The Encyclopedia of Natural Medicine, 3rd Ed.

Heart and Cardiovascular Health



The cardiovascular system is composed of the heart and blood vessels. Its primary functions are to deliver oxygen and vital nutrition to cells throughout the body as well as aid in the removal of cellular waste products. In achieving this goal, the human heart beats 100,000 times each day, pumping 2,500 to 5,000 gallons of blood through the 60,000 miles of blood vessels within our bodies. In an average lifetime, the heart will beat 2.5 billion times and pump 100 billion gallons of blood.

Obviously, we need to support the heart in its tireless efforts. Unfortunately, as a nation we are doing a very poor job of keeping our hearts healthy. Heart disease and strokes are our nation’s number one and number four killers, respectively. Together, these two conditions are responsible for at least 30% of all deaths in the United States. Both are referred to as “silent killers” because the first symptom or sign in many cases is a fatal event. The cause of both conditions is often atherosclerosis—hardening of the artery walls.

Atherosclerosis is the disease process underlying cardiovascular disease (CVD), an umbrella term that encompasses atherosclerosis of the coronary arteries [called coronary artery disease (CAD) or heart disease], heart attack (the medical term is myocardial infarction), blockage of a main artery in the lung (called pulmonary embolism), and stroke (also called cerebrovascular accident or CVA). The coronary arteries are blood vessels that supply the heart muscle with vital oxygen and nutrients. If the blood flow through these arteries is restricted or blocked, severe damage to or death of the heart muscle often occurs—a heart attack. In most cases, the artery blockage is due to a buildup of plaque, a combination of cholesterol, fatty material, and cellular debris. In the case of a stroke, it is an artery in the brain that is blocked.

Understanding Atherosclerosis

To fully understand the important ways that the various natural measures described in this chapter affect the health of the artery and the treatment of cardiovascular disease, it is necessary to examine closely the structure of an artery and the process of atherosclerosis.

Structure of an Artery

An artery is divided into three major layers:

1. The intima or endothelium is the internal lining of the artery. The intima consists of a layer of cells known as endothelial cells. Molecules known as glycosaminoglycans (GAGs) line the exposed endothelial cells to protect them from damage as well as promote repair. Beneath the surface endothelial cells is an internal elastic membrane composed of a layer of GAGs and other ground substances that provide support to the endothelial cells and separate the intima from the smooth muscle layer.


Structure of an Artery

2. The media or middle layer consists primarily of smooth muscle cells. Interposed among the cells are GAGs and other ground substances that provide support and elasticity to the artery.

3. The adventitia or external elastic membrane consists primarily of connective tissue, including GAGs, providing structural support and elasticity to the artery.

The Process of Atherosclerosis

No single theory of the development of atherosclerosis satisfies all investigators. However, the most widely accepted explanation theorizes that the lesions of atherosclerosis begin as a response to injury to the cells lining the inside of the artery, the intima. Details of the progression of atherosclerosis are illustrated below.

Causes of Atherosclerosis

Prevention of CVD involves reducing and, when possible, eliminating risk factors. Risk factors are divided into two primary categories: major risk factors and other risk factors. Keep in mind that some of the other risk factors have been shown to be more important than the so-called major risk factors. For example, a strong argument could be made that insulin resistance and elevations in high-sensitivity C-reactive protein (hsCRP), a marker for inflammation, are much more important than elevated cholesterol levels. It is also important to point out that the risk for a heart attack increases exponentially with the number of risk factors.


The Development of Atherosclerosis

A. The initial step in the development of atherosclerosis is a weakening of the GAG layer that protects the endothelial cells. As a result, the endothelial cell is exposed to damage by free radicals and other injurious factors. Immune, physical, mechanical, viral, chemical, and drug factors have all been shown to induce damage to the endothelial cells and lead to plaque development.

B. Once the endothelial lining has been damaged, these sites of injury become more permeable to plasma constituents, especially lipoproteins (fat-carrying proteins). The binding of lipoproteins to glycosaminoglycans leads to a breakdown in the integrity of the ground substance matrix and causes an increased affinity for cholesterol. Once significant damage has occurred, monocytes (large white blood cells) and platelets adhere to the damaged area, where they release growth factors that stimulate smooth muscle cells to migrate from the media into the intima and replicate.

C. The local concentration of lipoproteins and platelets also leads to the migration of smooth muscle cells from the media into the intima, where they undergo proliferation. The smooth muscle cells dump cellular debris into the intima, leading to further development of plaque.

D. A fibrous cap (consisting of collagen, elastin, and glycosaminoglycans) forms over the intimal surface. Fat and cholesterol deposits accumulate.

E. Plaque continues to grow until eventually it either blocks the artery directly or ruptures to form a clot that travels throughout the general circulation until it occludes a blood vessel. Plaque instability is associated with a significantly greater risk for heart attack or stroke.1 Thus, reducing inflammation and other factors that promote plaque instability is an important target.

Risk Factors for Atherosclerosis

• Major risk factors

  images Smoking

  images Elevated blood cholesterol levels (especially oxidized LDL)

  images High blood pressure

  images Diabetes

  images Physical inactivity

• Other risk factors

  images Elevation in high-sensitivity C-reactive protein

  images Insulin resistance

  images Low thyroid function

  images Low antioxidant status

  images Low levels of essential fatty acids

  images Increased platelet aggregation

  images Increased fibrinogen formation

  images Low levels of magnesium and/or potassium

  images Elevated levels of homocysteine

  images Type A personality

Clinical Evaluation

Since CVD is such a major cause of death, we recommend consulting a physician in order to have a complete cardiovascular assessment that can include these tests:

Laboratory tests

• Total cholesterol (oxidized LDL is more predictive)

• Low-density-lipoprotein (LDL) cholesterol

• High-density-lipoprotein (HDL) cholesterol

• High-sensitivity C-reactive protein

• Lipoprotein(a), Lp(a)

• Fibrinogen

• Homocysteine

• Ferritin (an iron-binding protein)

• Lipid peroxides

Other procedures

• Exercise stress test

• Electrocardiography

• Echocardiography

Association of Major Risk Factors with the Incidence of Atherosclerosis



Presence of one of the major risk factors


High cholesterol and high blood pressure


High cholesterol and a smoker


High blood pressure and a smoker


Smoker, high blood cholesterol, and high blood pressure




To help determine your overall risk for having a heart attack or stroke, we have developed the following risk-determinant scale. Although this risk assessment does not take into consideration several important factors such as your level of fibrinogen and your coping style, the score provides a good indication of your relative risk for a heart attack or stroke. Each of these risk factors is discussed below.

Risk Determination Scale for Heart Disease and Stroke









Blood pressure (systolic)

< 125




≥ 165

Blood pressure (diastolic)

< 90




≥ 115

Smoking (cigarettes per day)





≥ 30

Heredity I*


> 65



< 35

Heredity II





≥ 4

Diabetes duration (years)





> 15

Total cholesterol (mg/dl)

< 200




≥ 275

HDL (high-density-lipoprotein) cholesterol (mg/dl)

≥ 75




< 35

Total cholesterol/HDL ratio

< 3




≥ 6.5

High-sensitivity CRP

< 1




> 4

Exercise (hours per week)

> 4





Supplemental EPA/DHA (mg) intake

> 600




< 100

Vitamin C, vitamin E, selenium, PCOs, lutein supplementation (number of items)






Average daily servings of fruits and vegetables

> 5






< 35




> 65



* Age of patient when he or she had a first heart attack or stroke.

