The Great Cholesterol Myth (32 page)

We’re going to advise you about which tests you should ask your doctor for and why. We’ll recommend which foods you should incorporate into your diet, if you haven’t already.

And we’re also going to discuss the emotional and psychological risk factors for heart disease, which need to be taken just as seriously as the physical ones. We’ll give you specific tools to help lower these risk factors.

We hope by now you’re convinced that total cholesterol is a meaningless number and should be the basis for absolutely nothing in your treatment plan. The old division into “good” (HDL) cholesterol and “bad” (LDL) cholesterol is out of date and provides only marginally better information than a “total” cholesterol reading. As we’ve said, both good and bad cholesterol have a number of different components (or subtypes) that behave quite differently, and the twenty-first-century version of a cholesterol test should always tell you exactly which subtypes you have. Anything less is not particularly useful and should never be the sole basis on which a treatment plan or a statin drug is recommended. That’s why the LDL particle size test is the first test we recommend.

Although LDL cholesterol is known as the “bad” cholesterol, the fact is that it comes in several shapes and sizes, as does HDL cholesterol, the so-called “good” kind. These different subtypes of cholesterol behave very differently. Seen under a microscope, some LDL particles are big, fluffy, and harmless. Some are small, dense, “angry,” and much more likely to become oxidized, slipping through the cells that line the walls of the arteries (the endothelium) and beginning the inflammatory cascade that leads to heart disease.

Tests are now available that measure LDL particle size, and that’s the information you really want to have. If you have a pattern A cholesterol profile, most of your LDL cholesterol is the big, fluffy kind, which is great; but if you have a pattern B profile, most of your LDL cholesterol is composed of the small, dense, atherogenic particles that cause inflammation and ultimately plaque. (Fortunately, you can change the distribution from small to buoyant by following the dietary and supplement recommendations in this book.)

One widely used test is called the
NMR LipoProfile
, and it analyzes the size of LDL particles by measuring their magnetic properties. Others—including the
Lipoprint
and the
Berkeley
(from the Berkeley HeartLab) use electrical fields to distinguish the size of the particles. Another test known as the
VAP
(Vertical Auto Profile) separates lipoprotein particles using a high-speed centrifuge.
¹
And still another is the
LPP
(or Lipoprotein Particle Profile). Any of these newer cholesterol tests can be offered by your doctor.

Taking a statin drug, or any other medication, based solely on the standard cholesterol test is a really bad idea. Ask your doctor for one of the newer particle tests. If he objects, make sure he has a darn good reason. It’s the only cholesterol test that matters.

CRP is a marker for inflammation that is directly associated with overall heart and cardiovascular health. In multiple studies, CRP has been identified as a potent predictor of future cardiovascular health—and, in our opinion, one that is far more reliable than elevated cholesterol levels. Biological characteristics that are associated with high CRP levels include
infections, high blood sugar, excess weight, and hypercoagulability of blood (sticky blood).

Fortunately, there is a simple test that your doctor can conduct to find out how much CRP is in your blood. Just make sure the high-sensitivity test
(hs-CRP)
is used. This test doesn’t take much time: Typically, blood is drawn from a vein located either on your forearm or on the inside of your elbow. The blood is then analyzed in several tests to determine the level of CRP present. (Dr. Sinatra’s recommendation for an optimal CRP level is less than 0.8 mg/dL.)

Fibrinogen is a protein that determines the stickiness of your blood by enabling your platelets to stick together. You need adequate fibrinogen levels to stop bleeding when you’ve been injured, but you also want to balance your fibrinogen levels to support optimal blood circulation and prevent unnecessary clotting. (In women younger than forty-five, Dr. Sinatra has seen far more heart attacks caused by improper blood clotting than by anything else.) Normal levels are between 200 and 400 mg/dL, and they may be elevated during any kind of inflammation.

