By Glenn S. Rothfeld, MD
           
The second most-asked question from my patients, next to “What’s my blood pressure?” is “What’s my cholesterol?”  Even my patients who have had nice low cholesterols, are on careful diets, and have no family risk, continue to ask me to check this particular lab test.  It’s a testimony to the success of public health efforts that everyone is so cholesterol-conscious.       

However, one fact remains:  over half of patients with atherosclerotic heart disease do not have high cholesterol or even other known risk factors like obesity, hypertension, or diabetes.  This means that there are other factors involved in fatal heart disease and stroke, factors that go beyond cholesterol and into a more comprehensive model of atherosclerosis.

To understand this new model, let’s look at how atherosclerosis happens.  The first event is now thought to be inflammation that results from an injury to the wall of the artery.  That injury might come from high blood pressure damage, from so-called free radical damage due to environmental exposure (including cigarette smoke), from substances in the body like insulin and homocysteine that irritate the wall of the artery, or from the abnormal metabolism found in diabetics.  It also seems to come from various infections, including herpes viruses and Chlamydia pneumonia infection, and it can come from wear and tear from stress hormones that are released into the bloodstream unchecked.

Whatever the cause of the injury, the wall of the artery gets altered, leading to inflammation, increase in the stickiness of platelets in the area, and an increase in a certain type of lipid called LDL (low density lipoprotein).  This LDL gets oxidized by the inflammatory substances, and becomes able to pass through the artery wall, leading to inflammation in the wall of the artery, bringing along fatty cells and clotting material.  The plaque that we associate with atherosclerosis is an accumulation of these fatty cells, clotting materials, and products of inflammation.

Thus, in order for atherosclerosis to form, we must have inflammation (from injury, infection, etc.), clotting (from sticky platelets and fibrin or clot formation), and LDL which has been oxidized (from blood cholesterol increases, and lack of proper antioxidants).  In modern medicine, we have been concentrating on the last piece (specifically, lowering LDL) and ignoring the inflammatory, clotting and oxidation parts of the whole picture.

Now, information has come out that improves our ability to measure heart disease risk, and to provide natural protection.  Several tests are available to measure cardiac risk more completely.  One simple blood test, called a C-reactive protein (CRP), is a measurement of the amount of inflammation in the circulatory system.  Multiple studies have shown that CRP measurements (specifically, the highly-sensitive form of CRP) can predict both stroke and heart disease.  In fact, almost all of the recent large cardiovascular studies (Women’s Health Study, Helsinki Heart Study, Physician Health Study, etc.) studied hs-CRP and demonstrated its predictive possibilities, a better predictor and lipid testing.

Another simple measurement is a homocysteine level.  Homocysteine is normally made by the body when certain proteins are broken down, and then harmlessly broken down further and excreted.  In certain people, however, the homocysteine is not broken down well due to a problem with an enzyme, and homocysteine stays in the body, where it is very damaging to the artery walls.

Clotting can be assessed by measuring fibrinogen levels.  Fibrinogen is the substance that is used in the body to form fibrin, or clot.  Stress raises fibrinogen levels and platelet stickiness, as does infection and inflammation.  Infections can be measured by antibody testing, although it’s not clear at this point that treating chronic infections makes a difference in heart disease.  Some studies are currently underway to look at this.

Finally, there are certain kinds of lipoproteins that are usually hereditary, and can be more damaging to the circulatory system when oxidized.  These are called “lipoprotein a” and usually abbreviated lp (a), and can be measured on a blood test.

To summarize, a complete cardiac risk evaluation, such as we perform at The Rothfeld Center, should include measurements of lipids (cholesterol, LDL/HDL, triglycerides), genetic lipid and metabolic abnormalities (lp [a], homocysteine), inflammation (hs-CRP), and clotting tendency (fibrinogen).  With all of this information, we can begin to put together a program to lessen cardiac risk.

Each of these risk factors can be approached naturally.  Lipid elevations, for instance, are treated medically with lipid lowering drugs called “statins.”  While these statin drugs are quite effective, there are some natural alternatives.  One, called red yeast rice, stimulates some natural “statin” activity in the body, lowering total cholesterol and LDL, and raising HDL, the protective cholesterol.  Inositol hexaniacinate, a non-flush form of vitamin B3, also safely lowers cholesterol.  Other natural lipid-lowering agents include pantothenic acid, garlic, fish oils and gugulipids, the resins of the gugul tree of India.

Antioxidants play an important role in protecting the circulation from oxidation and inflammation.  Vitamin E has crossed the line into mainstream acceptability as a cardiac antioxidant.  Vitamin C and selenium are other common antioxidants.  Coenzyme-Q-10, which carries energy in the cells, acts as protection for the circulation.  Co-Q-10 also is blocked by statin drugs, and giving it with statins seems to help ward off the side effects of fatigue and muscle aching.  Herbal antioxidants include substances containing polyphenol compounds (PCs).  These include pure olive oil, red wine, green tea, ginger and licorice, among others.  Taking supplements with these compounds and eating a diet rich in olive oil can be healthy for the heart.

Clotting in the circulation can be managed by taking a low dose of aspirin each night, which makes the platelets less sticky.  Ginkgo biloba, fish oils and vitamin E also have an anti-sticky effect on the platelets.  Bromelaine, a natural enzyme from pineapple, is known to break down fibrin, and can be taken to help lessen clotting.  Recent enzyme products made from soy products and (believe it or not) earthworms have also been studied for their clot-busting activity.

Elevated homocysteine treatment is simple.  Folic acid and B12 (and sometimes B6) assist the enzyme that breaks down homocysteine, and usually this problem is alleviated by taking the proper vitamins.

A comprehensive cardiovascular protection program should include testing for these risk factors, taking the appropriate supplements, following a “Mediterranean” type diet which is high in olive oil, exercising regularly (this has a positive effect on all of the risk factors), and managing stress.  If we follow this type of program, we can move “beyond cholesterol” to full and vigorous circulatory health!