 Number of immediate family members having had a heart attack before the age of 50.

 Total cholesterol divided by HDL.

Risk = sum of all five columns; 14–20 = very low risk; 21–30 = low risk; 31–40 = average risk; 41–50 = high risk; ≥ 51 = very high risk.


A Closer Look at Risk Factors


Cigarette smoking is perhaps the most important risk factor for CVD, as statistical evidence reveals smokers have a 70% greater risk of death from CVD than nonsmokers.2 The more cigarettes smoked and the longer a person has smoked, the greater the risk of dying from a heart attack or stroke. Overall, the average smoker dies seven to eight years sooner than the nonsmoker.

Tobacco smoke contains more than 4,000 chemicals, of which more than 50 substances have been identified as carcinogens. These chemicals are extremely damaging to the cardiovascular system. Specifically, these chemicals are carried in the bloodstream on low-density lipoprotein (LDL) cholesterol, where they either damage the lining of the arteries directly or damage the LDL molecule (creating oxidized LDL), which then damages the arteries. An elevated LDL level worsens the effect of smoking because more cigarette toxins travel through the cardiovascular system. Smoking contributes to elevated cholesterol presumably by damaging feedback mechanisms in the liver, which control how much cholesterol is being manufactured.3 Smoking also promotes platelet aggregation and elevated fibrinogen levels, two other independent risk factors important for CVD because they tend to result in the formation of blood clots. In addition, it is a well-documented fact that cigarette smoking is a factor contributing to high blood pressure.4

Even passive exposure to cigarette smoke is damaging to cardiovascular health, as convincing evidence links environmental (secondhand or passive) smoke to CVD. Analysis of 10 population-based studies indicates a consistent dose-response effect related to exposure.5 In other words, the more you are exposed to cigarette smoke, the greater your risk for CVD. Evidence indicates that nonsmokers appear to be more sensitive to smoke, including its deleterious effects on the cardiovascular system. Environmental tobacco smoke actually has a higher concentration of some toxic constituents. Data after short- and long-term exposure to environmental tobacco smoke show changes in the lining of the arteries and in platelet function as well as exercise capacity similar to those found in active smokers. In summary, passive smoking is a relevant risk factor for CVD. In the United States it is estimated that more than 37,000 heart disease deaths each year are attributable to environmental smoke.

The good news is that the magnitude of risk reduction achieved by smoking cessation in patients with CVD is quite significant. Results from a detailed meta-analysis showed a 36% reduction in relative risk of mortality for patients with coronary artery disease who quit compared with those who continued smoking.6

Various measures—including nicotine-containing skin patches or chewing gum, acupuncture, and hypnosis—have all been shown to provide some benefit in helping patients to quit smoking.7 For more information on strategies to stop smoking, see the chapter “A Health-Promoting Lifestyle.”

Elevated Blood Cholesterol Levels

The evidence overwhelmingly demonstrates that elevated cholesterol levels greatly increase the risk of death due to CVD, especially elevations in LDL cholesterol.8 It is currently recommended that the total blood cholesterol level be less than 200 mg/dl. In addition, it is recommended that LDL be less than 130 mg/dl, HDL greater than 40 mg/dl in men and 50 mg/dl in women, and triglycerides less than 150 mg/dl.

Cholesterol is transported in the blood by lipoproteins. The major categories of lipoproteins are very-low-density lipoprotein (VLDL), LDL, and HDL. Because VLDL and LDL are responsible for transporting fats (primarily triglycerides and cholesterol) from the liver to body cells while HDL is responsible for returning fats to the liver, elevations of either VLDL or LDL are associated with an increased risk for developing atherosclerosis, the primary cause of a heart attack or stroke. In contrast, elevations of HDL are associated with a low risk of heart attacks.

The ratios of total cholesterol to HDL cholesterol and LDL to HDL are referred to as cardiac risk factor ratios because they reflect whether cholesterol is being deposited into tissues or broken down and excreted. The ratio of total cholesterol to HDL should be no higher than 4.2, and the ratio of LDL to HDL should be no higher than 2.5. The risk of heart disease can be reduced dramatically by lowering LDL while simultaneously raising HDL levels. For every 1% drop in the LDL level, the risk of a heart attack drops by 2%. Conversely, for every 1% increase in HDL level, the risk for a heart attack drops 3% to 4%.8,9

For more information on elevated blood cholesterol and lipoproteins, see the chapter “High Cholesterol and/or Triglycerides.”


Atherosclerosis is one of the key underlying factors in the development of many chronic complications of diabetes. Individuals with diabetes have a two- to threefold higher risk of dying prematurely of heart disease or stroke than those who are not diabetic, and 55% of deaths in diabetic patients are caused by CVD. However, even mild insulin resistance and poor glucose control have been shown to have a dramatic impact on the incidence and progression of CVD. For more information, see the chapter “Diabetes.”

High Blood Pressure

Elevated blood pressure is often a sign of considerable atherosclerosis and a major risk factor for heart attack or stroke. In fact, the presence of hypertension is generally regarded as the most significant risk factor for stroke. For more information, see the chapter “High Blood Pressure.”

Physical Inactivity/Lack of Exercise

A sedentary lifestyle is another major risk factor for CVD. Roughly 54% of adult Americans report little or no regular physical activity, and there is also a sharp decline in regular exercise among children and adolescents.10 But not only does being active protect against the development of CVD, it also favorably modifies other CVD risk factors, including high blood pressure, blood lipid levels, insulin resistance, and obesity. Exercise is also important in the treatment and management of patients with CVD or increased risk, including those who have hypertension, stable angina, a prior heart attack, peripheral vascular disease, or heart failure, or who are recovering from a cardiovascular event. For more information, see the chapter “A Health-Promoting Lifestyle.”

Other Risk Factors

In addition to the major risk factors for CVD (smoking, elevated cholesterol, high blood pressure, diabetes, physical inactivity, and obesity), a number of other factors have, on occasion, been shown to be more significant than the so-called major risk factors. In fact, more than 300 different risk factors have been identified. Although there is considerable evidence that all of these risk factors and more can play a significant role in the development of atherosclerosis, much of the current research has focused on the central roles of inflammatory processes and insulin resistance.11

Inflammatory mediators influence many stages in the development of atherosclerosis, from initial leukocyte recruitment to eventual rupture of the unstable atherosclerotic plaque. In particular, high-sensitivity C-reactive protein, a blood marker that reflects different degrees of inflammation, has been identified as an independent risk factor for CAD. The hsCRP level has been shown to be a stronger predictor of cardiovascular events than LDL level, but screening for both biological markers provides better prognostic information than screening for either alone.12

Elevations in hsCRP are closely linked to insulin resistance, a condition in which cells of the body become unresponsive to the hormone insulin (see the chapter “Diabetes” for more information).13 Insulin resistance is a key underlying factor not only in type 2 diabetes but also in metabolic syndrome, defined as a combination of at least three of the following metabolic risk factors:

• A waist-to-hip ratio greater than 1 for men and greater than 0.8 for women

• Triglycerides greater than 150 mg/dl, and low HDL (below 40 mg/dl in men and below 50 mg/dl in women)

• High blood pressure (equal to or greater than 130/85 mm Hg)

• Insulin resistance or glucose intolerance (fasting blood sugar levels above 101 mg/dl)

• High blood levels of fibrinogen or plasminogen activator inhibitor

• Elevated high-sensitivity CRP

Metabolic syndrome has become increasingly common in the United States. It is now estimated that more than 60 million U.S. adults may have it.