Fibrinogen has been identified as an independent risk factor for cardiovascular disease and is associated with the traditional risk factors as well. In one study, fibrinogen levels were significantly higher among subjects with cardiovascular disease than among those without it.
²

There are two ways to test for fibrinogen. The first is the
Clauss method
and the second is a newer test called the
FiF
(immunoprecipitation functional intact fibrinogen) test, which was developed by American Biogenetic Sciences.
³
The FiF test is the better one because it shows a stronger association with cardiovascular disease than the Clauss method does.
⁴
If the FiF test isn’t available, use the Clauss method—it still has a strong association with cardiovascular disease, even if it’s not quite as accurate as the newer test.

If you have a family history of heart concerns, you must check your serum fibrinogen level. Women who smoke, take oral contraceptives, or are postmenopausal usually have higher fibrinogen levels.

Worth noting: This test hasn’t caught on with many doctors because there are no direct treatments for elevated levels. But supplements such as nattokinase, discussed in
chapter 7
on supplements, can work well to “thin” the blood and prevent unwanted clotting. Adding omega-3 fatty acids to your diet may also help.

Ever wonder why so many vitamin manufacturers offer multiple vitamins “without iron”? Here’s why: Iron is one of those weird substances where if you don’t have enough you can have some real problems (e.g., iron-deficiency anemia), but if you have too much, look out! Iron is highly susceptible to oxidation. (Imagine someone leaving a barbell from your gym outside in the rain for a couple of days. It’s going to rust like crazy. That’s oxidation.)

Iron levels in the body are cumulative (stored in the muscles and other tissues), and unless iron is lost
through menstruation or by donating blood, over the years toxic levels can build up in the system. Although this danger always exists for men, it becomes a real risk for women after menopause. Both of us are adamant that no one but premenopausal women should ever take vitamins with iron, or supplemental iron of any kind, unless prescribed by a doctor.

Iron overload—technically called
hemochromatosis
—can actually contribute to heart disease. Researchers measure iron in the blood by measuring a form of it called
ferritin
. A 1992 study by Finnish researchers examined the role of iron in coronary artery disease. After studying 1,900 Finnish men between the ages of forty-two and sixty for five years, the researchers found that men with excessive levels of ferritin had an elevated risk of heart attack, and that every 1 percent increase in ferritin translated into a 4 percent increase in heart attack risk.
⁵

Those with high levels of ferritin were more than twice as likely to have heart attacks than those with lower levels. The authors of this study concluded that ferritin levels may be an even stronger risk factor for heart disease than high blood pressure or diabetes is.
⁶
It’s certainly a more important risk factor than high cholesterol.

If your ferritin levels are high, consider donating blood every so often, or ask your doctor to consider a therapeutic phlebotomy. (Dr. Sinatra’s recommendation for an optimal serum ferritin level is less than 80 mg/L for women and less than 90 mg/L for men.)

Worth noting: One consideration regarding supplemental vitamin C is that it helps the body absorb iron better. If you have a problem with iron levels, keep your supplemental vitamin C to less than 100 mg a day.

Lp(a) is a type of cholesterol-carrying molecule that contains one LDL (low-density lipoprotein) molecule chemically bound to an attachment protein called
apolipoprotein(a)
. In a healthy body, Lp(a) isn’t much of a problem. It circulates and carries out repair and restoration work on damaged blood vessels. The protein part of it promotes blood clotting. So far, so good.

The problem is, the more repair you need on your arteries, the more Lp(a) is utilized, and that’s when things get ugly. Lp(a) concentrates at the site of damage, binds with a couple of amino acids within the wall of a damaged blood vessel, dumps its LDL cargo, and starts to promote the deposition of oxidized LDL into the wall, leading to more inflammation and ultimately to plaque.

Also, Lp(a) promotes the formation of blood clots on top of the newly formed plaque, which narrows the blood vessels further. If the clots are large enough, they can block an artery. (Most heart attacks are due to either a large clot developing in vessels with moderate-to-severe narrowing or a plaque rupture that blocks the artery.)

Elevated Lp(a) is a very serious risk factor. A very high percentage of heart attacks happen to people with high Lp(a) levels. Dr. Sinatra thinks Lp(a) is one of the most devastating risk factors for heart disease and one of the hardest to treat.

