The Great Cholesterol Myth (29 page)

When you’re under constant (chronic) stress, you secrete
more
hormones, such as epinephrine and the glucocorticoids, which prepare the body to fight or flee. At the same time, you make
less
of other hormones, such as growth hormone. Why? Because at this point, at least from the body’s point of view, these hormones are a big waste of time.

When your life is at stake, or your body
thinks
it is, your body does an instant evaluation (like a triage nurse) and decides what’s essential and what’s not. When you’re running for your life, it doesn’t make much sense to invest energy in reproductive or digestive functions, and it doesn’t make sense to increase circulation to the stomach or the ears. What
does
make sense is keeping you alive, so the body diverts blood from the gut and sends it to the legs (so you can run faster). It doesn’t bother with little extras, such as growth hormone or sex hormones, because if you’re not going to be around past dinnertime, what’s the point? Instead, it mobilizes all of its resources to combat the immediate life-threatening problem at hand.

This “triage” phenomenon was first noted around 1833 by a bunch of physician scientists treating a man with a gunshot wound.
³
When the docs were about to patch him up, they noticed, not surprisingly, that he had a significant amount of red and rosy blood flow beneath where his guts were exposed. Then, for some reason—who knows, maybe he didn’t like the doctors’ aftershave—the guy got pissed off and angry. His body treated his anger and pissed-off-ness as an emergency, and his stress response kicked in immediately. Suddenly that red and rosy blood they were seeing in his guts turned pink and pale. It was almost as if all that deep red blood had disappeared!

So what happened?

What the docs were witnessing was a vivid visual example of the triage phenomenon described earlier. Stress hormones divert blood flow from the areas that aren’t immediately necessary to your survival and send it to where it can do the most good in an emergency—the heart, lungs, and running muscles. That’s why the blood in the guts of the guy with the gunshot wound changed color.

So your body perceives a life-threatening emergency (and remember, your body makes no distinction between an “old-school” emergency, such as an attacking lion, and the modern version of the same thing, such as being stuck for hours on the freeway). But releasing stress hormones that divert blood from nonessential to essential areas is only the beginning. You also need to get
more
blood into your system, or at least make sure you don’t lose any of the blood you already have! (Remember, from an evolutionary and historical point of view, most life-threatening “emergencies” carried with them the distinct possibility of blood loss!)

Now what does your body do? It makes more of a certain type of red blood cell called a
platelet.
Platelets stick together and form clots, which, when you think about it, is a pretty spiffy protection against the possibility of bleeding out.

So stress hormones trigger the production of platelets, a good thing in the short run when your body is anticipating the possibility of a major bloodletting
wound, but not such a good thing in the long run. When stress hormones are constantly in the “on” position, you’re
overproducing
platelets. Inevitably, the platelets begin to stick together, and your blood thickens. They combine with other red and white blood cells, as well as with a compound called
fibrin,
to form a kind of “super clot” called a
thrombus
. When a thrombus blocks an artery that leads to the heart muscle, you have a heart attack.

Okay, so what else does your body have to do in a life-threatening emergency to ensure that you stay alive? Divert blood from nonessential areas to essential, check. Make sure you don’t lose any more blood than you absolutely have to by making more platelets so that you can clot more easily, check. But wait! What about
replacing
any blood that you might lose in battle? You’re going to need replacement blood, and where the heck is that going to come from?

Glad you asked.

Because there are no blood transfusions available in the African Serengeti, you’re going to have to make your own blood. The first thing you’ll need is water, which is found in the kidneys! The kidneys are sitting around, peacefully filtering water and getting ready to send it out into the universe in the form of urine, but now, with the new demand for water, your stress hormone–fueled body runs down to the kidneys and says, “Wait! Hold the presses! Don’t send that water out into the universe, because we’re gonna need it right here to make more blood!” And because the kidneys really don’t speak English, this message is sent to them via a hormone aptly named the
anti-diuretic hormone
, or ADH, which tells the body to reabsorb water from the kidneys and put it into circulation to increase blood volume.

Brilliant. And it all makes total sense from the point of view of survival.

But what happens when you do this chronically?

Let’s take a look.

See, if you increase the volume of your blood pressure for thirty seconds while you run from a lion, you are one smart dude, from an evolutionary point of view at least. But elevate it for weeks, and you have chronic hypertension. And this is exactly the state that many of us are in today—heart attacks waiting to happen. According to the World Health Organization (WHO), hypertension is one of the most important causes of premature death worldwide, and it’s certainly one of the most important risk factors for heart disease.
⁴
Let’s take a look at why.

When blood pressure increases, the heart starts pumping blood with more force, pushing the blood vessels outward in response to the sheer power of it. (Imagine a garden hose hooked up to a fully opened fire hydrant. The garden hose would look like it’s about to burst!)

In response to this distending, the blood vessels build up more muscle around them (more layers of rubber on the garden hose), which now makes the vessels more rigid. This in turn requires even
more
pressure to get the blood through them, which means—not
surprisingly—your blood pressure goes even higher.

If blood pressure is increased, the heart muscles pay the price. Because blood is being pumped out with more force, it slams back with more force as well. And the area that takes the brunt of this returning blood under high force is the left ventricle. The muscle there begins to enlarge—a condition known as
left ventricular hypertrophy
—and that sets the heart up for irregularities.

Now we’ll discuss how this can cause inflammation and trigger the whole chain of events that leads to heart disease, a chain of events in which cholesterol is the most minor of players.