Therapeutic Considerations

Prevention of a heart attack or stroke involves reducing risk factors. The major risk factors—smoking, obesity, physical inactivity, diabetes, and hypertension—are detailed in other chapters. The point we want to make here is that there is significant evidence that simply adopting a healthy diet and lifestyle dramatically reduces CVD-related mortality. In a prospective trial enrolling more than 20,000 men and women, it was found that the combination of four healthy behaviors (not smoking; being physically active; moderate alcohol intake; and consuming at least five servings of fruit and vegetables per day) reduced total mortality fourfold compared with the absence of all these behaviors.14

In addition to these healthful lifestyle behaviors, we will also discuss antioxidant status, elevated hsCRP, and fibrinogen levels.


The chapter “A Health-Promoting Diet” features a comprehensive dietary approach that will help both with the prevention and treatment of CVD and with the improvement of blood lipid profiles. In particular, it is important to reduce the intake of saturated fat and trans-fatty acids while increasing the consumption of vegetables, fruit, dietary fiber, monounsaturated fats, and omega-3 fatty acids. An important dietary goal is to improve the structure and composition of cell membranes by making available essential structural components like the monounsaturated and omega-3 fatty acids and by preventing oxidative and free radical damage to these structures by consuming a high level of antioxidants and phytochemicals.

One of the most widely studied dietary interventions in CVD is the traditional Mediterranean diet, which reflects food patterns typical of some Mediterranean regions in the early 1960s.15 As we discussed in the chapter “A Health-Promoting Diet,” the original Mediterranean diet had the following characteristics:

• Olive oil is the principal source of fat.

• The diet centers on an abundance of plant foods.

• Foods are minimally processed, and people focus on fresh, seasonal, locally grown foods.

• Fresh fruit is the typical everyday dessert, with sweets containing concentrated sugars or honey consumed only a few times a week at most.

• Dairy products (principally cheese and yogurt) are consumed in low to moderate amounts daily.

• Fish is consumed regularly.

• Poultry and eggs are consumed in moderate amounts (up to four times weekly) or not at all.

• Red meat is consumed in low amounts.

• Wine is consumed in low to moderate amounts, normally with meals.

In one study, the effect of the Mediterranean diet on the lining of blood vessels and hsCRP was examined in patients with metabolic syndrome.16 Patients in the intervention group were instructed to follow the Mediterranean diet and received detailed advice on how to increase their consumption of whole grains, fruits, vegetables, nuts, and olive oil; patients in the control group followed the American Heart Association (AHA) diet. After two years, patients following the Mediterranean diet regularly ate more foods rich in monounsaturated fat, polyunsaturated fat, and fiber and had a lower ratio of omega-6 to omega-3 fatty acids. Compared with patients on the control diet, patients on the intervention diet had significantly reduced levels of hsCRP and other inflammatory mediators; improved blood vessel function; and greater weight loss.

Although several components of the Mediterranean diet deserve special mention, it is important to stress that the total benefits reflect an interplay among many beneficial compounds rather than any single factor.17

In addition, it is critical to follow a low-glycemic-load diet. A study of more than 48,000 participants following a low-glycemic diet for an average of eight years found that the consumption of foods with a high glycemic load increased the risk of CVD in women by 68%; women in the highest glycemic-load quartile had a relative risk of 2.2 for CHD compared with those in the lowest quartile.18

Olive Oil and Omega-3 Fatty Acids

One of the most important aspects of the Mediterranean diet may be the combination of olive oil and the intake of omega-3 fatty acids. Olive oil contains not only monounsaturated fatty acid (oleic acid) but also several antioxidant agents that may account for some of its health benefits. In addition to a mild effect in lowering LDL and triglycerides, olive oil increases HDL level and helps prevent LDL from being damaged by free radicals.19

In addition to olive oil, the benefits of the longer-chain omega-3 fatty acids EPA and DHA for cardiovascular health have been demonstrated in more than 300 clinical trials. These fatty acids exert considerable benefits in reducing the risk for CVD. Supplementation with EPA and DHA has little effect on cholesterol levels but does lower triglyceride levels significantly, as well as produce a myriad of additional beneficial effects, including reduced platelet aggregation, improved function of the lining of blood vessels and arterial flexibility, improved blood and oxygen supply to the heart, and a mild reduction in blood pressure.20

The levels of EPA and DHA within red blood cells have been shown to be highly significant predictors of heart disease. This laboratory value has been termed the omega-3 index. An omega-3 index of 8% was associated with the greatest protection, whereas an index of 4% was associated with the least. In one analysis, the omega-3 index was shown to be the most significant predictor of CVD compared with hsCRP, total cholesterol, LDL, HDL, and homocysteine. Researchers subsequently determined that a total of 1,000 mg EPA + DHA per day is required to achieve or surpass the 8% target of the omega-3 index.21,22

The findings about the omega-3 index are not surprising, as a wealth of information has documented a clear relationship between dietary intake of omega-3 fatty acids and the likelihood of developing CVD: the higher the omega-3 fatty acid intake, the lower the likelihood of CVD. It has been estimated that raising the levels of long-chain omega-3 fatty acids through diet or supplementation may reduce overall cardiovascular mortality by as much as 45%.23,24

In general, for preventive effects against CVD, the dosage recommendation is 1,000 mg EPA + DHA per day; for lowering triglycerides, the dosage is 3,000 mg per day. In a double-blind study, after eight weeks of supplementation, a daily dosage of 3.40 g EPA + DHA lowered triglycerides by 27%, while a lower dosage of 0.85 g had no effect. These results clearly indicate that lowering triglycerides requires dosages of 3 g EPA + DHA per day.25

Although the longer-chain omega-3 fatty acids exert more pronounced effects than alpha-linolenic acid, a shorter-chain omega-3 fatty acid (derived from vegetable sources such as flaxseed oil and walnuts), it is important to point out that the two populations with the lowest rates of heart attack have a relatively high intake of alpha-linolenic acid: the Japanese who inhabit Kohama Island and the inhabitants of Crete.26,27 Typically, Cretans have a threefold higher serum concentration of alpha-linolenic acid than members of other European countries, owing to their frequent consumption of walnuts and the vegetable purslane.26 Of course, another important dietary factor in both the Kohamans and the Cretans is their use of oleic-acid-containing oils. However, although the oleic acid content of the diet offers some degree of protection, the rates of heart attack among the Kohamans and Cretans are much lower than those in populations that consume only oleic acid sources and little alpha-linolenic acid. The intake of alpha-linolenic acid is viewed as a more significant protective factor than oleic acid.

