Diet and nutritional issues play an important role in the primary and secondary prevention of coronary heart disease (CHD). Atherogenic diet, sedentary lifestyle, and weight gain can lead to both abnormal lipid and metabolic profiles as well as increased CHD risk. Adoption of a healthy lifestyle has beneficial effects on the lipid profile and is a crucial part of the treatment of individuals who have multiple metabolic risk factors (“the metabolic syndrome”). Moreover, data on the value of diet and lifestyle in reducing oxidant stress, thrombotic tendencies, chronic inflammation, and ischemic sudden death continue to emerge.

The American Heart Association’s (AHA) recommended population or “healthy” diet focuses on healthy eating patterns and foods. It recommends an overall healthy eating pattern with general advice that should help physicians to counsel on obesity, hypertension, and hypercholesterolemia. For individuals who have medical problems that necessitate consumption of a therapeutic cardiovascular diet, consultation with a dietitian for medical nutrition therapy is recommended for guidance in making the necessary lifestyle changes. To reduce levels of low-density lipoprotein cholesterol (LDL-C), the earlier AHA Step II diet restricted saturated fatty acids to less than 7% of energy and dietary cholesterol to less than 200 mg/d. The current AHA dietary module to reduce LDL-C preserves this recommendation and also recommends a reduction in trans fatty acids (TFAs). For individuals with multiple metabolic risk factors and obesity, treatment begins with caloric restriction and increased energy expenditure. For those with elevated blood pressure, a low-sodium regimen with increased emphasis on fruits and vegetables, nonfat dairy products, and weight reduction, if needed, is recommended.

The response to diet is variable and increasingly is shown to be genetically based. Therapeutic diets that reduce risk factors must be targeted to the specific characteristics of the individual (e.g., high LDL-C level, metabolic syndrome, hypertension). These individual characteristics may also underlie individual responsiveness to diet.

Understanding the response of the individual to various dietary components is useful, because some people may use the therapeutic diet to reach their LDL-C goal or reduce their need for medication to reach LDL-C goals. The response of LDL-C to dietary cholesterol is highly variable. People with combined forms of hyperlipidemia may be the most sensitive to diet. Dietary options such as plant sterol and stanol esters taken as margarines reduce cholesterol absorption significantly and can reduce LDL-C by 10% or more. Most saturated fats raise blood cholesterol, although stearic acid is an important exception. It is converted to oleic acid and is essentially neutral in lowering blood cholesterol. Because saturated fats play a major role in raising LDL-C, restriction of saturated fats along with weight control are the hallmarks of effective cholesterol-lowering diets. Other factors are important. TFAs, when consumed in high amounts, can raise LDL-C, lower high-density lipoprotein
cholesterol (HDL-C) and lipoprotein (a) [Lp(a)]. Sources high in TFAs, such as hydrogenated vegetable oils in stick margarine, cookies, biscuits, and cakes, should be avoided. Butter contains cholesterol and saturated fat and is cholesterol raising compared with soft margarine. Therapeutic diets should be low in both saturated fatty acids and TFAs.

Mediterranean-style diets have proven to be both attainable and effective in reducing health risks over the long term. The use of monounsaturated fats such as canola and olive oil in place of saturated fats in this kind of diet is especially beneficial in those with metabolic syndrome or diabetes. A diet with unsaturated fats does not lower HDL-C as much as when additional carbohydrate is used to lower saturated fat intake. Regardless of the fats used, calories must be counted as excess calories—unsaturated or not—can lead to weight gain, higher triglycerides (TG) and lower HDL-C. Reducing excess body weight can be a crucial factor in improving lipid profile. The addition of regular exercise to changes in diet can be particularly beneficial in helping a patient maintain weight loss. Recent data suggest that omega-3 fatty acids play a cardioprotective role. Marine sources of omega-3 fatty acids appear to reduce cardiovascular events by a nonlipid mechanism, most likely anti-arrhythmic in nature. Plant sources of omega 3-fatty acids rich in linolenic acid as seen in canola and safflower oils, English walnuts, and flaxseed may also contribute increased omega-3 fatty acid blood levels and reduced cardiac events.

Alone or in combination, vitamins cannot be recommended for reduction of cardiovascular risk. Indeed, mega-vitamin combinations may interfere with the beneficial action of niacin on HDL-C and angiographic progression. Diets that emphasize sources of antioxidants in fruits, vegetables, nuts, and whole-grain products are recommended.

The contemporary practice of preventive cardiology requires an understanding of diet and lifestyle prescriptions both in the prevention and treatment of CHD. An essential component is restriction of fatty acids that raise LDL-C. Epidemiologic, clinical trial, and nonhuman primate evidence demonstrate a consistent relationship between increased intakes of saturated dietary fat, elevated blood cholesterol, and CHD (1). Therapeutic diets that require additional LDL-C lowering can emphasize not only restriction of dietary saturated fat, but also sources of TFA and dietary cholesterol. The use of plant sterol/stanols and soluble fiber can result in even more LDL-C lowering. These strategies may permit LDL-C goals to be realized without starting or adding LDL-C–lowering medication.

In addition, the development of atherogenic dyslipidemia characterized by high TG, low HDL-C and small, dense LDL-C (2) requires a specific focus on improving the atherogenic
diet, sedentary behaviors, and weight gain associated with this pattern. For individuals with impaired glucose tolerance, an important component of the metabolic syndrome, the prescription of lifestyle change that embraces a healthy diet, regular exercise, and weight loss may be particularly effective in preventing the progression to diabetes and the increased CHD risk that this entails (3,4). A recent evidence-based review of popular diets for cardiovascular disease (CVD) felt that there was a consistent basic science and clinical trial base to support the benefit of the Mediterranean-style diet for cardioprotection (5). Therapeutic diets and associated preventive measures such as weight reduction and/or smoking cessation have resulted in significant reductions in total mortality (6), CHD death (7,8), angiographic progression (9,10), and angina (11). Careful reviews of clinical trials and diets (5,12) emphasize the key role of omega 3 fatty acids in improving CHD survival in high-risk populations. Thus, a dietary prescription can be thought of as having these components:

Since pioneering experiments in rabbits almost a century ago, we have known that dietary cholesterol causes marked elevations of blood cholesterol in laboratory animals. In contrast, dietary cholesterol causes a variable response in blood cholesterol when tested in humans (30). If one looks only at tightly controlled studies, on average, the response of blood cholesterol to dietary cholesterol is approximately 10 mg/dL per 100 mg dietary cholesterol per 1,000 Kcal (31).