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(Circulation. 2002;106:3253.)
© 2002 American Heart Association, Inc.

ATP III Final Report

V. Adopting Healthful Lifestyle Habits to Lower LDL Cholesterol and Reduce CHD Risk

	1. Population approach: promoting a base of healthy life habits

Top 1. Population approach:... 2. General approach to... 3. Components of the... 4. Management of the... 5. Practical approach to... 6. Improving patient adherence...

 
NCEP advocates a two-pronged approach for reducing CHD risk: the population approach and the clinical strategy. The two are closely linked. The population approach, which is outlined in the 1990 report of the Population Panel,^5,6 is designed to lower risk in the whole population through adoption of healthy life habits including a healthy diet, weight control, and increased physical activity. The clinical strategy is described in the ATP reports. This section summarizes the population approach and connects it to the clinical strategy. The clinical management team must recognize that they are an integral part of the population approach and contribute to it by providing education and guidance to the patient with high serum cholesterol and the patient's family.

The health community has provided the American public with consistent messages on cardiovascular risk reduction for the past four decades. These messages have encouraged avoidance or cessation of cigarette smoking, reduction of intakes of saturated fats and cholesterol, achieving and maintaining a healthy body weight, regular physical activity, and routine medical check-ups for blood pressure and cholesterol. Table V.1-1 (derived from the Healthy People 2010 publication)⁶²⁰ reports the current status of the U.S. population on various healthy lifestyle habits and compares it with the goals for 2010.

View this table: [in this window] [in a new window]   Table V.1-1. Status Report on Healthy Lifestyle Habits: Healthy People 2010

Although progress has been made, it is clear that much more is needed to bring about the changes required to achieve the goals for 2010. The physician has an important role to play in this effort to help attain these goals.

The NHLBI, American Heart Association, and other organizations have mounted a major effort to reduce risk factors for CHD in the United States. Not only is there continuing research on improved methods for risk reduction, but national educational programs have also been put into effect. Table V.1-2 lists some of the Web sites of the programs sponsored by the U.S. Government.

View this table: [in this window] [in a new window]   Table V.1-2. Government-Sponsored Web Sites for Public Information: An Effective Way to Implement the Public Health Approach

Physicians and other health professionals have the opportunity to implement the public health and clinical approaches to risk reduction through interaction with patients and their families. Even in persons who are not candidates for clinical management of high serum cholesterol, control of other risk factors and preventive efforts convey the broader public health message to the patient. The physician's advice is valued and considered more credible than mass media or non-targeted educational campaigns. The physician can affect the public health arena in many ways. Table V.1-3 compares the role of the physician and other health professionals in the implementation of the public health approach with their role in the clinical management of risk factors through lifestyle changes.

View this table: [in this window] [in a new window]   Table V.1-3. The Role of the Physician and Other Health Care Professionals in Implementing the Population and Clinical Approaches to Lifestyle Modification

	2. General approach to therapeutic lifestyle changes (TLC)

Top 1. Population approach:... 2. General approach to... 3. Components of the... 4. Management of the... 5. Practical approach to... 6. Improving patient adherence...

 
ATP III recommends a multifactorial lifestyle approach to reducing risk for CHD. This approach is designated therapeutic lifestyle changes (TLC) and includes the following components (see Table V.2-1):

View this table: [in this window] [in a new window]   Table V.2-1. Essential Components of Therapeutic Lifestyle Changes (TLC)

• Reduced intakes of saturated fats and cholesterol
  
• Therapeutic dietary options for enhancing LDL lowering (plant stanols/sterols and increased viscous [soluble] fiber)
  
• Weight reduction
  
• Increased regular physical activity
  

Reduced intakes of saturated fats and cholesterol and other therapeutic dietary options for LDL-lowering (plant stanols/sterols and increased viscous fiber) are introduced first for the purpose of achieving the LDL cholesterol goal. After maximum reduction of LDL cholesterol is achieved with dietary therapy, emphasis shifts to management of the metabolic syndrome and its associated lipid risk factors (elevated triglycerides and low HDL cholesterol). A high proportion of patients with the metabolic syndrome are overweight/obese and sedentary; for them, weight reduction therapy and physical activity guidance is required to obtain further CHD risk reduction beyond that achieved by LDL lowering. At all stages of dietary therapy, physicians are encouraged to refer patients to registered dietitians or other qualified nutritionists for medical nutrition therapy, which is the term for the nutrition intervention and guidance provided by a nutrition professional.

ATP III recommendations for ranges of other macronutrient intakes in the TLC Diet are given in Table V.2-2. Note that the recommendation for total fat ranges from 25 percent to 35 percent of total calories. To improve overall health, ATP III's lifestyle therapies generally contain the recommendations embodied in the Dietary Guidelines for Americans (2000).²⁴¹

View this table: [in this window] [in a new window]   Table V.2-2. Macronutrient Recommendations for the TLC Diet

The overall composition of the TLC Diet is consistent with the recommendations of the Dietary Guidelines for Americans (2000) (Table V.2-3). The dietary principles delineated in the Dietary Guidelines need not and should not be sacrificed for the purpose of LDL lowering. Furthermore, adherence to Dietary Guidelines recommendations should contribute to a reduction in risk beyond LDL lowering.

View this table: [in this window] [in a new window]   Table V.2-3. Dietary Guidelines for Americans (2000)241

Figure V.2-1 presents one model illustrating the general approach to dietary therapy.

View larger version (17K): [in this window] [in a new window]   Figure V.2-1. A Model of Steps in Therapeutic Lifestyle Changes (TLC)

During the first three months of dietary therapy, priority is given to lowering LDL cholesterol. In the first visit, the physician should address a few key questions and obtain an overall assessment of the individual's current life habits:

• Does the patient consume excess calories in the form of LDL-raising nutrients?
  
• Is the patient overweight or obese? Is abdominal obesity present?
  
• Is the patient physically active or inactive?
  
• If the patient is overweight/obese and/or physically inactive, is the metabolic syndrome present? (See Table II.6-1.)
  

To assess intakes of LDL-raising nutrients, the ATP III panel devised a brief Dietary CAGE that may be helpful (Table V.2-4). These questions are not a substitute for a systematic dietary assessment, which is usually carried out by a nutrition professional. CAGE questions can be used to identify the common food sources of LDL-raising nutrients—saturated fat and cholesterol—in the patient's diet. Also in the first visit, advice is given to begin moderate physical activity, but serious attempts to achieve weight loss can be delayed briefly to concentrate first on reducing intakes of LDL-raising nutrients. At any and every stage of dietary therapy, effective dietary modification will be facilitated by consultation with a registered dietitian or other qualified nutritionist for medical nutrition therapy. (Subsequently, the term nutrition professional will refer to a registered dietitian or qualified nutritionist.)

View this table: [in this window] [in a new window]   Table V.2-4. Dietary CAGE Questions for Assessment of Intakes of Saturated Fat and Cholesterol

After approximately 6 weeks, the physician should evaluate the LDL cholesterol response. If the LDL cholesterol goal has been achieved, or if progress in LDL lowering has occurred, dietary therapy should be continued. If the LDL goal is not achieved, the physician has several options to enhance LDL lowering. First, dietary instructions can be reexplained and reinforced. The assistance of a nutrition professional for more formal instruction and counseling (medical nutrition therapy) is especially valuable at this time. Second, therapeutic dietary options for LDL lowering (plant stanols/sterols and increased viscous fiber) will also enhance LDL lowering. Plant stanols/sterols are currently incorporated into special margarines, which are available directly to consumers. The stanol/sterol contents are listed on the food label. They may be available in other products in the future. Viscous fiber can be increased by emphasizing certain foods: cereal grains, fruits, vegetables, and dried beans, peas, and legumes (see Table V.2-5).

View this table: [in this window] [in a new window]   Table V.2-5. Food Sources of Viscous (Soluble) Fiber

After another 6 weeks, the response to dietary therapy should be evaluated. If the LDL cholesterol goal is achieved, the current intensity of dietary therapy should be maintained indefinitely. If the patient is approaching the LDL goal, consideration should be given to continuing dietary therapy before adding LDL-lowering drugs. If it appears unlikely that the LDL goal will be achieved with dietary therapy alone, drug therapy should be considered (see Section IV).

Thereafter, the metabolic syndrome, if present, becomes the target of therapy (see Section II). First-line therapy for the metabolic syndrome is weight control and increased physical activity. Again, referral to a nutrition professional for medical nutrition therapy to assist in weight reduction is recommended.

Finally, long-term monitoring for adherence to TLC is required. Revisits are indicated every 4-6 months during the first year of therapy and every 6-12 months in the long term. If a person is started on drug therapy, more frequent visits are advised.