Nuts and Seeds

Higher consumption of nuts and seeds has been shown to significantly reduce the risk of CVD in large population-based studies, including the Nurses Health Study, the Iowa Health Study, and the Physicians Health Study.28Researchers estimate that substituting nuts for an equivalent amount of carbohydrates in an average diet resulted in a 30% reduction in heart disease risk. Researchers calculated an even more impressive risk reduction, 45%, when fat from nuts was substituted for saturated fats (found primarily in meat and dairy products). Nuts have a cholesterol-lowering effect, which partly explains this benefit, but they are also a rich source of arginine. By increasing nitric oxide levels, arginine may help to improve blood flow, reduce blood clot formation, and improve blood fluidity (the blood becomes less viscous and therefore flows through blood vessels more easily).

Walnuts appear to be especially beneficial because they are also a rich source of both antioxidants and alpha-linolenic acid. In one study, men and women with high cholesterol were randomly assigned to a cholesterol-lowering Mediterranean diet or to a diet of similar energy and fat content in which walnuts replaced approximately 32% of the energy from monounsaturated fat (olive oil). Participants followed each diet for four weeks. Compared with the Mediterranean diet, the walnut diet improved endothelial cell function (it increased endothelium-dependent vasodilation and reduced levels of vascular cell adhesion molecule-1). The walnut diet also significantly reduced total cholesterol (–4.4%) and LDL (–6.4%).29

Vegetables, Fruits, and Red Wine

An important contributor to the benefits noted with the Mediterranean diet is the focus on carotenoid- and flavonoid-rich fruits, vegetables, and beverages (e.g., red wine). Numerous population studies have repeatedly demonstrated that a higher intake of dietary antioxidants significantly reduces the risk of heart disease and stroke. Higher blood levels of antioxidant nutrients are also associated with lower levels of hsCRP.30 The importance of antioxidant intake in the prevention and treatment of CAD is discussed further below.

Two valuable sources of antioxidants in the Mediterranean diet are tomato products and red wine. Tomatoes are a rich source of the carotene lycopene. In large clinical studies evaluating the relationship between carotene status and heart attack, lycopene but not beta-carotene was shown to be protective. Lycopene exerts greater antioxidant activity compared with beta-carotene in general but specifically against LDL oxidation.31

The cardiovascular protection offered by red wine is popularly referred to as the “French paradox.” The French consume more saturated fat than people in the United States and the United Kingdom yet have a lower incidence of heart disease; red wine consumption has been suggested as the reason. Presumably this protection is the result of flavonoids and other polyphenols in red wine that protect against oxidative damage to LDL and help to reduce levels of inflammatory mediators.16,32 However, moderate alcohol consumption alone has also been shown to be protective in some studies, exerting positive effects on ratios of HDL to LDL and CRP as well as levels of fibrinogen (although red wine typically has the most significant effects).33 Importantly, the effects of alcohol on CVD risk, morbidity, and total mortality are counterbalanced by alcohol’s addictive and psychological effects; excessive alcohol consumption results in depletion of glutathione and an increased risk of colon cancer.

The major benefits of red wine consumption in protecting against CVD may ultimately be the effects that the polyphenols have on improving the function of the cells that line the blood vessels.34 The consumption of green tea and dark chocolate, like that of red wine, has also been shown in population studies to be associated with a reduced risk for CVD. As with red wine, much of the benefit from green tea and chocolate may be the result of several different mechanisms, including improving endothelial cell function.35

Other foods and beverages rich in antioxidant content have shown benefit in fighting atherosclerosis. Pomegranate (Punica granatum) juice appears to be particularly useful. It is remarkably rich in antioxidants, such as soluble polyphenols, tannins, and anthocyanins. Animal research has indicated that components of pomegranate juice can retard atherosclerosis, reduce plaque formation, and improve arterial health. Human clinical studies have supported the role of pomegranate juice (240 ml/day) in benefiting heart health.3638 An important caveat with pomegranate juice or any beneficial fruit juice (blueberry, cherry, grape, etc.) is that it can be a significant source of simple sugars, so consume in moderation. Keep the serving size no greater than 4 to 6 fl oz and drink it no more than twice per day.

Lowering Cholesterol Levels

Lowering total cholesterol as well as LDL and triglycerides is clearly associated with reducing CVD risk. For more information, see the chapter “High Cholesterol and/or Triglycerides.”


Dietary antioxidant nutrients such as lycopene, lutein, selenium, vitamin E, and vitamin C have been shown in population-based studies to offer significant protection against the development of CVD. Fats and cholesterol are particularly susceptible to free radical damage. When damaged, fats and cholesterol form lipid peroxides and oxidized cholesterol, which can then damage the artery walls and accelerate the progression of atherosclerosis. Antioxidants block the formation of these damaging compounds.

Although diets rich in antioxidant nutrients have consistently shown tremendous protection against CVD, clinical trials using antioxidant vitamins and minerals have produced inconsistent results.39,40 This failure may be due to several factors, most importantly the fact that the human antioxidant system is a complex system of interacting components. It is unlikely that any single antioxidant would be proven to be effective, especially in the absence of a supporting cast. Most antioxidants require some sort of “partner” antioxidant, allowing them to work more efficiently. The most salient example of this is the partnership between the two primary antioxidants in the human body, vitamins C and E. Vitamin C is an aqueous-phase antioxidant, while vitamin E is a lipid-phase antioxidant. Although some studies have shown that supplementation with these nutrients reduces atherosclerotic lesions, more protection is probably required to ensure optimal effect.41

In addition to vitamin C, vitamin E also requires selenium and CoQ10 to work efficiently (as discussed in more detail later). Another shortcoming of many of the studies on antioxidant nutrients is the lack of consideration given to the importance of phytochemicals and plant-derived antioxidants, which, in addition to having benefits on their own, are well known to potentiate the activities of vitamin and mineral antioxidants. Phytochemicals such as carotenes (especially lycopene and lutein) and flavonoids are especially important in fighting free radical damage. Most scientific reviews on antioxidant supplements devote significant attention to studies of beta-carotene, because they have involved more than 70,000 subjects, but such studies fail to differentiate the facts that synthetic beta-carotene was used and that beta-carotene is of little importance in protecting against LDL oxidation. (Unlike lycopene and lutein, beta-carotene does not become incorporated into LDL effectively, although it may help protect the endothelium.)

Lutein may turn out to be the most significant carotene in the battle against atherosclerosis. On the basis of analysis of the different subtypes of LDL, lycopene, beta-carotene, and cryptoxanthin were mainly located in the larger, less dense LDL particles, whereas lutein and zeaxanthin tended to be found in the smaller, denser LDL particles. Because the smaller, denser LDL subtype is more easily oxidized, lutein and zeaxanthin are particularly important in protecting against damage to LDL.42

Other vitamins and minerals may also be important in supporting the effectiveness of antioxidants. Taking a multivitamin/multimineral supplement seems appropriate. In one double-blind study, CRP levels were significantly lower in the multivitamin group than in the placebo group, with the reduction in CRP levels most evident in patients who had elevated levels (equal to or greater than 1 mg/L) at baseline.43Researchers found that serum vitamin B6and vitamin C levels were inversely associated with CRP level.

