The Great Cholesterol Myth (8 page)

Contrary to cholesterol’s negative reputation, your body simply can’t function without it. It’s found in every single cell and is so essential that the lion’s share of the cholesterol in your body is actually
made
by your body, specifically by the liver, which produces this fatty, waxy substance precisely
because
it is so essential to the health of your cells.

The cholesterol you eat has a minimal effect on your blood levels of cholesterol, which is why the admonition to eat less of it and the prominent listing of cholesterol on food nutrition labels are not as significant as we are led to believe they are. If you eat
less
cholesterol,
your liver will simply take up the slack and make more. If you eat
more
of it, the liver makes l
ess
. It is primarily, overwhelmingly made in the liver, though small amounts are made in other locations. For all intents and purposes, “manufacturing central” is the liver, and this is what responds to the “eat more/make less, eat less/make more” seesaw. The Framingham Heart Study found that there was virtually
no difference
in the amount of cholesterol consumed on a daily basis by those who went on to develop cardiovascular disease and those who did not. Egg-white omelet eaters, take note!

Cholesterol’s ability to fight toxins may be one reason why it’s found at the site of arterial injuries caused by inflammation. But blaming cholesterol for those injuries is a little like blaming firemen for fire.

As we said earlier, cholesterol is the basic raw material that your body makes into vitamin D; sex hormones such as estrogen, progesterone, and testosterone; and the bile acids needed for digestion. The emphasis on lowering cholesterol as much as possible is not only misguided but also dangerous. Studies show that those at the lowest end of the cholesterol spectrum have a
significantly
increased risk of death from myriad conditions and situations unrelated to heart disease, including, but not limited to, cancer, suicide, and accidents.

Accidents and suicides? Really? Yes. Here’s the connection: You need cholesterol to make brain cells. A cholesterol level too low (around 160 mg/dL) has, in fact, been linked to depression, aggression, and cerebral hemorrhages. (The connection to sex drive will be discussed later in
chapter 6
—it’s a doosey!)

The membranes of your cells contain a ton of cholesterol because it helps maintain their integrity and also facilitates cellular communication. The consistency of the cell membrane has to be just right—hard enough to act as a barrier to all sorts of molecular riff-raff but pliable and soft enough to allow access to the molecules that need to get inside. Essentially, you
need
cholesterol for memory. Lower cholesterol too much and it can easily promote a kind of global amnesia; with too little cholesterol in the cell membranes, nerve transmission can be affected. It’s no surprise to us that Duane Graveline, M.D.—a former flight surgeon and astronaut who received international recognition for his research on zero gravity deconditioning—gave his book about the memory loss he experienced after taking statin drugs the ominous title
Lipitor: Thief of Memory
.

Cholesterol is also one of the important weapons your body uses to fight infections. It helps neutralize toxins produced by bacteria that swarm into the
bloodstream from the gut when the immune system is weakened. When you have an infection, the total blood level of cholesterol goes up, but HDL (which we’ll define in a moment) falls because it’s being used up in the fight. Cholesterol’s ability to fight toxins may be one reason why it’s found at the site of arterial injuries caused by inflammation. But blaming cholesterol for those injuries is a little like blaming firemen for the fire.

Now here’s an interesting fact of which you might not have been aware: It’s actually impossible to measure cholesterol directly in the bloodstream. Being a fatty substance, cholesterol is not soluble in water or blood. So how does it get in the bloodstream? Simple. Your liver coats it with a “protein wrapper” and bundles it with a few other substances (such as triglycerides); packaging it in this protective shell allows it to enter your circulatory system, much like stones would float in the ocean if they were contained in a buoyant, waterproof container. In our case, the protein wrapper acts like a passport, allowing cholesterol to travel throughout your bloodstream. It’s these packages, known as
lipoproteins
, that we actually measure when we measure our cholesterol levels.

We know these cholesterol–protein combinations as HDL (
high-density lipoprotein
) and LDL (
low-density lipoprotein
). Both contain cholesterol and triglycerides, but the percentages are different, and the two types of lipoproteins have different functions in the body. LDL, known as “bad” cholesterol, carries cholesterol to the cells that need it, while HDL, known as “good” cholesterol, picks up the excess and carries it back to the liver.

But this old idea of “good” and “bad” cholesterol is a wholly outdated concept.

We now know that there are many different “subtypes” of both HDL and LDL, and they do very different things. LDL, the imprecisely named “bad” cholesterol, has several different subtypes, and not all of them are bad at all—quite the contrary.