The information shown in Table V.2-6 may be helpful for the physician both for dietary and lifestyle assessment and for guidance of the patient adopting TLC recommendations. The table is compiled from current ATP III dietary recommendations, Dietary Guidelines for Americans (2000),²⁴¹ Obesity Education Initiative (OEI) guidelines for weight reduction,^78,79 and the Surgeon General's Report on Physical Activity.²³⁸

View this table: [in this window] [in a new window]   Table V.2-6. Guide to Therapeutic Lifestyle Changes (TLC)

	3. Components of the TLC Diet

Top 1. Population approach:... 2. General approach to... 3. Components of the... 4. Management of the... 5. Practical approach to... 6. Improving patient adherence...

 
a. Major nutrient components
The major LDL-raising dietary constituents are saturated fat and cholesterol. A reduction in intakes of these components is the core of the TLC Diet. The scientific foundation for the relationship between high intakes of saturated fat and increased LDL levels dates back several decades and consists of several lines of evidence: observational studies, metabolic and controlled feeding studies, and clinical studies, including randomized clinical trials. These data have been reviewed in detail in previous reports of the NCEP,^1,2,5,6 the U.S. Dietary Guidelines Committees,²⁴¹ and the American Heart Association.³⁹³ The other major nutrients—unsaturated fats, protein, and carbohydrates—do not raise LDL cholesterol levels. In developing an LDL-lowering diet for ATP III, consideration was given not only to these long-established factors but also to new and emerging data that support the importance of the appropriate distribution of other nutrients that are related to cardiovascular health as well as general health. Therefore, the rationale for the recommendations for each component of the TLC diet will be described briefly.

1) Saturated fatty acids
Saturated fatty acids are a major dietary determinant of LDL cholesterol level.²⁴¹ The effects of saturated fatty acids on serum total cholesterol (and LDL cholesterol) levels have been studied extensively.⁶²² Several meta-analyses and reviews have been carried out to estimate the impact of saturated fatty acids on cholesterol levels.^623,624 These analyses indicate that for every 1 percent increase in calories from saturated fatty acids as a percent of total energy, the serum LDL cholesterol rises about 2 percent. Conversely, a 1 percent reduction in saturated fatty acids will reduce serum cholesterol by about 2 percent. Recent trials confirm the efficacy of diets low in saturated fatty acids for lowering LDL levels. For example, the DELTA Study⁶²⁵ investigated the effects of reducing dietary saturated fatty acids from 15 percent of total calories to 6.1 percent of total calories. On the diet low in saturated fatty acids, LDL cholesterol was reduced by 11 percent. Another study, beFIT,^626,627 tested effects of an NCEP therapeutic diet in individuals with hypercholesterolemia with and without hypertriglyceridemia. Compared to the participants' baseline diet, LDL cholesterol levels were reduced on the therapeutic diet by approximately 8 percent. Large-scale randomized controlled trials have been carried out to assess the safety of reduced intakes of saturated fatty acids and cholesterol in children and have found no evidence for compromised growth or development.^628,629

Evidence statements: There is a dose response relationship between saturated fatty acids and LDL cholesterol levels. Diets high in saturated fatty acids raise serum LDL cholesterol levels (A1). Reduction in intakes of saturated fatty acids lowers LDL cholesterol levels (A1, B1).

 

The beneficial effects of reducing saturated fatty acids and cholesterol in the diet can be enhanced by weight reduction in overweight persons. Several studies have shown that LDL cholesterol levels can be lowered through weight reduction in overweight persons.^78,79 And most important, as shown in the MRFIT study, weight reduction will enhance serum cholesterol lowering brought about by a reduction in intakes of saturated fatty acids and cholesterol.^630,631

Evidence statements: Weight reduction of even a few pounds will reduce LDL levels regardless of the nutrient composition of the weight loss diet (A2), but weight reduction achieved through a calorie-controlled diet low in saturated fatty acids and cholesterol will enhance and sustain LDL cholesterol lowering (A2). Recommendation: Weight loss through reduced caloric intake and increased levels of physical activity should be encouraged in all overweight persons. Prevention of weight gain also should be emphasized for all persons.

 

Epidemiological studies show that populations that consume high amounts of saturated fatty acids and cholesterol have a high risk for CHD.^19,632 The evidence that lowering serum cholesterol levels by decreasing intakes of saturated fatty acids reduces the risk for CHD has been demonstrated in the meta-analysis by Gordon.^409,410 This analysis included six robust dietary trials, in aggregate including 6,356 person-years of follow up. It showed that lowering serum cholesterol levels by reducing the intake of saturated fatty acids significantly decreased the incidence of CHD by 24 percent. There was also a trend toward a decrease in coronary mortality (21 percent) and total mortality (6 percent). No increase in non-CVD mortality was found.

The data from dietary trials, in combination with the results of controlled clinical trials with cholesterol-lowering medications,^455,633 document that reducing serum cholesterol and LDL cholesterol by diet alone or with pharmacological means will reduce CHD endpoints. The current American diet contains an average of about 11 percent of total calories as saturated fatty acids. The major sources of saturated fatty acids in the diet are high-fat dairy products (whole milk, cheese, butter, ice cream, and cream); high-fat meats; tropical oils such as palm oil, coconut oil, and palm kernel oil; and baked products and mixed dishes containing dairy fats, shortening, and tropical oils. To maximize LDL cholesterol lowering by reducing saturated fatty acid intake in the therapeutic diet, it will be necessary to lower intakes from the population mean intake of approximately 11 percent to <7 percent of total energy.

Evidence statements: High intakes of saturated fatty acids are associated with high population rates of CHD (C2). Reduction in intake of saturated fatty acids will reduce risk for CHD (A1, B1). Recommendation: The therapeutic diet to maximize LDL cholesterol lowering should contain less than 7 percent of total calories as saturated fatty acids.

 

2) Trans fatty acids
Trans fatty acids are those in which double bonds are in the trans configuration. They are generally produced by hydrogenation of vegetable oils but some are found naturally in animal fats. Substantial evidence from randomized clinical trials indicates that trans fatty acids raise LDL cholesterol levels, compared with unsaturated fatty acids.^634-646 These studies also show that when trans fatty acids are substituted for saturated fatty acids, HDL cholesterol levels are lower,⁶⁴⁷ with a dose response effect observed. Recent United States data show that the use of liquid vegetable oil or semiliquid margarine results in the most favorable total and LDL cholesterol levels and ratios of total cholesterol to HDL cholesterol, whereas the use of butter or stick margarine results in the worst lipid levels.⁶³⁴ In addition, evidence from some epidemiological cohort studies suggests that high intakes of trans fatty acids are associated with higher risk for CHD.^648-651 Whether this association is due to adverse effects of trans fatty acids on lipoproteins, to other adverse actions, or to confounding variables is uncertain.

The mean U.S. level of trans fatty acids intake is about 2.6 percent of total energy (compared with saturated fatty acids intake of 11 percent of energy). Major sources of trans fatty acids in the diet include products made from partially hydrogenated oils such as baked products including crackers, cookies, doughnuts, breads, and products like french fries or chicken fried in hydrogenated shortening. Animal sources including dairy products provide smaller amounts of trans fatty acids. Soft margarines, tub and liquid, and vegetable oil spreads have low amounts of trans fatty acids. Some margarines and spreads are now trans-fatty acid free. Some hydrogenation of vegetable oils is the primary technology currently used to provide form to food products, so that they can be eaten out of the hand, rather than with a spoon.

Evidence statements: Trans fatty acids raise serum LDL cholesterol levels (A2). Through this mechanism, higher intakes of trans fatty acids should increase risk for CHD. Prospective studies support an association between higher intakes of trans fatty acids and CHD incidence (C2). However, trans fatty acids are not classified as saturated fatty acids, nor are they included in the quantitative recommendations for saturated fatty acid intake of <7 percent of calories in the TLC Diet. Recommendation: Intakes of trans fatty acids should be kept low. The use of liquid vegetable oil, soft margarine, and trans fatty acid-free margarine are encouraged instead of butter, stick margarine, and shortening.

 

3) Dietary cholesterol
Dietary cholesterol causes marked hypercholesterolemia in many laboratory animals, including nonhuman primates. High intakes of cholesterol in humans, however, do not cause such a marked increase in serum cholesterol. Nonetheless, controlled metabolic studies in humans indicate that high cholesterol intakes raise LDL cholesterol levels. The degree of rise varies from person to person, as is true for all nutrients. Meta-analyses of studies done in controlled settings confirm the LDL-raising action of dietary cholesterol.^652,653 A recent meta-analysis showed that dietary cholesterol raises the ratio of total to HDL cholesterol, adversely affecting the serum cholesterol profile.⁶⁵⁴ A lesser effect of dietary cholesterol has been found in studies carried out in the outpatient setting;⁶⁵⁵ in this circumstance, failure to detect the full effect of dietary cholesterol is likely related to lack of tight metabolic control. On average, the response of serum cholesterol to dietary cholesterol as revealed in tightly controlled studies is approximately 10 mg/dL per 100 mg dietary cholesterol per 1000 kcal.^656,657

In the past 40 years, there has been a progressive decline in intakes of dietary cholesterol. This has been the result of decreased intakes of eggs, high-fat meat, and high-fat dairy products. This reduction in cholesterol intake, along with a substantial reduction in the proportion of calories from saturated fatty acids, corresponds with the decline in serum cholesterol levels that has occurred in the U.S. population over four decades.⁶⁵⁸ At present, the average U.S. daily consumption of cholesterol is 256 mg, higher for men (331 mg) than for women (213 mg).⁶⁵⁹ Eggs contribute about one-third of the cholesterol in the food supply and this fraction has increased somewhat in recent years.⁶⁶⁰ Other sources of dietary cholesterol include animal products, dairy, meats, poultry, and shellfish.