Vitamin E

Although clinical studies have shown inconsistent effects, it is clear that vitamin E does play a role in the protection against oxidation of LDL because of its ability to be easily incorporated into the LDL molecule. Furthermore, there is a clear-cut dosage effect (i.e., the higher the dosage of vitamin E, the greater the degree of protection against oxidative damage to LDL). Although dosages as low as 25 mg were originally shown to offer some protection, it appears that doses greater than 400 IU are required to produce clinically significant effects.4446 However, what is probably of greatest importance is to use vitamin E within the context of a comprehensive dietary and supplementation strategy to boost antioxidant status.

Vitamin E supplementation may offer help in protecting against heart disease and strokes because of its ability to do the following:

• Reduce LDL oxidation and increase plasma LDL breakdown

• Inhibit excessive platelet aggregation

• Increase HDL levels

• Reduce CRP levels

• Improve endothelial cell function

• Improve insulin sensitivity

Two early large-scale studies with relatively low dosages of vitamin E supplementation demonstrated a significant reduction in the risk of heart attack or stroke. The Nurses Health Study of 87,245 female health care professionals concluded that those who took 100 IU of vitamin E daily for more than two years had a 41% lower risk of heart disease compared with nonusers of vitamin E supplements.47 The Physicians Health Study of 39,910 male health care professionals found similar results: a 37% lower risk of heart disease with the intake of more than 30 IU of supplemental vitamin E daily.48 Subsequent studies, however, have been inconsistent in showing any benefit at all. In fact, in some studies vitamin E supplementation was shown to be associated with an increased risk for CVD death.49 Again, an important consideration is that vitamin E has a very narrow antioxidant effect and may not be effective unless paired with complementary antioxidants.

Some of the disappointing results may also have been due to the choice of synthetic vitamin E (D,L-alpha tocopherol) in one of the large studies vs. the more active natural form (D-alpha tocopherol). There is also the problem of the interference by statin drugs in vitamin E and CoQ10 metabolism; this interference increases the need for both compounds. Vitamin E and CoQ10 work synergistically, and each is required for the regeneration of the other. For example, CoQ10 is present in the blood in both oxidized (inactive) and reduced (active) form. During times of increased oxidative stress or low vitamin E levels, more CoQ10 will be converted to its oxidized form. Thus, by providing higher levels of vitamin E, the biological activity and function of CoQ10 are enhanced, and vice versa. Several studies in humans and animals have shown that the combination of vitamin E and CoQ10 works better than either alone. For example, in a study of baboons, where supplementation with vitamin E alone reduced CRP levels, co-supplementation with CoQ10 significantly enhanced this effect of vitamin E. Similar results have been seen in other animal studies of other factors associated with atherosclerosis, including LDL oxidation and lipid peroxide content within the aorta.5052

In addition to CoQ10, vitamin E also requires adequate selenium status for optimal antioxidant effects. Selenium functions primarily as a component of the antioxidant enzyme glutathione peroxidase. This enzyme works closely with vitamin E to prevent free radical damage to cell membranes. Studies looking only at vitamin E’s ability to reduce cancer and heart disease are often faulty because they fail to factor in the critical partnership between selenium and vitamin E, not to mention the interrelationship between vitamin E and CoQ10. Several studies have clearly demonstrated that low selenium status is significantly associated with coronary artery disease.53,54 Failure to co-supplement with selenium as well as vitamin C and CoQ10 may be a major reason for the inconsistent results in intervention trials with vitamin E supplementation alone.

Finally, when you are taking vitamin E, it is important to take mixed tocopherols (that is, all the forms of vitamin E found in food) rather than simply d-alpha-tocopherol.

Vitamin C

Vitamin C works as an antioxidant in aqueous (watery) environments in the body, both outside and inside cells. It is the first line of antioxidant protection in the body. Its primary antioxidant partner is vitamin E, as this antioxidant is fat-soluble. Along with CoQ10, vitamin C is also responsible for regenerating vitamin E after it has been oxidized in the body, thus potentiating the antioxidant benefits of vitamin E.55Vitamin C works along with antioxidant enzymes such as glutathione peroxidase, catalase, and superoxide dismutase as well. Vitamin C has been shown to be extremely effective in preventing LDL from being oxidized, even in smokers.56 Vitamin C and E supplementation, 500 mg and 272 IU per day respectively for six years, has been shown to reduce the progression of carotid atherosclerosis by 53% in men and 14% in women.57

A high dietary intake of vitamin C has been shown to significantly reduce the risk of death from heart attacks and strokes, as well as all other causes, including cancer, in numerous population studies. One of the most detailed studies analyzed the vitamin C intake of 11,348 adults over five years and divided them into three groups: (1) less than 50 mg dietary intake per day, (2) more than 50 mg per day dietary intake with no vitamin C supplementation, and (3) more than 50 mg dietary intake plus vitamin C supplementation (estimated to be equal to or greater than 300 mg).58 Analysis showed that the average death rate (for CVD and overall mortality) was up to 48% lower in the high-intake group than in the low-intake group. These differences correspond to an increase in longevity of five to seven years for men and one to three years for women.

Dozens of observational and clinical studies have shown that vitamin C levels correspond to total cholesterol and HDL.5961 In one of the best-designed studies, it was shown that the higher the vitamin C content of the blood, the lower the total cholesterol and triglycerides and the higher the HDL.61 The benefits for HDL were particularly impressive. For each 0.5 mg/dl increase in vitamin C content of the blood, there was an increase in HDL of 14.9 mg/dl in women and 2.1 mg/dl in men. This study is significant in having demonstrated that the association of vitamin C and HDL levels persists even in well-nourished individuals with normal serum levels of vitamin C who supplement their diets with additional vitamin C.

