Policosanol Stabilizes Atherosclerotic Plaque
Among the Many Benefits of Policosanol ...
Policosanol Stabilizes
Atherosclerotic Plaque

Stabilization may reduce the chances of plaque
rupture, which can lead to heart attack and stroke
By Dr. Edward R. Rosick

When your heart speaks, take good notes.
— Judith Campbell

he heart is considered by romantics to be the most wondrous organ in the human body (the brain thinks otherwise), and it has inspired countless songs, poems, and epigrams that have enriched our lives and gladdened our . . . hearts. This fist-sized, hollow mass of unique cardiac muscle is one of the first organs to become fully formed, while we’re still embryos. Once the heart starts its life-giving rhythm—long before we are even born—it continues beating every second of every day for the rest of our lives.

If you live to be 80, with an average resting heart rate of 70 beats per minute (100,000 beats per day), your heart will have beat about 3 billion times! And at about 5 quarts of blood per minute (at rest), it will have pumped well over 50 million gallons (about 220 thousand tons) of blood during that time.

That’s pretty impressive, but for millions of Americans, unfortunately, the statistics concerning diseases of the heart and its blood vessels are grim. Coronary artery disease (CAD), the most significant and dangerous type of cardiovascular disease, affects almost 13 million American men and women and is the leading cause of death in this country. Many of these deaths are unexpected; according to the American Heart Association, about 335,000 Americans die of CAD every year without being hospitalized or admitted to an emergency room. Most of these events are classified as sudden cardiac death (SCD), and in 90% of the cases, there is evidence of CAD.

Atherosclerosis Can Begin When We’re Still Young

Now, if you’re a youngster in your 20s or 30s, you might be thinking, “I’m too young to be worrying about a disease like CAD, which affects only old people.” That, however, would be a mistake. We’ve known for half a century that atherosclerosis can begin in childhood, especially in our society, where good diet and regular exercise are the exception rather than the rule. A recent study has confirmed that coronary atherosclerosis indeed begins at an early age and that atherosclerotic lesions are present in one in six American teenagers.1

Atherosclerosis is thought to be initiated when there’s an insult (medical jargon for injury) to the inner lining of our arteries, caused by factors such as hypertension, hyperglycemia (high blood sugar), nicotine, the destructive amino acid homocysteine, or reactive oxygen species, including free radicals. The immune system responds by sending specialized white blood cells called macrophages to the site of the injury to prevent infection. The accumulation of these cells, however, causes localized inflammation, which can cause still more damage. Macrophages are implicated throughout the entire atherosclerotic process, which is accelerated by high cholesterol levels.

How Does Your Plaque Grow?

The process entails a buildup of soft, sticky plaque, which consists mainly of fatty substances (especially cholesterol), macrophages, cellular debris, and, often, calcium deposits, all held in place by a capsule of connective tissue. As plaques become embedded in the lining of the arteries and grow larger, they can cause a thickening and hardening of the arterial walls (the word atherosclerosis comes from the Greek athera, gruel, and sklerosis, hardness).

The arteries thus become less able to dilate properly in response to the need for reduced blood pressure or increased blood flow to various tissues. Worse still, the sheer volume of the plaques can significantly obstruct blood flow, depriving the affected organs and tissues of adequate oxygen and vital nutrients.

As plaques continue to grow, the immune system, sensing harm to the arteries, responds with proteins called cytokines to help repair the damage. This, however, causes the accumulation of more macrophages (which themselves produce certain cytokines) at the plaque sites, leading to even more inflammation and more plaque buildup. A vicious cycle is established that can have dire consequences, especially for the heart and brain.

Plaque Stability Is Crucial

Although it was formerly thought that all plaques were dangerous, scientists now believe otherwise. High-precision imaging studies, e.g., have shown that even large plaques can be asymptomatic. The extent to which a plaque represents a real danger to its host depends not just on its size and location, but also on its stability, i.e., its tendency to hold together and not rupture under adverse circumstances.

Both exertion and the TC/HDL-C
ratio were statistically associated with
acute plaque rupture, independently
of age and other cardiac risk factors.

If a plaque does rupture, a thrombus (blood clot) is likely to form at the site. This is potentially dangerous, because sooner or later it can break free and become lodged in an artery somewhere downstream, shutting off blood circulation to the tissue served by that artery. Depending on where in the body this occurs, the result can be anything from localized mild tissue damage to gangrene of an extremity to a heart attack or stroke.

Plaque Rupture Can Cause Sudden Cardiac Death

The vital importance of plaque stability was underscored by a recent study on the link between plaque rupture and sudden cardiac dealth.2 American researchers studied the hearts of 141 men (average age 51) with severe CAD who had succumbed to SCD. For the purposes of this study, cardiac death (or coronary death) was defined as natural death not attributable to any cause other than the heart and in which at least one coronary artery was at least 75% obstructed by atherosclerotic plaque, with or without an attached thrombus. Death was considered to be sudden only if it had occurred within 6 hours of the onset of symptoms (as confirmed by witnesses) or (if there were no witnesses) within 24 hours of the last time the victim was seen alive in his normal state of health.