Some epidemiological data, namely the Western Electric Study, suggest dietary cholesterol increases heart disease risk independently of its effect on serum LDL cholesterol levels.⁶⁶¹ In contrast, data from two prospective cohort studies, the Nurses Health Study and the Health Professionals Study, found no significant association between frequency of reported egg consumption and CHD, except among diabetic women.⁶⁶²

Evidence statements: Higher intakes of dietary cholesterol raise serum LDL cholesterol levels in humans (A2, B1). Through this mechanism, higher intakes of dietary cholesterol should raise the risk for CHD. Reducing cholesterol intakes from high to low decreases serum LDL cholesterol in most persons (A2, B1). Recommendation: Less than 200 mg per day of cholesterol should be consumed in the TLC Diet to maximize the amount of LDL cholesterol lowering that can be achieved through reduction in dietary cholesterol.

 

4) Monounsaturated fatty acids
The most common form of monounsaturated fatty acids is oleic acid, which occurs in the cis form. Substitution of cis-monounsaturated fatty acids for saturated fatty acids results in a fall in LDL cholesterol levels.⁶²⁴ Moreover, substitution of monounsaturated fatty acids for saturated fatty acids results in little or no decrease in HDL cholesterol and does not increase triglycerides as occurs with very high intakes of carbohydrates (>60 percent of total energy).^624,663-665

Monounsaturated fatty acids—as part of a diet that is low in saturated fatty acids and cholesterol and rich in vegetables, fruits, and grain products—have received increased attention as being potentially beneficial for risk reduction because of their association with low rates of CHD in olive-oil consuming populations of the Mediterranean basin.^19,20,632 Despite epidemiological support for higher intakes of monounsaturated fatty acids, there are no controlled clinical trials that are designed to compare effects of monounsaturated and saturated fatty acids on CHD endpoints. This lack of data contrasts with several trials that replaced saturated fat with polyunsaturated fat.

Evidence statements: Monounsaturated fatty acids lower LDL cholesterol relative to saturated fatty acids (A2, B2). Monounsaturated fatty acids do not lower HDL cholesterol nor raise triglycerides (A2, B2). Evidence statement: Dietary patterns that are rich in monounsaturated fatty acids provided by plant sources and rich in fruits, vegetables, and whole grains and low in saturated fatty acids are associated with decreased CHD risk (C1). However, the benefits of replacement of saturated fatty acids with monounsaturated fatty acids has not been adequately tested in controlled clinical trials. Recommendations: Monounsaturated fatty acids are one form of unsaturated fatty acid that can replace saturated fatty acids. Intake of monounsaturated fatty acids can range up to 20 percent of total calories. Most monounsaturated fatty acids should be derived from vegetable sources, including plant oils and nuts.

 

5) Polyunsaturated fatty acids
Polyunsaturated fatty acids, consisting mainly of n-6 linoleic acid, reduce LDL cholesterol levels when substituted for saturated fatty acids. At high intakes, linoleic acid also can produce small reductions in HDL cholesterol and triglycerides, although these responses are variable. Compared to cis-monounsaturated fatty acids, polyunsaturated fatty acids often cause a slightly greater reduction in LDL cholesterol levels.⁶²⁴

Several controlled clinical trials have compared the effects of polyunsaturated fatty acids, as a replacement for saturated fatty acids, on coronary endpoints.⁶⁵⁷ Meta-analysis of trial results indicates that substitution of polyunsaturated fatty acids for saturated fatty acids reduces risk for CHD.^409,410,624 This positive result is supported by research in primates that indicates that polyunsaturated fatty acids are antiatherogenic when substituted for saturated fatty acids.⁶⁶⁶

Despite evidence of CHD risk reduction from polyunsaturated fatty acids, there are no large populations that have consumed large quantities of polyunsaturated fatty acids for long periods. Thus, high intakes have not been proven safe in large populations; this introduces a note of caution for recommending high intakes.

Evidence statements: Linoleic acid, a polyunsaturated fatty acid, reduces LDL cholesterol levels when substituted for saturated fatty acids in the diet (A1, B1). Polyunsaturated fatty acids can also cause small reductions in HDL cholesterol when compared with monounsaturated fatty acids (B2). Controlled clinical trials indicate that substitution of polyunsaturated fatty acids for saturated fatty acids reduces risk for CHD (A2, B2). Recommendations: Polyunsaturated fatty acids are one form of unsaturated fatty acids that can replace saturated fat. Most polyunsaturated fatty acids should be derived from liquid vegetable oils, semi-liquid margarines, and other margarines low in trans fatty acids. Intakes of polyunsaturated fat can range up to 10 percent of total calories.

 

6) Total fat
Among the fatty acids that make up the total fat in the diet, only saturated fatty acids and trans fatty acids raise LDL cholesterol levels.⁶⁵⁷ Thus, serum levels of LDL cholesterol are independent of intakes of total fat per se. ATP II^1,2 advised limiting total fat in Step I and Step II diets to 30 percent of calories primarily as a means of achieving lower intakes of saturated fatty acids. The focus of the dietary approach to reducing CHD risk then and now is on dietary fatty acids that raise LDL cholesterol concentrations.

Evidence statement: Unsaturated fatty acids do not raise LDL cholesterol concentrations when substituted for carbohydrates in the diet (A2, B2). Recommendation: It is not necessary to restrict total fat intake for the express purpose of reducing LDL cholesterol levels, provided saturated fatty acids are reduced to goal levels.

 

For many years, other public health groups have recommended low intakes of total fat in an effort to curtail obesity and to reduce the risk for some forms of cancer. These recommendations were based largely on experiments in laboratory animals and cross-cultural studies. Several short-term studies also suggest that higher fat intakes (>35 percent of calories) modify the body's metabolism in ways that favor fat accumulation.^667-672 However, isocaloric exchange of fat for carbohydrate does not produce weight gain over a period of many months.^673,674 Further, although some prospective studies have suggested a relationship between the percentage of dietary fat and obesity,^675,676 recent prospective studies (or meta-analysis of studies) have failed to detect a causative link between them.^677,678 Evidence related to these areas is reviewed in detail in the recent rationale report of the Dietary Guidelines for Americans (2000).²⁴¹

Studies in laboratory animals and cross-cultural studies have suggested a relationship between fat intake and risk for certain cancers.^679-682 Moreover, a major clinical trial is presently underway to determine whether low-fat diets will reduce risk for breast cancer in women; this trial is a component of the Women's Health Initiative⁶⁸³ and is scheduled to end in 2005.

Even so, recent prospective studies have not confirmed an association between fat intake and cancer.^684-687 Thus, a strong recommendation to reduce fat intake for the purpose of preventing cancer does not seem warranted at this time.²⁴¹

The Dietary Guidelines for Americans (2000)²⁴¹ noted that some investigators are concerned that recommendations that emphasize lower total fat intakes (<30 percent of energy) may have led to an overconsumption of carbohydrates, contributing to an increased prevalence of obesity. Moreover, very high intakes of carbohydrates (>60 percent of calories) in overweight/-obese persons can aggravate some of the risk factors of the metabolic syndrome.^{663,664,688-691} These latter responses have led some investigators to propose that populations with a high prevalence of insulin resistance and the metabolic syndrome should avoid very high-carbohydrate diets and should consume relatively more unsaturated fatty acids.⁶⁹²

Evidence statement: The percentage of total fat in the diet, independent of caloric intake, has not been documented to be related to body weight or risk for cancer in the general population.241 Short-term studies suggest that very high fat intakes (>35 percent of calories) modify metabolism in ways that could promote obesity (C2). On the other hand, very high carbohydrate intakes (>60 percent of calories) aggravate some of the lipid and nonlipid risk factors common in the metabolic syndrome (A2, B2, C2). Recommendations: Dietary fat recommendations should emphasize reduction in saturated fatty acids. Further, for persons with lipid disorders or the metabolic syndrome, extremes of total fat intake—either high or low—should be avoided. In such persons, total fat intakes should range from 25-35 percent of calories. For some persons with the metabolic syndrome, a total fat intake of 30-35 percent may reduce lipid and nonlipid risk factors.

 

7) Carbohydrate
When carbohydrates are substituted for saturated fatty acids, the fall in LDL cholesterol levels equals that with monounsaturated fatty acids. However, compared with monounsaturated fatty acids, substitution of carbohydrate for saturated fatty acids frequently causes a fall in HDL cholesterol and a rise in triglyceride.^{624,663,689,693} This effect apparently persists in the long term, as suggested by differences in population lipid levels in the presence of different habitual diets.^694,695 When carbohydrate is consumed along with high-fiber diets, however, the rise in triglycerides or fall in HDL cholesterol has been reported to be reduced.^693,696,697

Digestible carbohydrates include starches (complex carbohydrates) and sugar. Some foods, such as whole grains, vegetables, and some fruits, contain viscous fiber that helps to lower LDL cholesterol as well (see Table V.2-5). Sugars and starches occur naturally in many foods that also supply other important nutrients. Examples of these foods include fat-free and low-fat dairy products, fruits, some vegetables, breads, cereals, and grains. Inclusion of these foods helps provide daily recommended intakes of essential nutrients.²⁴¹

An old concept receiving recent attention is the "glycemic" potential of different foods. Glycemic index refers to the value obtained by feeding a carbohydrate load and measuring the level of blood glucose. Study of this factor is complicated because there is a wide range in the glycemic index for each group of foods, attributed to factors such as its form when eaten, the way it is processed, how it is chewed, how it is emptied from the stomach, and an individual's physiologic and metabolic responses.⁶⁹⁸ To date the glycemic index has not been widely accepted as a practical means by which to select specific carbohydrate-containing foods for dietary therapy.²⁴¹

Evidence statement: When carbohydrate is substituted for saturated fatty acids, LDL cholesterol levels fall (A2, B2). However, very high intakes of carbohydrate (>60 percent of total calories) are accompanied by a reduction in HDL cholesterol and a rise in triglyceride (B1, C1). These latter responses are sometimes reduced when carbohydate is consumed with viscous fiber (C2); however, it has not been demonstrated convincingly that viscous fiber can fully negate the triglyceride-raising or HDL-lowering actions of very high intakes of carbohydrates. Recommendation: Carbohydrate intakes should be limited to 60 percent of total calories. Lower intakes (e.g., 50 percent of calories) should be considered for persons with the metabolic syndrome who have elevated triglycerides or low HDL cholesterol. Regardless of intakes, most of the carbohydrate intake should come from grain products, especially whole grains, vegetables, fruits, and fat-free and low-fat dairy products.