In summary, vitamin C lowers the risk of CVD by doing the following:62,63

• Acting as an antioxidant

• Strengthening the collagen structures of the arteries

• Lowering total cholesterol, Lp(a), and blood pressure

• Raising HDL levels

• Inhibiting platelet aggregation

• Promoting the breakdown of fibrin (a component of blood clots and arterial plaque)

• Reducing markers of inflammation

• Regenerating vitamin E

Grape Seed and Pine Bark Extracts

One of the most beneficial groups of plant flavonoids is the procyanidolic oligomers (PCOs). Although PCOs exist in many plants as well as in red wine, commercially available sources of PCO include extracts from grape seeds and the bark of the maritime (Landes) pine. These extracts offer protection through several different mechanisms, including their antioxidant activity and effects on the endothelial cells that line blood vessels.64,65

Miscellaneous Risk Factors

Platelet Aggregation

Excessive platelet aggregation, or clumping, is another risk factor for heart disease and stroke. Once platelets aggregate, they release potent compounds that dramatically promote the formation of atherosclerotic plaque, or they can form a clot that can lodge in small arteries and produce a heart attack or stroke. The adhesiveness of platelets is determined largely by the type of fats in the diet and the level of antioxidants. While saturated fats and cholesterol increase platelet aggregation, omega-3 oils (both short-chain and long-chain) and monounsaturated fats have the opposite effect.6668

In addition to the monounsaturated and omega-3 fatty acids, antioxidant nutrients, and flavonoids, vitamin B6 also inhibits platelet aggregation and lowers blood pressure and homocysteine levels.69,70 In one study, the effect of vitamin B6 (pyridoxine HCl) supplementation on platelet aggregation, plasma lipids, and serum zinc levels was determined in 24 healthy male volunteers (19 to 24 years old) given either pyridoxine at a dosage of 5 mg/kg or a placebo for four weeks.69 Results demonstrated that pyridoxine inhibited platelet aggregation by 41% to 48%, while there was no change in the control group. Pyridoxine prolonged both bleeding and coagulation time but not over physiologic limits. It had no effect on platelet count. Pyridoxine was also shown to lower total plasma lipids and cholesterol levels considerably from pretreatment levels. Total plasma lipids were reduced from 593 to 519 mg/dl, and total cholesterol was reduced from 156 to 116 mg/dl. HDL increased from 37.9 to 48.6 mg/dl. Serum zinc levels increased from 96 to 138 mg/dl.

In another study, a significant inverse graded relation was observed between the serum level of an active form of vitamin B6—pyridoxal-5-phosphate (P5P)—and both CRP and fibrinogen.70 Low P5P concentrations were associated with a calculated 89% increase in CVD. These results provide clear evidence of the possible role of vitamin B6 supplementation in reducing the risk of atherosclerotic mortality.

Garlic preparations standardized for alliin content as well as garlic oil have also demonstrated inhibition of platelet aggregation. In one study, 120 patients with increased platelet aggregation were given either 900 mg per day of a dried garlic preparation containing 1.3% alliin or a placebo for four weeks.71 In the garlic group, spontaneous platelet aggregation disappeared, the microcirculation of the skin increased by 47.6%, plasma viscosity decreased by 3.2%, diastolic blood pressure dropped from an average of 74 to 67 mm Hg, and fasting blood glucose concentration dropped from an average of 89.4 to 79 mg/dl.


Fibrinogen is a component of blood clots and atherosclerotic plaque. Elevated fibrinogen levels are another clear risk factor for CVD. Early clinical studies stimulated detailed population-based investigations into the possible link between fibrinogen and CVD. The first such study was the Northwick Park Heart Study in the United Kingdom. This large study involved 1,510 men 40 to 64 years of age who were randomly recruited and tested for a range of clotting factors including fibrinogen. At the four-year follow-up, there was a stronger association between cardiovascular deaths and fibrinogen levels than that for cholesterol. This association has now been confirmed in at least five other large population-based studies.72

Natural therapies designed to promote the breakdown of fibrin (fibrinolysis) include exercise, omega-3 oils, niacin, garlic, and nattokinase. Nattokinase is a protein-digesting enzyme isolated from a fermented soy product called natto. Nattokinase has potent fibrinolytic and thrombolytic (clot-busting) activity that has shown significant potential in improving CVD.73 Typical dosage is 100 mg (2,000 FU) once or twice per day.

In addition, the Mediterranean diet alone significantly reduces fibrinogen and other markers of inflammation.74 Adherence to the Mediterranean diet was shown to be associated with a 20% lower CRP level, 17% lower another marker of inflammation (interleukin-6 level), 15% lower homocysteine level, and 6% lower fibrinogen level.


Homocysteine, an intermediate in the conversion of the amino acid methionine to cysteine, can damage the lining of arteries as well as the brain. If a person is functionally deficient in folic acid, vitamin B6, or vitamin B12, there will be an increase in homocysteine. Elevated homocysteine levels are an independent risk factor for heart attack, stroke, or peripheral vascular disease. Elevations in homocysteine are found in approximately 20 to 40% of patients with heart disease and are significantly associated with CVD.7578

Although folic acid supplementation (400 mg per day) alone can reduce homocysteine levels in many subjects, given the importance of vitamins B12 and B6 to proper homocysteine metabolism, all three should be used together. In one study the suboptimal levels of these nutrients in men with elevated homocysteine levels were 56.8%, 59.1%, and 25% for folic acid, vitamin B12, and vitamin B6, respectively, indicating that folic acid supplementation alone would not lower homocysteine levels in many cases.79 In other words, folic acid supplementation will lower homocysteine levels only if there are adequate levels of vitamins B12 and B6.

In 1998 the FDA mandated the fortification of food products with folic acid. Although homocysteine levels have decreased modestly since then, the effect on mortality has been minor at best.80 This indicates the importance of more aggressive supplementary measures to reduce homocysteine-associated cardiovascular risk and the need to address all three nutrients, not just one.

Type A Personality

Type A behavior is characterized by an extreme sense of time urgency, competitiveness, impatience, and aggressiveness. This behavior carries with it a twofold increase in CHD compared with non-type-A behavior.8183 Particularly damaging to the cardiovascular system is the regular expression of anger. In one study, the relationship between habitual anger as a coping style, especially anger expression, and serum lipid concentrations was examined in 86 healthy subjects.82 Habitual anger expression was measured on four scales: aggression, controlled affect, guilt, and social inhibition. A positive correlation between serum cholesterol level and aggression was found. The higher the aggression score, the higher the cholesterol level. A negative correlation was found between the ratio of LDL to HDL and controlled affect score—the greater the ability to control anger, the lower this ratio. In other words, those who learn to control anger experience a significant reduction in the risk for heart disease, while an unfavorable lipid profile is linked with a predominantly aggressive (hostile) anger coping style.

Anger expression also plays a role in CRP levels. In one study, greater anger and severity of depressive symptoms, separately and in combination with hostility, were significantly associated with elevations in CRP in apparently healthy men and women.83 Other mechanisms explaining the link between the emotions, personality, and CVD include increased cortisol secretion, endothelial dysfunction, hypertension, and increased platelet aggregation and fibrinogen levels.84

Ten Tips to Help You Improve Your Coping Strategies

1. Do not starve your emotional life. Foster meaningful relationships. Provide time to give and receive love in your life.

2. Learn to be a good listener. Allow the people in your life to really share their feelings and thoughts uninterruptedly. Empathize with them; put yourself in their shoes.

3. Do not try to talk over somebody. If you find yourself being interrupted, relax; do not try to outtalk the other person. If you are courteous and allow someone else to speak, eventually (unless the person is extremely rude) he or she will respond likewise. If not, explain that he or she is interrupting the communication process. You can do this only if you have been a good listener.

4. Avoid aggressive or passive behavior. Be assertive, but express your thoughts and feelings in a kind way to help improve relationships at work and at home.

5. Avoid excessive stress in your life as best you can by avoiding excessive work hours, poor nutrition, and inadequate rest. Get as much sleep as you can.