Of the 141 men, 116 died while at rest (e.g., sitting at home or at work, driving a car, or sleeping), and 25 died during or shortly after strenuous physical exertion (e.g., carrying heavy objects, moving furniture, pushing a car, playing basketball, or having sex) or during emotional stress brought on by such things as public speaking, a court appearance, or an altercation of some kind.

The researchers were interested in the relationship between acute plaque rupture and SCD in the two groups of deceased men (the Exertion group and the Rest group). The findings from the autopsied hearts of these men provided no surprises, but a clear and ominous warning. Of the 25 hearts in the Exertion group, 68% (17) showed acute plaque rupture in a coronary artery, while only 24% (6) showed stable plaque; the remainder showed some plaque erosion but not acute rupture. The 116 hearts in the Rest group presented a very different picture: only 23% (27) showed acute plaque rupture, while 52% (60) showed stable plaque; most of the remainder showed plaque erosion, and a few showed healing plaque ruptures.

A Recipe for Disaster

The great majority of the men in the Exertion group had led sedentary lives and were not physically well conditioned—a recipe for disaster when they undertook strenuous activities. The autopsies showed that the men in the Exertion group had, on average, a significantly higher ratio of total cholesterol (TC) to HDL-cholesterol (the “good cholesterol”) than did the men in the Rest group. In other words, the Exertion group had less HDL-C in relation to their TC than did the Rest group, a fact that emphasizes the importance of maintaining high HDL-C levels as well as low levels of TC and LDL-cholesterol (the “bad cholesterol”). The virtue of HDL-C is that it represents cholesterol in the process of being removed from our arteries rather than being deposited there.

In this study, both exertion and the TC/HDL-C ratio were statistically associated with acute plaque rupture, independently of age and other cardiac risk factors, such as smoking and hypertension. The researchers concluded that strenuous activity is an independent risk factor for plaque rupture in men with severe CAD.

The message of this study is twofold: (1) avoid plaque like the plague; and (2) if you can’t do that, at least try to keep your plaque as stable as possible. You’ve undoubtedly heard the first prescription many times, in one form or another, but the second one is probably new to you. How in the world can one affect the stability of one’s own plaque, deep down in those inaccessible arteries?

Policosanol—A Versatile Agent for Heart Health

One answer may lie with policosanol, a safe, natural supplement that is known to exert beneficial effects on lipid profiles in people with high cholesterol levels, as well as in people with type 2 diabetes and in postmenopausal women. Policosanol produces strong reductions in total cholesterol and LDL-cholesterol, as well as significant reductions in triglycerides (fats) and significant increases in HDL-cholesterol. By simultaneously decreasing total cholesterol and increasing HDL-cholesterol, policosanol strongly decreases that important TC/HDL-C ratio, a marker of good cardiovascular health. (See “Policosanol Improves Every Measure of Blood Cholesterol” and “Policosanol Keeps Your Arteries Healthy” in the October and November 2002 issues, respectively.)

Policosanol’s health benefits are not limited to improving lipid profiles, however. Among the varied cardiovascular benefits that have been attributed to this substance in scientific studies are the ability to inhibit blood clotting (anticoagulant action), to improve blood-pumping ability (left-ventricular function) and exercise capacity, to inhibit lipid peroxidation, to inhibit plaque growth, and to reduce the pain associated with walking (intermittent claudication). (For more on these topics and on policosanol’s potential for improving cognitive function, see “Policosanol Improves Cardiovascular Health” and “One Hundred Reasons for Taking Policosanol” in the December 2002 and January 2003 issues, respectively.)

Gotu Kola’s TTFCA Also Stabilizes Plaque

The traditional herb gotu kola (Centella asiatica) has a long history of use for a variety of human ills. Modern science has focused on the use of a high-potency extract of gotu kola called TTFCA (total triterpenic fraction of Centella asiatica) for treating chronic venous insufficiency; this is a functional deterioration of the veins in the legs, often leading to poor circulation, varicose veins, and edema (swelling).

In 2001, a team of Italian researchers published an extensive series of studies of the effects of TTFCA on various aspects of arterial and venous function, including two randomized, placebo-controlled, human clinical trials that investigated low-density plaque composition and stability.1,2 The objective was to modify the plaque’s composition so as to increase its density. This, in turn, should make the plaques more stable and thus less likely to rupture, which could lead to a potentially fatal thrombosis.

Using ultrasound techniques for visualizing and measuring plaque in the arteries of living subjects, the researchers focused in one study on the carotid arteries,1 and in the other study on the femoral arteries.2 In both studies, groups of middle-aged patients were given either placebo or 60 mg of TTFCA thrice daily (180 mg/day) for 12 months, and in both cases, the results were similar. Whereas there was little or no improvement in the controls, the TTFCA-treated individuals showed substantial gains in plaque density and stability.