 

8) Protein
Dietary protein in general has little effect on serum LDL cholesterol level or other lipoprotein fractions. However, substituting soy protein for animal protein has been reported to lower LDL cholesterol⁶⁹⁹ (see Section V.3.b.3). Plant sources of protein are predominantly legumes, dry beans, nuts, and, to a lesser extent, grain products and vegetables, which are low in saturated fats and cholesterol. Animal sources of protein that are lower in saturated fat and cholesterol include fat-free and low-fat dairy products, egg whites, fish, skinless poultry, and lean meats.

b. Additional dietary options for LDL lowering
1) Increasing viscous fiber in the diet
Recent reports indicate that viscous (soluble) forms of dietary fiber can reduce LDL cholesterol levels. In contrast, insoluble fiber does not significantly affect LDL cholesterol.⁷⁰⁰ On average, an increase in viscous fiber of 5-10 grams per day is accompanied by an approximately 5 percent reduction in LDL cholesterol.^701,702 In a meta-analysis of 67 trials related to oats, pectin, guar, and psyllium, a small but significant reduction in serum total and LDL cholesterol was noted for all sources of viscous fiber in ranges of 2-10 grams per day.⁷⁰³ Thus, at present, there is general agreement that viscous fiber (e.g., oats, guar, pectin, and psyllium) decreases serum cholesterol and LDL cholesterol. Because of the favorable effect of viscous fiber on LDL cholesterol levels, the ATP III panel recommends that the therapeutic diet be enriched by foods that provide a total of at least 5-10 grams of viscous fiber daily (see Table V.2-5). Even higher intakes of 10-25 grams per day can be beneficial.

Some investigators report that the consumption of viscous (soluble) fiber (provided by oats, barley, psyllium, pectin-rich fruit, and beans) produces a reduction in HDL cholesterol concentration.⁶⁹⁹ Other reviews report little, no, or inconsistent effect on HDL cholesterol.^704,705

Evidence statement: 5-10 grams of viscous fiber per day reduces LDL cholesterol levels by approximately 5 percent (A2, B1). Recommendation: The use of dietary sources of viscous fiber is a therapeutic option to enhance LDL cholesterol lowering.

 

2) Plant stanols/sterols
Recent studies have demonstrated that LDL-lowering effect of plant sterols, which are isolated from soybean and tall pine-tree oils. Plant sterols can be esterified to unsaturated fatty acids (creating sterol esters) to increase lipid solubility. Hydrogenating sterols produces plant stanols and, with esterification, stanol esters. The efficacy of plant sterols and plant stanols is considered to be comparable.^706,707 Because lipids are needed to solubilize stanol/sterol esters, they are usually available in commercial margarines. The presence of plant stanols/sterols is listed on the food label. When margarine products are used, persons must be advised to adjust caloric intake to account for the calories contained in the products.

Data show that plant-derived stanol/sterol esters at dosages of 2-3 g/day lower LDL-C levels by 6-15 percent with little or no change in HDL cholesterol or triglyceride levels.^707-713 The more recent among these studies indicate that maximal lowering of LDL cholesterol occurs at intakes of plant stanol/sterol esters of 2 g/day. LDL reductions also occur in individuals who have both hypercholesterolemia and type 2 diabetes⁷¹⁴ and in children with hypercholesterolemia.⁷¹⁵ A greater percent lowering of LDL occurs in older people than in younger people.⁷¹⁶ No studies have been conducted to determine the effect of plant stanols/sterols on CHD risk, although Law⁷¹⁶ has recently projected that their use should double the beneficial effect on CHD risk achieved by reducing dietary saturated fatty acids and cholesterol.

Plant sterols/stanols reduce absorption of dietary carotenoids, and decreased levels of plasma beta-carotene have been observed subsequent to consumption of margarines that contain either stanol ester or sterol ester.⁷⁰⁶ Whether carotenoid decreases are deleterious is unknown, but prudence calls for adhering to current recommendations for intakes of fruits and vegetables with consumption of plant stanols/sterols.

Evidence statement: Daily intakes of 2-3 grams per day of plant stanol/sterol esters will reduce LDL cholesterol by 6-15 percent (A2, B1). Recommendation: Plant stanol/sterol esters (2 g/day) are a therapeutic option to enhance LDL cholesterol lowering.

 

3) Soy protein
Soy protein included in a diet low in saturated fatty acids and cholesterol can lower levels of total cholesterol and LDL cholesterol in individuals with hypercholesterolemia. Recent reviews^717,718 gave particular weight to 16 well-controlled trials that reported intakes of saturated fatty acids and cholesterol. More than half of the studies used more than 40 g/day soy protein in some form. One report⁷¹⁹ indicated that 25 g/day soy protein in a diet low in saturated fatty acids and cholesterol lowers LDL cholesterol levels by about 5 percent.

The specific processing of the soybean determines the characteristics of soy protein, such as the content of isoflavones, fiber, and saponins. There is some evidence that an LDL-lowering effect is dependent upon isoflavone content⁷²⁰ but conclusive data are lacking. Since there are inconsistent findings regarding both the dose and the potential benefit of soy protein, soy protein's major role in LDL-lowering may be to help reduce the intake of animal food products with their higher content of saturated fatty acids.

Evidence statement: High intakes of soy protein can cause small reductions in LDL cholesterol levels, especially when it replaces animal food products (A2, B2). Recommendation: Food sources containing soy protein are acceptable as replacements for animal food products containing animal fats.

 

c. Other dietary factors that may reduce baseline risk for CHD
Epidemiological studies strongly suggest that other nutrient factors affect baseline risk for CHD. For example, in the Mediterranean region, where the diet is rich in fruits and vegetables, whole grains, ocean fish, and unsaturated fatty acids, the risk for CHD appears to be lower than predicted by the major risk factors. In contrast, in regions without this dietary pattern, such as Eastern Europe and Russia, CHD rates are higher than predicted by the prevalence of CHD risk factors. Such observational data provide a basis for a general recommendation for a dietary pattern that is consistent with a low baseline population risk. The Dietary Guidelines for Americans (2000),²⁴¹ were crafted to facilitate reduction in baseline risk for CHD (Table V.2-3).

In addition, nutritional research has focused on several specific factors that may have unique properties to reduce risk for CHD. The status of these emerging dietary factors are reviewed below and summarized in evidence statements.

1) n-3 (omega-3) polyunsaturated fatty acids
Polyunsaturated fatty acids of the n-3 (omega-3) type occur as alpha-linolenic acid (18:3), primarily in certain vegetable sources such as soybean, canola oil and English walnuts, and in fish oils as eicosapentaenoic acid (EPA) (20:5) and docosahexaenoic acid (DHA) (22:6) (marine n-3 fatty acids).

Moderate fish consumption has been associated with reduced sudden cardiac death or reduced CHD mortality in several prospective cohort studies^721-723 but not in others.^724,725 One study found a trend toward increased relative risk of CHD death with marine n-3 fatty acids. A nested, case-control study found an inverse relationship between risk for sudden cardiac death and both reported intake of marine n-3 fatty acids and red blood cell n-3 fatty acid level.⁷²⁶ Postulated mechanisms for the effects of marine n-3 fatty acids on CHD risk include favorable effects on cardiac rhythm, platelet aggregation, inflammatory responses, and serum triglyceride levels. High intakes of marine n-3 fatty acids reduce triglyceride levels;⁷²⁷ this effect appears to be secondary to decreased VLDL production.⁷²⁸ Generally, marine n-3 fatty acids have no effect on LDL cholesterol levels, but large doses have been shown to reciprocally increase LDL cholesterol levels in persons with hypertriglyceridemia.⁷²⁹ Recent data indicate that some fish have a high mercury content and the toxic effects of mercury could attenuate protective effects of fish.^730,731