6. Avoid stimulants such as caffeine and nicotine. Stimulants promote the fight-or-flight response and tend to make people more irritable in the process.

7. Take time to build long-term health and success by performing stress-reduction techniques and deep breathing exercises.

8. Accept gracefully those things over which you have no control. Save your energy for those things that you can do something about.

9. Accept yourself. Remember that you are human and will make mistakes from which you can learn along the way.

10. Be more patient and tolerant of other people. Follow the golden rule.

Magnesium and Potassium Deficiency

Magnesium and potassium are absolutely essential to the proper functioning of the entire cardiovascular system. Their critical roles in preventing heart disease and strokes are now widely accepted. In addition, there is a substantial body of knowledge demonstrating that supplementation of magnesium, potassium, or both is effective in treating a wide range of cardiovascular disease, including angina, arrhythmias, congestive heart failure, and high blood pressure. In many of these applications, magnesium or potassium supplementation has been used for more than 50 years.

The average intake of magnesium by healthy adults in the United States ranges from 143 to 266 mg per day. This level is well below even the recommended daily intake (RDI) of 350 mg for men and 300 mg for women. Food choices are the main reason. Because magnesium occurs abundantly in whole foods, many nutritionists and dietitians assume that most Americans get enough magnesium in their diets. But most Americans are not eating whole, natural foods. They are consuming large quantities of processed foods. Because food processing removes a large portion of a food’s magnesium, most Americans are not getting the RDI for magnesium.

The best dietary sources of magnesium are tofu, legumes, seeds, nuts, whole grains, and green leafy vegetables. Fish, meat, milk, and most commonly eaten fruits are quite low in magnesium. Most Americans consume a low-magnesium diet because their diet is high in low-magnesium foods such as processed foods, meat, and dairy products.

People dying of heart attacks have been shown to have lower heart magnesium levels than people of the same age dying of other causes.85 Low magnesium levels contribute to atherosclerosis and CVD via many mechanisms including disruption of the protective factors within the lining of the arteries.86

Intravenous magnesium therapy has now emerged as a valued treatment measure in acute heart attack.8789 The major obstacle to its becoming the preferred method for saving a person’s life may be a financial interest. Magnesium is cheap compared with new high-tech, high-priced, genetically engineered drugs currently being promoted by drug companies. The treatment of heart attacks is big business in the United States: each year more than 1.5 million U.S. citizens experience one. Although many other parts of the world are now using magnesium therapy for heart attack because of its effectiveness, low cost, safety, and ease of administration, it plays second fiddle to the high-tech drugs in the United States.

During the past decade, eight well-designed studies involving more than 4,000 patients have demonstrated that intravenous magnesium supplementation during the first hour of admission to a hospital for acute heart attack reduces immediate and long-term complications as well as death rates. The beneficial effects of magnesium in heart attack relate to its ability to do the following:

• Improve energy production within the heart

• Dilate the coronary arteries, resulting in improved delivery of oxygen to the heart

• Reduce peripheral vascular resistance, resulting in reduced demand on the heart

• Inhibit platelets from aggregating and forming blood clots

• Reduce the size of the blockage

• Improve heart rate and arrhythmias

Vitamin D Deficiency

Data from a detailed study involving more than 8,000 subjects indicate that individuals with vitamin D levels below 30 ng/ml had at higher risk for CVD.90 Another study of more than 3,000 men and women found that those in the lowest quartile of vitamin D blood levels had a more than a twofold increase in CVD mortality.91

Preventing a Second Heart Attack

People who have experienced a heart attack or stroke and live through it are extremely likely to experience another. To prevent future cardiovascular events, the primary focus is, of course, still on controlling the major cardiac risk factors (e.g., high cholesterol levels, hypertension, cigarette smoking, diabetes, physical inactivity). But many physicians recommend low-dose aspirin (e.g., usually 325 mg per every other day or 81 mg—one “baby” aspirin—per day) to reduce the risk of a subsequent heart attack. However, there may be more effective alternatives, especially for those who cannot tolerate aspirin therapy. Furthermore, although it is becoming increasing popular to recommend dosages of aspirin lower than 325 mg every other day there are few (if any) data to support these lower dosage recommendations.

Aspirin Therapy

Let’s first take a look at studies with aspirin. It has been shown to decrease the risk of CVD events (heart attack or stroke) in people who have never had a heart attack as well as in those with a history of a heart attack. In the Physicians Health Study, there was a 44% reduction in the risk of a first heart attack with the use of 325 mg aspirin every other day. Since this study, three additional randomized trials including both men and women have shown aspirin to be effective in the prevention of a first heart attack. Among the 55,580 subjects, aspirin use was associated with a statistically significant 32% reduction in the risk of a first heart attack and a significant 15% reduction in the risk of all other important vascular events, but it had no significant effects on nonfatal stroke or death due to a heart attack or stroke. Evaluation of the data from the Physicians Health Study indicated that those with the highest CRP had the greatest decrease in risk, 55.7%, vs. 13.9% in those with the lowest CRP. It seems reasonable to reserve the use of aspirin as a primary prevention strategy for individuals with high CRP values.92

As of 2012 there have been seven prospective randomized placebo-controlled trials involving almost 15,000 survivors of heart attack that have examined the use of aspirin to reduce the incidence of recurrent heart attack and death due to a heart attack. These trials have used several doses of aspirin ranging from 325 to 1,500 mg per day, and enrolled patients at various intervals after the heart attack, ranging from four weeks to five years. None of the studies demonstrated a statistically significant reduction in mortality with aspirin use. However, when all the results from these studies were pooled, aspirin was shown to reduce the mortality rate from all causes as well as cardiovascular deaths. The mortality rate for all causes in the aspirin group was 5.8%, compared with 8.3% in the placebo group, indicating a reduction in mortality by 30% with aspirin.93,94

Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with a significant risk of peptic ulcer. However, most studies documenting the relative frequency of peptic ulcers as a consequence of NSAIDs have focused on the drugs’ use in the treatment of arthritis and headaches. The risk of gastrointestinal bleeding due to peptic ulcers has been evaluated for aspirin at daily dosages of 300, 150, and 75 mg. Essentially there is an increased risk of gastrointestinal bleeding due to peptic ulcers at all dosage levels. However, the dosage of 75 mg per day was associated with a lower risk, a 2.3-fold increased risk of ulcers compared with 3.9-fold increased risk at 300 mg per day and 3.2-fold risk at 150 mg per day.95

Because it is unknown whether 75 mg per day of aspirin is helpful in preventing a second heart attack or stroke, most physicians recommend at least 300 mg. To prevent death due to a stroke, the dosage necessary appears to be 900 mg. However, these dosage recommendations carry with them a significant risk for developing a peptic ulcer but may be appropriate for high-risk patients unwilling to adopt the natural approach.