  1. Cesarone MR, Belcaro G, Nicolaides AN, et al. Increase in echogenicity of echolucent carotid plaques after treatment with total triterpenic fraction of Centella asiatica: a prospective, placebo-controlled, randomized trial. Angiology 2001 Oct;52 Suppl 2:S19-25.
  2. Incandela L, Belcaro G, Nicolaides AN, et al. Modification of the echogenicity of femoral plaques after treatment with total triterpenic fraction of Centella asiatica: a prospective, randomized, placebo-controlled trial. Angiology 2001 Oct;52 Suppl 2:S69-73.

Monkey Business

Adding to this already impressive list, a new study in Cuba has shown that policosanol can stabilize atherosclerotic plaque by altering its composition, thus reducing the risk of rupture and thrombosis (the formation of a thrombus).3 The subjects in this study were stump-tailed macaques (Macaca arctoides), chosen because their anatomy, cardiovascular physiology, and tendency to develop atherosclerosis are similar to those of humans.

The Cuban researchers randomized 14 adult male macaques into three groups: a control group (six monkeys) that received a low-fat, protein-rich diet, and two treatment groups (four monkeys each) that were fed the same diet along with policosanol at either 2.5 or 25 mg per kg of body weight daily for 54 weeks. Then the monkeys were killed, and the researchers examined their cardiac as well as noncardiac arteries for evidence of atherosclerotic lesions.

Policosanol Stabilizes Atherosclerotic Plaque

The frequency of severe lesions, as well as thickening of the artery walls, was significantly lower in the monkeys given policosanol. Just as importantly, the plaque composition differed significantly among the three groups: in a dose-dependent manner, policosanol had inhibited the accumulation of proinflammatory macrophages in the plaques (good). It had also reduced the levels of the protein carrier of cholesterol in LDL-cholesterol (good), and it increased the levels of the protein carrier of cholesterol in HDL-cholesterol (good). In slightly fractured English, the authors concluded,

These results suggest the policosanol potential benefit on plaque composition and stability and could explain the protective effects of policosanol on atherosclerosis development.

It’s worth noting that similar results were found with the statin drug cerivastatin, using rabbits instead of monkeys.4 Although cerivastatin was pulled from the market in 2001 because of potentially severe side effects, other cholesterol-lowering statins remain in widespread use and are very effective. A few of these drugs have gone head-to-head with policosanol in scientific studies, and policosanol has generally performed as well as or better than the statins (see, e.g., “Policosanol—A Better Alternative to Statin Drugs” and “Cholesterol Showdown: Policosanol vs. Atorvastatin” in the May 2002 and May 2003 issues, respectively).

Let Policosanol Take Care of Your Heart

With the high-fat, high-calorie diet that most of us consume, it’s almost inevitable that we’ll accumulate some atherosclerotic plaque during our life. Although it’s important to make every effort to avoid this—by not smoking and by eating a healthy diet and exercising regularly—it’s also important to try to stabilize the plaque that has already formed. Policosanol, an effective and extremely safe supplement, may be the way to keep your cholesterol down and your plaque stable so that your heart can continue beating long into your golden years.


  1. Tuzcu EM, Kapadia SR, Tutar E, et al. High prevalence of coronary atherosclerosis in asymptomatic teenagers and young adults. Circulation 2001; 103:2705-10.
  2. Burke AP, Farb A, Malcom GT, et al. Plaque rupture and sudden death related to exertion in men with coronary artery disease. JAMA 1999;281: 921-6.
  3. Noa M, Mas R. Protective effect of policosanol on atherosclerotic plaque on aortas in monkeys. Arch Med Res 2005;36:441-7.
  4. Aikawa M, Rabkin E, Sugiyama S, et al. An HMG-CoA reductase inhibitor, cerivastatin, suppresses growth of macrophages expressing matrix metalloproteinases and tissue factor in vivo and in vitro. Circulation 2001; 103:276-83.

Policosanol for Heart Support

Policosanol extracted from Hawaiian sugar cane is a primary choice for a heart-healthy nutrient. An advanced formulation will also contain three other heart-healthy nutrients: niacin, a B-vitamin that lowers cholesterol; coenzyme Q10, a vital antioxidant and energy molecule that can be depleted by cholesterol-lowering agents; and green tea extract, which has a protective action on heart function. [The niacin may be in the form of inositol hexanicotinate (IHN), which does not produce the notorious “flushing” effect of niacin itself.]

The recommended daily serving of policosanol in 20 mg and 1200 mg of niacin, divided and taken in equal servings throughout the day.

Edward R. Rosick, D.O., is an attending physician and clinical asst. prof. of medicine at Pennsylvania State University, where he specializes in preventive and alternative medicine. He also holds a master’s degree in healthcare administration.

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