Four clinical trials suggest that n-3 fatty acids from marine or plant sources reduce sudden death and overall death in populations with pre-existing cardiovascular disease. The DART trial⁷³² was a relatively large secondary prevention trial in which subjects advised to eat fatty fish had a 29 percent reduction in 2-year all-cause mortality compared with those not so advised, although myocardial infarction and coronary death were not specifically reduced. The Lyon Heart Trial⁷³³ included increased intakes of alpha-linolenic acid as part of a "Mediterranean" diet. Compared to the control group, subjects consuming the Mediterranean diet had fewer coronary events. The authors attributed some of the benefit to higher intakes of n-3 fatty acids. In a small supplement trial, Singh et al.⁷³⁴ treated patients with suspected acute myocardial infarction with fish oil capsules (EPA 1.08 g/day) or mustard oil (alpha-linolenic acid 2.9 g/day) or placebo. After one year, total cardiac events were significantly less in the groups on fish oil and mustard seed oil supplements. Further, the large placebo-controlled, but unblinded Italian GISSI Prevention trial⁷³⁵ administered fish oil supplements containing n-3 fatty acids (1 g/day fish oil, n = 2836 subjects) and compared coronary outcomes to controls (n = 2828). The group receiving fish-oil supplements had a 14 percent reduction in total death and a 17 percent reduction in cardiovascular death. Other clinical trials are less suggestive of benefit from n-3 fatty acids. Angiographic data fail to show that marine n-3 fatty acids modify coronary lumen size.^736,737 Also, fish oil administration apparently does not prevent restenosis after coronary angioplasty.⁷³⁸ Additional studies are underway to determine the effect of n-3 fatty acids on CHD risk in the U.S. population.²⁴¹

Based on these findings, the Dietary Guidelines for Americans (2000)²⁴¹ noted that some fish, such as salmon, tuna, and mackerel, contain omega-3 fatty acids that are being studied to determine if they offer protection against heart disease. No quantitative recommendations for n-3 fatty acids were made for the general public.

Evidence statement: The mechanisms whereby n-3 fatty acids might reduce coronary events are unknown and may be multiple. Prospective data and clinical trial evidence in secondary CHD prevention suggest that higher intakes of n-3 fatty acids reduce risk for coronary events or coronary mortality (A2, C2). Recommendation: Higher dietary intakes of n-3 fatty acids in the form of fatty fish or vegetable oils are an option for reducing risk for CHD. This recommendation is optional because the strength of the evidence is only moderate at present. ATP III supports the American Heart Association's recommendation that fish be included as part of a CHD risk-reduction diet. Fish in general is low in saturated fat and may contain some cardioprotective n-3 fatty acids. However, a dietary recommendation for a specific amount of n-3 fatty acids is not being made (See Section VI for ATP III recommendations on n-3 supplements for reducing risk for CHD.)

 

2) Vitamins/antioxidants
a) Folic acid and vitamins B₆ and B₁₂
Folic acid and vitamins B₆ and B₁₂ play a role in the metabolism of homocysteine, and levels of these vitamins correlate inversely with homocysteine levels. Data from the Framingham Heart Study suggest that the mandated fortification of cereal grains with folic acid has lowered population mean homocysteine levels as well as the prevalence of hyperhomocysteinemia.³⁰⁷ Many cross-sectional case-control studies and some prospective cohort studies show a positive association between plasma homocysteine levels and CVD risk^297,739-743 but other prospective cohort studies do not.^300,744-746

Despite the fact that homocysteine levels can be reduced with supplements of folate, B₆, and B₁₂, it is not known whether reduction of plasma homocysteine levels by diet and/or vitamin supplements will reduce CVD risk.⁷⁴³ Several randomized trials are underway to determine if folic acid, vitamin B₆, and vitamin B₁₂ will be effective in reducing the risk of heart disease.³⁰⁴

The Institute of Medicine has recently published dietary recommendations for folate for the general population.⁷⁴⁷ The recommended dietary allowance (RDA) for folate is 400 micrograms per day. This level of intake was deemed adequate to provide any reduction in risk for cardiovascular disease that can be obtained from dietary folate. An upper limit for folate derived from fortified food or supplements was estimated to be 1000 micrograms per day.

Evidence statement: According to the Institute of Medicine, the RDA for folatefor adults is 400 micrograms per day, and the upper limit is 1000 micrograms per day. There are no published randomized controlled clinical trials to show whether lowering homocysteine levels through dietary intake or supplements of folate and other B vitamins will reduce the risk for CHD. Recommendation: ATP III endorses the Institute of Medicine RDA for dietary folate, namely, 400 micrograms per day. Folate should be consumed largely from dietary sources.

 

b) Antioxidants
Oxidative stress is a putative cause of atherosclerotic disease. In experimental studies, oxidation of LDL is an important step in the development and progression of CHD. Thus, a large body of research has been directed towards the potential of antioxidants for reducing CHD risk. Antioxidants under investigation include ascorbic acid (vitamin C), alpha-tocopherol (vitamin E), beta-carotene, ubiquinone (coenzyme Q10), bioflavonoids, and selenium.

Several studies in laboratory animals support the concept that antioxidants are antiatherogenic.⁷⁴⁸ Some, but not all, epidemiological data lend additional support to the concept that dietary antioxidants can reduce risk for CHD.⁷⁴⁸ Generally, in populations that consume a dietary pattern rich in fruits and vegetables and other foods high in antioxidants, there is a reduced risk of CHD.

Several controlled clinical trials have been carried out to determine whether supplementation with antioxidants reduces risk for CHD. The Linxian study in China found that supplements of beta-carotene (15 mg/d), vitamin E (30 mg/d), and selenium (15 mcg/d), given at levels obtained from foods, were associated with a non-significant 10 percent decrease in CVD mortality.⁷⁴⁹ In the Alpha-Tocopherol, Beta Carotene Cancer Prevention Study, supplementation with betacarotene had no beneficial effect on the incidence of myocardial infarction.⁷⁵⁰ Another trial,⁷⁵¹ found no benefit (or harm) for CHD incidence after 12 years of beta-carotene supplementation in 22,071 male physicians. Finally, in the CARET study, a non-significant 26 percent increase in cardiovascular mortality was reported in a group supplemented with beta-carotene.⁷⁵²

In the Alpha-Tocopherol, Beta Carotene Cancer Prevention Study, supplementation with small doses of vitamin E in Finnish male smokers had only a marginal effect on incidence of fatal CHD, whereas it had no effect on incidence of nonfatal myocardial infarction.⁷⁵⁰ In a secondary prevention trial among patients with CHD, vitamin E supplementation (400 or 800 IU per day during 1.5 years) in the Cambridge Heart Antioxidant Study (CHAOS), significantly reduced the risk for recurrent MI (77 percent). No effect was demonstrated for CVD mortality. A non-significant increase in total mortality was observed in the vitamin E group.⁷⁵³ Two large-scale clinical trials in patients with established CHD failed to demonstrate a protective effect of vitamin E supplementation on subsequent cardiovascular events.^510,735,754

Thus, in spite of the theoretical benefits of antioxidant vitamins for reducing risk for CHD, this potential has so far not been found in controlled clinical trials that have used a variety of antioxidant mixtures and doses. The failure to demonstrate benefit in controlled trials does not eliminate the possibility of benefit. It does, however, dilute confidence in benefit and stands in the way of a solid recommendation for high intakes of antioxidants for CHD prevention.

The Institute of Medicine has recently released recommendations for Dietary Reference Intakes (DRIs) for antioxidant vitamins. A specific recommendation was not made for beta-carotene because it has not been shown to be an essential nutrient nor have clinical trials demonstrated benefit for reduction in risk for either cardiovascular disease or cancer. The RDA for vitamin C was increased to 75 mg/day for women and 90 mg/day for men. The RDA for Vitamin E was set at 15 mg/day. Vitamin E supplementation was not recommended for prevention of chronic disease because of a lack of convincing evidence of benefit.

Evidence Statement: Oxidative stress and LDL oxidation appear to be involved in atherogenesis. However, clinical trials to date have failed to demonstrate that supplementation of the diet with antioxidants will reduce risk for CHD (A2). Recommendation: Evidence of CHD risk reduction from dietary antioxidants is not strong enough to justify a recommendation for antioxidant supplementation to reduce CHD risk in clinical practice. ATP III supports current recommendations of the Institute of Medicine's RDAs for dietary antioxidants, i.e., 75 mg and 90 mg per day for women and men, respectively, for vitamin C and 15 mg per day for vitamin E.

 

3) Moderate intakes of alcohol
Observational studies consistently show a J-shaped relation between alcohol consumption and total mortality. Moderate alcohol consumption is associated with lower mortality, and higher consumption with higher mortality. The lower mortality appears to be related to CHD death, because CHD accounts for a significant proportion of total deaths. Case-control, cohort, and ecological studies indicate lower risk for CHD at low to moderate alcohol intake.⁷⁵⁵ A moderate amount of alcohol can be defined as no more than one drink per day for women and no more than two drinks per day for men.^756,757 This gender distinction takes into account differences in both weight and metabolism. Moreover, any cardiovascular benefit occurs not in the young age groups but in middle-aged adults, men 45 years of age or older and women 55 years of age or older.⁷⁵⁸ Mechanisms of putative risk reduction from moderate alcohol consumption are unknown; however, it could be due to an increase in HDL cholesterol and apo A-1 and modestly to an improvement in hemostatic factors.⁷⁵⁹ Prospective cohort studies suggest a similar relationship with CHD regardless of the type of alcoholic beverages consumed.⁷⁶⁰

The dangers of overconsumption of alcohol are well known. At higher levels of intake, adverse effects include elevated blood pressure, arrhythmia, and myocardial dysfunction.^755,757 Alcohol excess also predisposes to acute pancreatitis. Rarely it can precipitate pancreatitis by accentuating a pre-existing hypertriglyceridemia and chylomicronemia.⁷⁶¹ A pooled analysis shows that alcohol intake increases the risk of breast cancer in women.⁷⁶² Since up to 10 percent of U.S. adults misuse alcohol, advice about alcohol intake should be given carefully with both advantages and negatives presented.⁷⁶³ For some persons, the negatives of alcohol consumption will outweigh any advantage.