Dietary Alternatives to Aspirin

The best approach to preventing subsequent heart attacks may not be low-dose aspirin, especially in aspirin-sensitive patients. The first alternative to aspirin to be examined here is one too often overlooked by many physicians—diet. Several studies have shown that dietary modifications not only are more effective in preventing recurrent heart attack than aspirin but also can reverse the blockage of clogged arteries. In addition to the studies with the Mediterranean diet, three famous studies deserve special mention. The first was the Lifestyle Heart Trial, conducted by Dean Ornish.96 In this study, subjects with heart disease were divided into a control group and an experimental group. The control group received regular medical care, while the experimental group members were asked to eat a low-fat vegetarian diet for at least one year. The diet included fruits, vegetables, grains, legumes, and soybean products. Subjects were allowed to consume as many calories as they wished. No animal products were allowed except egg whites and 1 cup of nonfat milk or yogurt per day. The diet contained approximately 10% fat, 15% to 20% protein, and 70% to 75% carbohydrates (predominantly complex carbohydrates from whole grains, legumes, and vegetables).

The experimental group members were also asked to perform stress reduction techniques such as breathing exercises, stretching exercises, meditation, imagery, and other relaxation techniques for an hour each day and to exercise for at least three hours each week. At the end of the year, the subjects in the experimental group showed significant overall regression of atherosclerosis of the coronary blood vessels. In contrast, subjects in the control group who were being treated with regular medical care and following the standard AHA diet actually showed progression of their disease. Ornish stated: “This finding suggests that conventional recommendations for patients with CHD (such as a 30% fat diet) are not sufficient to bring about regression in many patients.”

Two other famous studies showing that diet can prevent further heart attacks in patients suffering a first heart attack highlight the importance of omega-3 fatty acids and again show the ineffectiveness of the AHA’s dietary recommendations. As stated previously, numerous population studies have demonstrated that people who consume a diet rich in omega-3 oils from either fish or vegetable sources have a significantly reduced risk of developing heart disease. Two famous intervention trials upheld this protective effect. In the Dietary and Reinfarction Trial (DART), it was only when the intake of omega-3 fatty acids (from fish) was increased that future heart attacks were reduced.97 In another study, the Lyon Diet Heart Study, increasing the intake of omega-3 fatty acids from plant sources (alpha-linolenic acid) was found to offer the same degree of protection as increased fish intake.98

Finally, we can’t emphasize enough that there are no side effects of a healthy diet comparable to the increased risk of ulcers and other problems from taking aspirin.

Other Considerations

Angiography, Coronary Artery Bypass Surgery, or Angioplasty?

A significant challenge for patients is weighing the benefits against the risks when they are referred for angiography, coronary artery bypass surgery, or angioplasty. As is fully discussed in the chapter “Angina,” these procedures are used far more frequently than is justified by objective evaluation of their appropriateness and efficacy. That chapter also gives advice for patient care when angiography, coronary artery bypass surgery, or angioplasty is unavoidable.

In one study, angiography performed on 205 consecutive patients showed an 82% accuracy in predicting heart disease, with a false-positive rate of 12% and a false-negative rate of 18%.

Earlobe Crease

The presence of a diagonal earlobe crease has been recognized as a sign of CVD since 1973. More than 30 studies have been reported in the medical literature. The earlobe is richly vascularized, and a decrease in blood flow over an extended period of time is believed to result in collapse of the vascular bed. This leads to a diagonal crease.99,100

In a study of 112 consecutive patients, the earlobe crease was highly correlated with demonstrable heart disease and less strongly with previous heart attack.99

The crease is seen more commonly with advancing age, until the age of 80, when the incidence drops dramatically. However, the association with heart disease is independent of age. Although the presence of an earlobe crease does not prove heart disease, it strongly suggests it, and examination of the earlobe is an easy screening procedure. The correlation does not hold with Asians, Native Americans, or children with Beckwith’s syndrome.100



• Atherosclerosis—hardening of the artery walls—is the underlying disease process in cardiovascular disease (CVD).

• Prevention of CVD involves reducing and, when possible, eliminating various risk factors.

• Cigarette smoking is perhaps the most important risk factor for CVD, as statistical evidence reveals smokers have a 70% greater risk of death from CVD than nonsmokers.

• The evidence overwhelmingly demonstrates that elevated cholesterol levels, especially elevations in LDL cholesterol, greatly increase the risk of death due to CVD.

• Physical activity and regular exercise protect against the development of CVD and also favorably modify other CVD risk factors including high blood pressure, blood lipid levels, insulin resistance, and obesity.

• High-sensitivity C-reactive protein, a blood marker that reflects different degrees of inflammation, has been identified as an independent risk factor for coronary artery disease.

• One of the most important aspects of the Mediterranean diet may be the combination of olive oil (a source of monounsaturated fats and antioxidants) and the intake of omega-3 fatty acids.

• Higher consumption of nuts and seeds has been shown to significantly reduce the risk of CVD in large population-based studies including the Nurses Health Study, the Iowa Health Study, and the Physicians Health Study.

• Dietary antioxidant nutrients such as lycopene, lutein, selenium, vitamin E, and vitamin C have been shown in population-based studies to offer significant protection against the development of CVD.

• Several studies have shown that dietary modifications not only are more effective in preventing recurrent heart attack than aspirin but also can reverse the blockage of clogged arteries.

• The presence of a diagonal earlobe crease has been recognized as a sign of CVD since 1973.



There is little doubt that in most cases atherosclerosis is directly related to diet and lifestyle. Treatment and prevention include reducing all known risk factors. In particular, it is important to work with your physician in identifying risk factors via laboratory evaluation of such factors as cholesterol, triglyceride, and CRP levels.


• Do not smoke.

• Achieve and maintain ideal body weight.

• Exercise on a regular basis.


• Follow the dietary guidelines given in the chapter “A Health-Promoting Diet.” Specifically, it is important to do the following:

  images Eat less saturated fat and cholesterol by reducing or eliminating the amounts of animal products in the diet.

  images Increase consumption of fiber-rich plant foods (fruits, vegetables, grains, legumes, nuts, and seeds).

  images Increase consumption of monounsaturated fats (e.g., nuts, seeds, and olive oil) and omega-3 fatty acids.

  images Follow a low-glycemic diet.

Nutritional Supplements

• Take a high-potency multivitamin and mineral formula according to the guidelines given in the chapter “Supplementary Measures.”

• Key individual nutrients:

  images Vitamin C: 250 to 500 mg one to three times per day

  images Vitamin E (mixed tocopherols): 100 to 200 IU per day

  images Vitamin D: 2,000 to 4,000 IU per day (ideally, measure blood levels and adjust dosage accordingly)

  images Vitamin B6: 25 to 50 mg per day

  images Folic acid: 800 mcg per day

  images Vitamin B12: 800 mcg per day

  images Magnesium: 250 to 400 mg per day

  images Fish oils: minimum 1,000 mg EPA + DHA per day

  images One of the following:

  – Grape seed extract (> 95% procyanidolic oligomers): 100 to 300 mg per day

  – Pine bark extract (> 95% procyanidolic oligomers): 100 to 300 mg per day

  – Some other flavonoid-rich extract with a similar flavonoid content, super greens formula, or other plant-based antioxidant that can provide an oxygen radical absorption capacity (ORAC) of 3,000 to 6,000 units or higher per day

  images Consider:

  – Nattokinase: 100 mg (2,000 FU) per day