Coming out of your heart is one huge blood vessel called the
ascending aorta
. After a certain distance, this vessel splits into two, a process called
bifurcation
. Each of these two vessels eventually splits into two
more
vessels, which keep bifurcating until you’re down to the little capillaries. Now when your blood pressure goes up, the bifurcation—the point where the vessel divides into two—is exactly the spot that gets the brunt of this bashing by the increased force, or blood pressure. Eventually you start to get what’s known in physics as
fluid turbulence
. (Think of a tube with fluid moving through it with more and more force; the fluid starts to resemble a miniature version of the water sloshing around a tunnel at a water park.) As the fluid—blood, in this case—slams into the weak spots with increasing force, you get little bits of scarring and tearing, which soon become inflamed. These spots of vessel damage attract more inflammatory cells (such as oxidized LDL cholesterol), which gets into the inflamed areas, sticking to them. Before you know it, you’ve got plaque.

You’ve also got damaged blood vessels. Healthy coronary blood vessels
vasodilate
(open) when you need more blood (e.g., when you’re running from a saber-toothed tiger). That makes sense—water flows more freely through a fire hose than through a garden hose, and blood flows more easily through a dilated (open) vessel than a constricted (closed) one. But when the coronary blood vessels are damaged, they no longer vasodilate. Just when you need them to open up the most, they actually
close up
, or constrict. Now the heart doesn’t get enough blood or oxygen, and you have something called
cardiac ischemia
(lack of oxygen to the heart). The heart muscle isn’t getting enough energy, and it hurts. The all-too-familiar name for this pain is
angina
.

And at the core of all this is inflammation.

“Twenty years ago, if you wanted to measure one thing to see how the cardiovascular system was doing, you’d measure your cholesterol,” Sapolsky said. “In recent years people have realized that cholesterol is important, but that
other
things are more important. If you have undamaged vessels there’s no place for cholesterol to stick to,” he explained. “If you don’t have inflammation, there’s no problem.”
⁵

A man wakes in the morning feeling unwell and complains of pain and distress in his chest and abdominal area. He is sweating profusely and gasping for air. His alarmed wife calls 911, but the man dies before the paramedics arrive.

Frequently, the first symptom of heart disease, at least the first symptom that gets
noticed,
is sudden death. (Sudden death tends to get people’s attention.) Unfortunately, there is no chastisement, no warning to mend our ways, no trade-off or time to bargain with fate. The heart, omnipotent organ that it is, demonstrates its power over us with one unforgiving defensive maneuver—it attacks us.

Clinical studies have found that from 40 to 50 percent of the time, the first recognized symptom of heart disease is a fatal heart attack, also known as sudden cardiac death (the number one killer of people between the ages of thirty-five and sixty). The big problem with cardiac disease is that it happens with little or no warning. It’s literally ominous in its silence. Ninety percent of individuals with heart disease are asymptomatic.

Many of us have heard stories about “voodoo death” (sudden death related to psychogenic stress), a concept researched in detail by the American physiologist Walter B. Cannon, who first introduced the word
homeostasis
and coined the term
fight or flight
. Cannon traveled around the world studying voodoo death in places such as Africa, the Pacific Islands, and Australia. According to Cannon, voodoo death defies the imagination of modern Western man. He cited a case in which a Maori woman died within a day after discovering that she had eaten a piece of fruit that came from a “tabooed” place.

Well, unless you believe that the fruit was cursed or had magical powers, there’s clearly another explanation, and it’s this: the person’s
belief
that the curse was inescapable. A common feature of such a belief, shared by many who believe in the supernatural, is a heightened emotional response. The stress hormones go crazy. The heart pumps blood like sailors bailing out a sinking ship—quickly and furiously. Blood pressure goes through the roof, causing vascular injury. The possessed woman, and other members of her family, believed that she was doomed to die. She had to deal with the sheer, unmitigated terror of the curse itself, compounded by the fact that she was physically and emotionallyisolated. She was all alone in a terrible struggle that eventually ended in death.

But how and why did she die?

Did the social isolation or despair cause a loss of hope and a willingness to die? Or was it the curse itself? Many voodoo deaths are commonly preceded by alienation, isolation, and lack of social support for the person enduring the experience. In the cases that he observed, Cannon concluded that the victims of voodoo death were overcome by terror at the exact moment that they found themselves without the safety net of a supportive environment. The combo was lethal. The victims accepted their deaths as a way to escape an intolerable, miserable situation.

But with all that, there’s still no perfect explanation for the physical mechanism of death. What went wrong? Did these people’s cholesterol levels suddenly jump?

Here’s what Cannon concluded: The overwhelming stimulation of the sympathetic nervous system provokes lethal electrical instability in the heart. In modern
terms, doctors would describe this whole “sudden death syndrome” as the result of
malignant arrhythmia culminating in ventricular fibrillation
, or
acute coronary spasms and myocardial infarction
—in other words, a heart attack.

What’s important here is not the exact
way
that the heart fails, but the fact that its breakdown—whatever the specifics—are
precipitated
by a profound loss of hope. Interestingly, Cannon observed that this profound loss of hope was so deep that all attempts to revive these individuals were fruitless.

Once again, we see that psychological belief can determine physical destiny, or at least have a profound influence on it.

Experimental research has demonstrated the impact of acute psychological stress on sudden cardiac death. In one study, 91 percent of patients who experienced sudden cardiac death but were then successfully resuscitated reported that they were experiencing acute psychological stress at the time of their “sudden death” experience. A typical scenario: A middle manager is winding down after a busy week. The economy is in recession. The guy has to cut costs. His overhead is ridiculously high. There’s a real potential of losing his job, and with the loss of his job would come a loss of self-esteem. He is not involved in a loving relationship and is isolated and depressed. He’s exercising at his local gym when he hears unexpected and disturbing news. He drops dead suddenly from a massive coronary.