Evidence Statement: Moderate intakes of alcohol in middle-aged and older adults may reduce risk for CHD (C2). However, high intakes of alcohol produce multiple adverse effects (C1). Recommendation: No more than two drinks per day for men and no more than one drink per day for women should be consumed. A drink is defined as 5 ounces of wine, 12 ounces of beer, or 1 ounces of 80 proof whiskey. Persons who do not drink should not be encouraged to initiate regular alcohol consumption.

 

4) Dietary sodium, potassium, and calcium
Many individuals with hypercholesterolemia also have hypertension (see Section VII.6). Evidence suggests that even those with normal blood pressure levels can reduce their chances of developing high blood pressure by consuming less salt.^160,161,657 Studies in diverse populations have shown that a high sodium intake is associated with higher blood pressure.⁷⁶⁴ Also, a high salt intake increases the amount of calcium excreted in the urine, and has been independently associated with bone loss at the hip.⁷⁶⁴ The Dietary Approaches to Stop Hypertension (DASH) trial has provided evidence that a dietary pattern high in fruits, vegetables, low-fat dairy products, whole grains, poultry, fish, and nuts and low in fats, red meat, and sweets--foods that are good sources of potassium, calcium, and magnesium—favorably influences blood pressure even when sodium levels are held constant,⁷⁶⁵ but when these nutrients are consumed in combination with a low sodium intake, 2400 mg or 1800 mg, blood pressure is lowered even more.⁷⁶⁶

Evidence statement: JNC VI160,161 provides a review of the evidence to support the concept that lower salt intake lowers blood pressure or prevents its rise. One clinical trial further shows that the effects of a dietary pattern high in fruits, vegetables, low-fat dairy products, whole grains, poultry. fish, and nuts and low in fats, red meat, and sweets--foods that are good sources of potassium, calcium, and magnesium--to reduce blood pressure are enhanced by a diet low in salt (A2). Recommendation: The Diet and Health report657 and JNC VI recommend a sodium intake of <2400 mg/d (no more than 100 mmol/day, 2.4g sodium or 6.4g sodium chloride). JNC VI further recommends maintaining adequate intakes of dietary potassium (approximately 90 mmol per day) and enough dietary calcium and magnesium for general health. ATP III affirms these recommendations for persons undergoing cholesterol management in clinical practice.

 

5) Herbal or botanical dietary supplements
The 10 top-selling herbal or botanical dietary supplements are cranberry, echinacea, evening primrose, garlic, ginkgo, ginseng, goldenseal, grape seed extract, St. John's wort, and saw palmetto.⁷⁶⁷ These botanical supplements are available in health food stores, pharmacies, and many supermarkets. Several of the compounds have been promoted as agents to reduce the risk of CHD. Data from controlled trials regarding efficacy and safety are limited, in part because existing food and drug laws do not require demonstration of safety and efficacy to support legal marketing of dietary supplements. Dietary supplements are regulated according to different standards than are drugs. In addition to concerns about efficacy and safety, there is a lack of standardization among brands of botanical supplements. As a result, the amount of bioactive constituent, by which the supplements are hypothesized to influence disease, can differ widely among brands. In the case of garlic, a few randomized controlled studies are available, but the preponderance of available evidence fails to establish that garlic reduces LDL cholesterol levels. Biological plausibility supports use of some supplements, but there are few controlled clinical trials to document benefit. Studies designed to evaluate efficacy for disease endpoints, long-term safety, and drug interaction have not been reported.

Evidence statement: Despite widespread promotion of several herbal or botanical dietary supplements for prevention of CHD, a paucity of data exists on product standardization, controlled clinical trials for efficacy, and long-term safety and drug interactions. Clinical trial data are not available to support the use of herbal and botanical supplements in the prevention or treatment of heart disease. Recommendation: ATP III does not recommend use of herbal or botanical dietary supplements to reduce risk for CHD. However, health care professionals should query patients to establish whether such products are being used because of the potential for drug interaction.

 

6) High protein, high total fat and saturated fat weight loss regimens
Periodically, weight-loss diets high in protein and fat and low in carbohydrate surge in popularity. Such diets will result in weight loss within a few weeks or months if calories are restricted. However, such diets have not been demonstrated to produce long-term weight loss in controlled trials. Although clinical trial data are lacking, several concerns have been expressed about the use of these diets in clinical weight reduction:

• Short-term, extreme diets rarely produce long-term weight reduction.
  
• High intakes of saturated fats can raise LDL cholesterol.
  
• Low intakes of fruits, vegetables, and grains can deprive persons of healthful nutrients and are not conducive to long-term health.
  

Diets popularized as low-carbohydrate, high-fat, high-protein regimens for rapid weight loss should not be confused with ATP III's easing restriction of the percentage of dietary fat for persons with the metabolic syndrome. The latter allows dietary fat to rise to 35 percent of total calories, provided it remains low in saturated fatty acids (<7 percent of total energy) and includes mostly unsaturated fats. This will reduce carbohydrate intake somewhat to prevent the actions of high-carbohydrate diets to raise triglycerides and reduce HDL cholesterol levels. The ATP III recommendation allows for the dietary variety outlined in the Dietary Guidelines for Americans (2000).²⁴¹

Evidence statement: High protein, high total fat and saturated fat weight loss regimens have not been demonstrated in controlled clinical trials to produce long-term weight reduction. In addition, their nutrient composition does not appear to be conducive to long-term health. Recommendation: High protein, high total fat and saturated fat weight loss regimens are not recommended for weight reduction in clinical practice.

 

	4. Management of the metabolic syndrome through life habit changes

Top 1. Population approach:... 2. General approach to... 3. Components of the... 4. Management of the... 5. Practical approach to... 6. Improving patient adherence...

 
a. Weight control
ATP II^1,2 recommended increased emphasis on weight reduction as part of LDL-lowering therapy for over-weight/obese persons who enter clinical guidelines for cholesterol management. ATP III confirms this recommendation. However, in ATP III, emphasis on weight reduction is delayed until after other dietary measures are introduced for LDL lowering (reduced intakes of saturated fatty acids and cholesterol and possibly other options for LDL lowering [plant stanols/sterols and increased dietary fiber]) (see Figure V.2-1). The delay in emphasizing weight reduction is to avoid overloading new patients with a multitude of dietary messages and to concentrate first on LDL reduction. After an adequate trial of LDL-lowering measures, attention turns to other lipid risk factors and the metabolic syndrome (see Figure V.2-1). Weight reduction then becomes a major focus of TLC. In 1998, the NHLBI published Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults from the Obesity Education Initiative (OEI).^78,79 This is an evidence-based report, and its recommendations for techniques of weight reduction are accepted by ATP III for persons undergoing management for cholesterol disorders. The ATP III report does not independently develop evidence statements beyond those in the OEI report. ATP III endorses the importance of weight control described in the OEI report. Indeed, weight control alone, in addition to lowering LDL cholesterol, favorably influences all of the risk factors of the metabolic syndrome.

b. Increased regular physical activity
ATP II also recommended increased emphasis on regular physical activity. In ATP III, the emphasis is reinforced with particular attention to its benefits for management of the metabolic syndrome. The recommendation for increased physical activity is introduced when TLC is initiated and the recommendation is reinforced when emphasis shifts to management of the metabolic syndrome (see Figure V.2-1). Physical inactivity is a major risk factor for CHD.^237,238 It raises risk for CHD in several ways, notably by augmenting the lipid and nonlipid risk factors of the metabolic syndrome. It further enhances risk by impairing cardiovascular fitness and coronary blood flow. Regular physical activity can help reverse these adverse effects. It can have favorable effects on the metabolic syndrome and can reduce VLDL levels, raise HDL cholesterol and, in some persons, lower LDL levels. Regular physical activity lowers blood pressure and reduces insulin resistance. It also has been reported to reduce risk for CHD independently of standard risk factors. The evidence base for the recommendation of increased physical activity as part of cholesterol management is presented in the U.S. Surgeon General's Report on Physical Activity²³⁸ and will not be detailed in this report. The purposes of regular exercise are to promote energy balance to maintain healthy body weight, to alleviate the metabolic syndrome, and to independently reduce baseline risk for CHD. In certain circumstances, a physician has the option of referring a patient to an exercise specialist for prescription and guidance in exercise training. Exercise specialists can complement nutrition professionals in implementation of TLC by guiding individuals in a healthy exercise program.

