endothelium, where it attempts to ingest the rising numbers of LDL cholesterol molecules that are being oxidized from the fatty diet. That white blood cell sends out a call for help to other white blood cells. More and more of them converge on the site, becoming engorged with bad cholesterol and eventually forming a bubble of fatty pus—an atheroma, or “plaque,” the chief characteristic of atherosclerosis.

Old plaques contain scar tissue and calcium. As they enlarge, they severely narrow and sometimes block the arteries (see Figure 4). A significantly narrowed artery cannot give the heart muscle a normal blood supply, and the heart muscle, thus deprived, causes chest pain, or angina. In some cases, the coronary arteries actually perform their own bypasses, growing extra branches—called “collaterals”—that go around the narrowed vessels.

However, it is not the old, larger plaques that put you most at risk for heart attacks. The most recent scientific evidence indicates that most heart attacks occur when younger and smaller fatty plaques rupture their outer lining, or cap, and bleed into the coronary artery.

As the plaque is formed, a fibrous cap develops at its roof, which is covered by a single layer of endothelium about as thick as a cobweb. For a while, thus protected, plaques lie quietly in place, doing little perceptible harm to the artery’s owner. But an insidious process is nonetheless under way. The white blood cells that raced to the rescue, now engorged with oxidized LDL cholesterol, are called “foam cells,” and begin to manufacture chemical substances that erode the cap of the plaque. The cap weakens to the thickness of a cobweb. And eventually, the shearing force of blood flowing over the weakened cap may cause it to rupture.

This is catastrophic. Plaque content or pus now oozes into the flowing bloodstream, and that constitutes a thrombogenic event: nature wants to heal the rupture, and so platelets are activated. They try mightily to stop the invading garbage by clotting the rupture. Thus begins a lethal cascade. The clot is self-propagating, and within minutes, the entire artery may become blocked.

With no more blood flowing through the blocked artery, the heart muscle that was nourished by it begins to die. This is the definition of myocardial infarction, or heart attack. If the person survives this attack, the dead portion of heart muscle scars. Multiple heart attacks and widespread scarring weaken the heart, sometimes causing it to fail. That condition is known as congestive heart failure. If the heart attack is extensive, if it results in an abnormal rhythmical contraction, or if the congestive heart failure is prolonged, the person may die.

If the same process of plaque formation occurs in a noncoronary artery, it can be just as dangerous. Whatever tissue the artery supplies—it could be the leg muscles or even the brain—will not receive its full measure of blood. What’s more, a piece of a plaque or a clot can break loose and be carried through the bloodstream, ultimately obstructing an artery far from its source.

Traditional cardiology has approached this disease primarily by relying on mechanical interventions. In angioplasty, for instance, a physician inserts a hollow tube into an artery in a leg or arm and guides it, using X-ray images, into the clogged coronary artery that is his target. A smaller catheter, with a deflated balloon at its tip, is then fed through the first. When it reaches the clogged area, the balloon is inflated—usually several times—to press the plaque against the artery wall, fracturing the plaque and the arterial wall, widening the vessel, and stripping away the delicate endothelial lining.

In recent years, the use of stents has become more common. A stent is a wire mesh tube that is inserted during angioplasty. When the balloon is inflated, the stent expands and locks into place inside the artery, holding it open after the balloon and catheter are withdrawn.

Bypass surgery is exactly what its name implies. The physician uses a short length of blood vessel from another part of the body to provide a way for blood to go around blockages in coronary arteries, much as a detour functions to route traffic around the congestion caused by an accident or by highway construction.

But as I have already argued, these interventions are aimed at alleviating the symptoms of coronary artery disease, not at curing the disease itself. And their results erode with the passage of time. Patients have second and third bypasses. Arteries widened with angioplasty tend to clog once again. Stents may have to be reopened because scar tissue reblocks the artery. The newer drug-eluting stents (coated with drugs to lessen the body’s natural healing response to the injury caused by the stent’s insertion) may also suddenly block after a few years because a clot forms where the endothelium was injured; the drug in the stent that prevents inflammation also inhibits the endothelium’s capacity to heal.

We can go directly to the bottom line. This is it: if you follow a plant-based nutrition program to reduce your total cholesterol level to below 150 mg/dL and the LDL level to less than 80 mg/dL, you cannot deposit fat and cholesterol into your coronary arteries. Period.

And although some patients may need cholesterol-lowering drugs to help them achieve those safe, low cholesterol levels, drugs alone are not the answer. Nutrition is the real key to saving your life in the long term. Eating the right way not only will help reduce your cholesterol levels, but also can work additional wonders you may never have imagined.