The most important subtypes of LDL are subtype A and subtype B. When most of your LDL is of the “A” type, you’re said to have a
pattern A
cholesterol profile. When most of your LDL is of the “B” type, you’re said to have a
pattern B
cholesterol profile. Simple, right? And absolutely essential to know for reasons soon to be made clear.

Subtype A is a big, fluffy molecule that looks like a cotton ball and does just about as much damage, which is to say none. Subtype B, however, is small, hard, and dense, like a BB gun pellet. It’s the real bad actor in the system, because it’s the one that becomes oxidized, sticks to the arterial walls, and starts the cascade of damage. Subtype B particles (what we might call the “bad” bad cholesterol) are atherogenic, meaning that they contribute significantly to heart disease. As we’ve already noted, big, fluffy LDL particles (the “good” bad cholesterol) are pretty much benign. Knowing you have a “high” LDL level is pretty much a useless piece of information
unless
you know how
much
of that LDL is the small, dense kind (harmful) and how much is the big, fluffy kind (not harmful in the least). Both of us would be totally comfortable having a high LDL number if the bulk of it was composed of the big, harmless, cotton ball–type molecules (the pattern A distribution).
That’s much more preferable than having a
lower
LDL number mostly composed of the BB gun pellet–type molecules (the pattern B distribution).

Unfortunately, most doctors are behind the times on this one. They look at that total LDL number—not the size and type—and if that number is even slightly higher than the lab says it should be, out comes the prescription pad. Pharmaceutical companies love when advisory committees—which are often heavily stacked with doctors who have financial ties to the pharmaceutical companies—recommend that we maintain lower and lower LDL levels, because that means a bigger and bigger market for cholesterol-lowering drugs. Sadly, most doctors do not perform the easily available tests—often covered by insurance—that determine your LDL.

You may recall from the first chapter that present-day health recommendations to reduce cholesterol by any means possible started with the Framingham Heart Study. In 1948, when the study began, cholesterol was only measured as “total” cholesterol. If you knew what your cholesterol was, you knew one specific number (200 mg/dL or 220 mg/dL, for example). As recently as 1961 we didn’t have the technology to distinguish between “good” and “bad” cholesterol (HDL and LDL), much less the newer technology that allows us to zero in on different subtypes of the so-called “bad” cholesterol, which, as you can see, is far from being all “bad” after all.

Even HDL, the so-called “good” cholesterol, isn’t
all
good. A study published in the December 2008 issue of the
FASEB Journal,
produced by the Federation of American Societies for Experimental Biology, challenged the conventional wisdom that simply having high levels of good cholesterol (HDL) and low levels of bad cholesterol (LDL) is necessary for good health. The researchers showed that even
good
cholesterol has varying degrees of quality and that
some
HDL cholesterol is actually bad news.

“For many years, HDL has been viewed as good cholesterol and has generated a false perception that the more HDL in the blood, the better,” said the lead researcher, Angelo Scanu, M.D., of the University of Chicago.
³
“It is now apparent that subjects with high HDL levels are not necessarily protected from heart
problems and should ask their doctors to find out whether their HDL is good or bad.” Scanu’s study found that the HDL of people with chronic diseases such as rheumatoid arthritis and diabetes is very different than the HDL of healthy individuals, even when their blood levels of HDL are similar. Normal, “good” HDL cholesterol reduces inflammation; dysfunctional, “bad” HDL does not.

Knowing you have a “high” LDL level is pretty much a useless piece of information unless you know
how much
of that LDL is the small, dense kind (harmful) and how much is the big, fluffy kind (not harmful in the least).

“This is yet one more line of research that explains why some people can have perfect cholesterol levels, but still develop cardiovascular disease,” said Gerald Weissmann, M.D., editor-in-chief of the
FASEB Journal
. “Just as the discovery of good and bad cholesterol rewrote the book on cholesterol management, the realization that some of the ‘good cholesterol’ is actually
bad
will do the same.”
⁴

The point is that there is, indeed, “bad” cholesterol—even “
ultra
-bad” cholesterol—but simply using a shotgun pharmaceutical approach to lowering all cholesterol doesn’t accomplish anything and has significant unwanted side effects, as we will see in
chapter 6
.

Now that the four main characters in our drama have been introduced—oxidation, inflammation, cholesterol, and the arterial walls—let’s see how they interact in real life, and how they work together to create a dangerous situation for your heart.

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.