	5. Practical approach to life habit changes

Top 1. Population approach:... 2. General approach to... 3. Components of the... 4. Management of the... 5. Practical approach to... 6. Improving patient adherence...

 
a. Role of the physician
The physician is crucial to initiating and maintaining the patient's dietary adherence. Physician knowledge, attitude, and motivational skills will strongly influence the success of dietary therapy. A positive attitude combined with effective dietary assessment, initiation of therapy, and followup are essential for initial and long-term adherence. The physician should try to determine the patient's attitude towards acceptance of and commitment to TLC. The physician's key responsibilities include: assessment of CHD risk, dietary assessment, explanation of the problem for the patient, decision about appropriate therapeutic plan, and description of the plan to the patient. The multiple benefits of lifestyle changes should be emphasized. The need for lifestyle change, even when drugs are prescribed, should be stressed. In this section, one model for the role of the physician in the institution and followup of dietary therapy will be described. This model can be modified according to the constraints of the practice setting. The key feature of this model is the introduction of dietary therapy in a stepwise manner, beginning with an emphasis on lowering LDL cholesterol and followed by a shift in emphasis to management of the metabolic syndrome, if the latter is present. The essential steps in this model are shown in Figure V.2-1.

1) Visit 1: Risk assessment, diet assessment, and initiation of therapeutic lifestyle change
Some persons do not qualify for immediate clinical management to lower LDL because their LDL level is not above the goal for their category of risk for CHD (see Section III). Nonetheless, the physican should appropriately control other risk factors, provide a public health message on overall risk reduction, and prescribe subsequent lipoprotein reevaluation as needed. Suggestions to assist the physician in conveying the public health message are outlined in Table V.1-3.

For persons who require dietary therapy, the first step is assessment of lifestyle habits. CAGE questions provide the physician with a way to rapidly assess current intakes of LDL-raising nutrients (Table V.2-4). A more detailed tool for both assessment and as a guide to TLC is available in Table V.2-6. Therapeutic change in the first visit should begin with the TLC diet. If the patient demonstrates a lack of basic knowledge of the principles of the TLC diet, the physician should consider referral to a nutrition professional for medical nutrition therapy.

2) Visit 2: Intensifying the TLC diet for LDL cholesterol lowering
Approximately 6 weeks after starting the TLC diet, lipoprotein analysis is repeated and assessed. If the LDL cholesterol goal is achieved by 6 weeks, the patient should be commended for his/her adherence and encouraged to continue lifestyle changes (Figure V.2-1). If the LDL goal has not been achieved, the LDL-lowering TLC should be intensified. Depending upon the patient's level of dietary adherence, various options exist. More vigorous reduction in saturated fats and cholesterol, adding plant stanols/-sterols (2 g/day), increasing viscous fiber (see Table V.2-5), and referral to a nutrition professional can all enhance LDL lowering.

The physician should not ignore the power of TLC to reduce CHD risk. Despite the marked advances in drug therapy for elevated LDL cholesterol level, ATP III places increased emphasis on nutrition and physical activity for cholesterol management and overall risk reduction. The low prevalence of CHD in populations that consume low intakes of saturated fats and cholesterol and high intakes of other healthful nutrients, and who maintain desirable body weight through balanced caloric intake and output, illustrate what can be achieved without drug therapy.⁶³² Moreover, specifically for LDL cholesterol reduction, the combination of several dietary modifications can produce a reduction in LDL levels that rivals reductions produced by standard doses of statins. LDL cholesterol responses shown in Table V.5-2 represent conservative estimates based on the literature. Although cumulative responses have not been documented by clinical trial, a sizable summed response from the multiple components of TLC is likely.

View this table: [in this window] [in a new window]   Table V.5-2. Approximate and Cumulative LDL Cholesterol Reduction Achievable By Dietary Modification

3) Visit 3: Decision about drug therapy; initiating management of the metabolic syndrome
If the LDL cholesterol goal has not been achieved after 3 months of TLC, a decision must be made whether to consider adding drug therapy. If drugs are started, TLC should be continued indefinitely in parallel with drug treatment. Although the apparent ease of drug use is appealing, the additive effect of TLC to drug therapy in LDL cholesterol lowering is substantial and should not be overlooked. For example, Hunninghake et al.⁷⁶⁹ reported an extra 5 percent lowering of LDL cholesterol when lovastatin therapy was combined with dietary therapy. This additional LDL cholesterol lowering equates to doubling the dose of the statin, due to the log-dose characteristics of statin usage. Other studies revealed a much greater LDL reduction when dietary therapy plus plant stanols were combined with statin therapy.^709,770 These dietary options, if successfully implemented, are preferable to progressively increasing doses of LDL-lowering drugs.

A second purpose of Visit 3 is to initiate lifestyle therapies for the metabolic syndrome, if it is present. Emphasis in TLC shifts to weight control and increased physical activity. The principles of weight control are described in the Obesity Education Initiative report.^78,79

Because of the complexities and frequent failures of long-term weight control in clinical practice, consideration should be given to referring overweight or obese individuals to a qualified nutrition professional for medical nutrition therapy.

A second element of treatment of the metabolic syndrome is to increase physical activity. The physician should provide specific recommendations for physical activity depending on the patient's physical well-being and social circumstances. Consideration also can be given to referral to an exercise specialist for guidance if this resource is available. Moderate, sustained exercise can cause a significant reduction in baseline risk for CHD. Examples of moderate intensity exercise that may be useful to individuals are listed in Tables V.2-6 and V.5-3. Moderate intensity physical activity should be promoted for most people. Moderate amounts of vigorous activity also can be beneficial for some individuals, provided safety is ensured. Suggestions to incorporate more exercise into daily life are shown in Table V.5-4.

View this table: [in this window] [in a new window]   Table V.5-3. Examples of Moderate* Physical Activity in Healthy Adults

View this table: [in this window] [in a new window]   Table V.5-4. Suggestions to Incorporate More Physical Activity into the Day

4) Visit N: Long-term follow-up and monitoring adherence to therapeutic lifestyle changes (TLC)
The patient who has achieved the goal LDL cholesterol as a result of TLC must be monitored for the long term. TLC is maintained indefinitely and reinforced by the physician and, as appropriate, by a nutrition professional if medical nutrition therapy is necessary. The patient can be counseled quarterly for the first year of long-term monitoring and twice yearly thereafter.

LDL cholesterol is measured prior to each visit, and the results are explained at the counseling session. When no lipoprotein abnormalities other than elevated LDL cholesterol are present, monitoring at 6-month intervals is appropriate. If elevated cholesterol level redevelops, the procedure outlined above for diet therapy of elevated LDL cholesterol should be reinstituted.

Persons who fail to achieve their goal LDL cholesterol by dietary therapy can be classified as having an inadequate response to diet. Such responses fall into four categories:

• Poor adherence. Some persons adhere poorly to diet modification despite intensive and prolonged dietary counseling. They are not ready to change for various reasons. Physician endorsement of the importance of diet is essential for facilitating increased interest on the part of the patient. If the patient admits a lack of willingness to change diet or other life habits, drug therapy may be the only reasonable option to effectively lower LDL.
  
• Gradual change. Some individuals modify eating habits only gradually. They may adhere poorly to diet in the first few months but eventually will modify their eating habits to meet the goals of therapy. Up to a year of instruction and counseling may be required for these persons. This is especially true for persons who are following a weight reduction plan. Ongoing follow-up and reinforcement is crucial for developing long-term adherence. A continued effort to achieve adherence to life-habit changes should not be abandoned if drug therapy is started.
  
• Poor responders. A minority of persons are non-responders to dietary therapy and will have high LDL cholesterol levels that are inherently resistant to dietary modification despite good adherence.^772-774 The mechanisms for this resistance are not well understood. Recognition of such persons is important, and care must be taken not to accuse them of failing to adhere to diet when they are non-responders. Drug therapy may be the only effective means of treatment of high blood cholesterol in such persons, but continued adherence to TLC is helpful for maintaining an overall healthful dietary pattern.
  
• Inadequate responders. Persons with severe elevations of LDL cholesterol often do respond to dietary therapy, but the cholesterol lowering achieved is inadequate to reach the LDL cholesterol goal. For such persons, a 3-month period of intensive diet therapy before adding drugs is not necessary.
  

b. Role of nurses, physician assistants, and pharmacists
Other health professionals associated with the physician facilitate patient management. The role of nutrition professionals is addressed in more detail below. Other health professionals—nurses, physician assistants, nurse clinicians, pharmacists, and other professionals—can participate in patient education (e.g., explaining the rationale for dietary change, goal setting, selection of appropriate foods, diet adherence), promoting behavioral changes, and monitoring dietary changes. These health professionals should receive appropriate training in dietary assessment, dietary education, and counseling. Hospital nurses play a vital role in guiding patients during hospital admissions for acute coronary events. NCEP and AHA offer various educational materials to assist in training health professionals.

c. Specific role of registered dietitians and other qualified nutrition professionals
Registered and/or licensed dietitians are certified providers of medical nutrition therapy (MNT), and qualify for Medicare reimbursement. Individual state licensure laws have established credentials for determining qualifications for nutrition counselors. Dietitians with expertise and experience in dietary counseling for lipid lowering can be especially effective in facilitating adherence to TLC. Registered dietitians and other licensed nutritionists can be located through local hospitals and state and district affiliates of the American Dietetic Association. The American Dietetic Association (www.eatright.org; 216 W. Jackson Blvd., Suite 800, Chicago, IL 60606-6995; 312-899-0040) maintains a roster of dietitians and responds to requests in writing or e-mail for assistance in locating a registered dietitian in a given area. Dietitians with particular expertise in cholesterol management are available in most large medical centers where they are often part of a multidisciplinary lipid clinic or cardiac rehabilitation team.