One reason doctors aren’t running out to test for Lp(a) all the time is that there are no real pharmaceutical interventions that work to lower it. In addition, Lp(a) levels are largely genetically determined and not very modifiable by lifestyle choices. However, your Lp(a) level can give you a good idea of your real risk for heart disease, and a high level may serve as a wake-up call to inspire you to work harder to improve your heart health using the strategies, foods, supplements, and lifestyle changes suggested in this book. That said, Dr. Sinatra feels that Lp(a) can be lowered with a combination of 1 to 2 g of fish oil, 500 to 2,500 mg of niacin (not the slow-release kind), and 200 mg of lumbrokinase.

Worth noting: Statin drugs can sometimes raise Lp(a) levels! This is mentioned on the warning labels of statin drug ads in the Canadian edition of the
New England Journal of Medicine
, but such labeling is not required by the Food and Drug Administration, so you won’t see it in ads published in the United States.
⁷

Homocysteine is an amino acid by-product that causes your body to lay down sticky platelets in blood vessels. Having some homocysteine is normal, but an excess might affect your cardiovascular health. Evidence shows that homocysteine contributes to atherosclerosis, reduces the flexibility of blood vessels, and helps make platelets stickier, thus slowing blood flow. Net result: There’s a direct correlation between high homocysteine levels and an increased risk of heart disease and stroke.

Elevated homocysteine strongly predicts both a first and a recurring cardiovascular incident (including death).
⁸
Too much homocysteine adversely affects the function of the endothelium, the all-important lining of the artery walls. It also increases oxidative damage and promotes inflammation and thrombosis—a regular evil trifecta for heart disease.
⁹
One study looked at more than 3,000 patients with chronic heart disease and found that a subsequent coronary event was 2.5 times more likely in patients with elevated levels of homocysteine. What’s more, each 5 μmol/L of homocysteine predicted a 25 percent increase in risk!
¹⁰

Fortunately, there’s an easy way to bring down homocysteine levels. All you have to do is give the body the three main nutrients it needs to metabolize homocysteine back into harmless compounds. The three nutrients are folic acid, vitamin B
₁₂
, and vitamin B
₆
. All it takes is about 400 to 800 mcg of folic acid, 400 to 1,000 mcg of B
₁₂
, and 5 to 20 mg of B
₆
. If you’ve had a heart attack or other cardiovascular event; if you have a family history of early heart disease; or if you have hypothyroidism, lupus, or kidney disease, consider asking your doctor to test your homocysteine levels. Finally, if you take drugs that tend to elevate homocysteine—theophylline (for asthma), methotrexate (for cancer or arthritis), or L-dopa (for Parkinson’s)—you should be tested. (Dr. Sinatra’s recommendation for an optimal homocysteine level is between 7 and 9 μmol/L.)

Interleukin-6 is important because it stimulates the liver to produce CRP. And we are learning that this inflammatory cytokine has a strong association with not only heart disease but also asthma. (Asthma is the result of airways swelling and constricting, so it makes sense that an inflammatory agent is behind the curtains here as well.) The Iowa 65+ Rural Health Study demonstrated that elevated levels of interleukin-6 and CRP were associated with an increased risk for both cardiovascular disease and general mortality in healthy older people.

Interleukin-6 may be an even better marker for inflammation than CRP is because these “precursor” levels rise earlier. If you’re concerned about inflammation and its effect on your heart, ask your doctor to do an interleukin-6 test. (Dr. Sinatra’s recommendation for an optimal interleukin-6 level is 0.0 to 12.0 pg/mL.)

Calcium is great—as long as it stays in the bones and teeth. One place you don’t want it is in the coronary arteries.

Coronary calcification is one of the major risk factors that predicts coronary heart disease and future heart attacks.
¹¹
The more calcium present, the greater the risk of suffering a heart attack. Men develop calcifications about ten to fifteen years earlier than women do. Calcification can be detected in the majority of asymptomatic men over fifty-five years of age and in women over sixty-five.