Medical nutrition therapy provided by a registered dietitian is a service that involves a comprehensive assessment of a patient's overall nutritional status, medical data, and diet history, followed by intervention to prescribe a personalized course of treatment.

The following medical nutrition therapy CPT Codes can be found in the American Medical Association Current Procedural Terminology: CPT 2001:⁷⁷⁵

• 97802 Medical nutrition therapy; initial assessment and intervention, individual face-to-face with the patient, 15 minutes each.
  
• 97803 Reassessment and intervention, individual face-to-face with the patient, 15 minutes each.
  
• 97804 Group (2 or more individual(s), 30 minutes each.
  

(For medical nutrition therapy assessment and/or intervention performed by a physician, see Evaluation and Management or Preventive Medicine service codes.)

CPT codes currently cover consideration of MNT for management of diabetes mellitus and renal disease.

1) Role of the nutrition professional in LDL-lowering therapy
When the physician chooses to consult a nutrition professional at Visits 1 or 2 for medical nutrition therapy, the goal is to enhance adherence to TLC. Medical nutrition therapy should start with dietary assessment, including the patient's motivational level and willingness to change. A dietary assessment questionnaire, MEDFICTS, which was originally developed for and printed in ATP II^1,2 is included in Diet Appendix A. Other cardiovascular dietary assessment tools are also available.^776-782 Proper assessment leads to a tailored dietary prescription. This prescription then goes to the physician, who can encourage adherence and monitor progress.

a) First: dietary assessment
A thorough and detailed assessment of the patient's knowledge, attitudes, and behavior regarding diet is essential for effective nutrition counseling. Assessment requires attention to dietary history, cultural influences, and current eating habits. It also includes recording the patient's weight and weight history, BMI, and waist circumference. The presence of abdominal obesity points to the metabolic syndrome. To assess current eating habits, the following information is needed:

• What times of the day does the patient usually eat?
  
• Are some meals routinely skipped?
  
• At what time does the patient eat his/her largest meal?
  
• Where are meals typically prepared and eaten (e.g., in a restaurant, work cafeteria, fast-food restaurant, deli, at home, or in the homes of others)?
  
• Are there occasions when stress increases food consumption?
  
• Are meals eaten at home purchased out and brought in, prepared from processed pre-packaged foods, or prepared fresh from the market?
  
• Which are favorite foods and what foods are disliked?
  
• Who is responsible for food shopping and preparation?
  
• What foods will be most difficult to increase or decrease?
  
• How well does the patient recognize serving sizes?
  

The nutrition professional should assess the patient's general knowledge of nutrition as it relates to elevated LDL cholesterol, the ability to read labels, educational level, motivation, attitudes toward diet, and the extent to which family members can facilitate dietary changes.

b) Dietary guidance on adopting the TLC Diet
To help patients adapt to the TLC Diet, the dietitian can:

• Focus on dietary patterns to facilitate LDL lowering. These patterns are consistent with the Dietary Guidelines for Americans (2000)²⁴¹ to achieve overall health and to further reduce baseline risk for CHD. This eating pattern is recommended for the entire family.
  
• Seek mutual agreement on an overall plan for diet modification as well as specific foods and eating habits that need to be changed. Emphasis goes first to dietary habits that affect LDL cholesterol levels. Highest on the list are foods rich in saturated fatty acids and cholesterol. The dietitian can review options for choosing preferred foods that lower LDL levels. The need for self-monitoring is reinforced; and simple approaches to tracking saturated fat, fiber, fruit, and vegetable intake are provided. Weight reduction includes learning how to control portion sizes. Also, documenting preparation and the quantities of different foods helps in long-term adherence. Practical teaching with measuring cups, spoons, food models, or even a food scale will enhance patient understanding. Keeping a food record during weekends and weekdays can facilitate discussion with the dietitian. Electronic (e-mail) links between dietitian and patient may enhance checking food records or reporting self-monitoring activities.
  
• Help patients identify sources of saturated fat in their usual diet, especially "hidden" fats in foods, such as baked goods, cheese, salad dressings, and other processed foods. Advice on alternative food choices, including snack foods, should be provided. For persons willing to prepare foods at home, appropriate techniques and cooking methods can be addressed. For those who eat out regularly, guidance on how to select from a menu and purchase premade take-out food should also be given.
  
• Apply motivational interviewing techniques to provide encouragement and to empower patients to choose wisely on different eating occasions. Gradual, step-wise changes in current eating habits are more likely to achieve long-term adherence than drastic changes. Starting with a specific food or food group, such as the type of milk used, how to reduce portion size of meats, how to substitute egg whites for whole eggs in baking, or how to use margarines and oils in the place of fats rich in saturated fatty acids are excellent topics to pursue. The dietitian should involve other individuals of significance (e.g., parents, spouse, and children) in dietary instructions.
  
• Recommend a variety of foods from all food groups to help achieve adequate nutrient intake: vegetables, fruits, grain products, potatoes and legumes, dairy products, and lean meat, poultry, and fish. Use of specially prepared processed foods, fat-free or fat modified snacks, desserts, etc. is not necessary, although some persons find these food choices appealing.
  
• Promote use of the Nutrition Facts food label to help patients learn to gauge saturated fat and cholesterol intakes. Saturated fat amounts listed on the Nutrition Facts food label correspond to 10 percent of calories; still lower intakes are needed to attain <7 percent. Persons should should be taught to routinely read the labels of all processed foods.
  

c) Specific foods and preparation techniques
Recommended food choices for the TLC Diet are summarized in Table V.2-6. This diet can be both tasty and nutritious. Many choices of high-quality and recommended foods are available in supermarkets, restaurants and as take-out options.

To decrease intake of saturated fat, total fat, and cholesterol, the emphasis of the diet should be on consumption of vegetables; fruits; breads, cereals, rice, legumes, and pasta; skim milk and skim milk products; and poultry, fish, and lean meat. There are many different eating styles in the United States that reflect diverse cultures and practices. Special attention to unique dietary preferences based on diverse cultures and eating habits can facilitate adoption of the TLC Diet. Sample menus are presented in Diet Appendix B.

Food preparation techniques should emphasize lower fat cooking and preparation methods (broiling, baking, grilling, steaming, poaching without added fat, trimming fat from meat, draining fat after cooking, and removing skin from poultry). Liquid vegetable oils high in unsaturated fatty acids (e.g. canola, corn, olive, rice bran, safflower, soybean, sunflower) are recommended in moderation. Since the major sources of saturated fat and total fat in the American diet are meat and high-fat dairy products, and since these foods as well as eggs are the major sources of dietary cholesterol, persons should limit consumption of foods containing butterfat such as whole milk (3.5 percent fat) and even reduced fat (2 percent) milk, butter, cheese, ice cream, cream, and pizza; fatty meats such as regular ground beef (hamburger), processed meats (hot dogs, sausage, bacon), and high-fat luncheon meats (bologna, salami, chopped ham products), as well as poultry skin. Low-saturated-fat substitutes, such as fat-free or 1 percent milk, soft margarine, low-fat cottage cheese, or low-fat or fat-free "ice cream" can be used. Egg yolks should be limited to 2 per week. Organ meats (liver, brain, sweetbreads) are rich sources of cholesterol and should be limited. Of the shellfish, only shrimp is moderately high in cholesterol and inclusion in the diet should be guided by the daily dietary cholesterol allowance. The vegetable oils rich in saturated fat—coconut oil, palm kernel oil, and palm oil—are used in some commercial foods and food products. Choose products that are labeled low saturated fat, e.g., 1 gram of saturated fat per serving, and meats that are labeled as lean.

Although persons need not purchase special foods for implementation of the TLC Diet, many new fat-modified products on the market may facilitate adherence to the TLC Diet.

d) Recommendations by food group
The following information about specific food choices can help persons adopt the TLC Diet.

• Breads, cereals, pasta, whole grains, potatoes, rice, dry peas, and beans (6 or more servings per day). These foods are high in complex carbohydrates and fiber, provide protein, and also are generally low in saturated fat, cholesterol, and total fat. Dry beans and peas are good sources of plant protein and are fiber-rich. They should be substituted for foods high in saturated fat, cholesterol, and total fat. Cereals can be eaten as snacks as well as for breakfast. Dry peas, beans, and legumes can be used in nutritious, tasty, lower fat entrees or accompaniments. Pasta, potatoes, rice, and vegetables can be combined with smaller amounts of lean meat, fish, or poultry for a tasty main dish that can provide less saturated fat and calories.
  
• Fruits and vegetables (5 or more servings per day). Fruits, vegetables, or both should be emphasized at each meal. They are major sources of vitamins C, E, and A, beta-carotene, other vitamins, fiber, and some minerals, and contribute to achieving the recommended allowances of these nutrients. Snacks and desserts that feature fruits and/or vegetables can be low in saturated fat, total fat, and cholesterol, and very nutritious.
  
• Fat-free or 1 percent dairy products (2-3 servings per day). Dairy products are important sources of protein, calcium, phosphorus, and vitamin D. Fat-free milk and other fat-free or low-fat dairy products provide as much or more calcium and protein than whole milk dairy products, with little or no saturated fat. Fat-free milk or 1 percent fat milk, fat-free or low-fat cheese (e.g., 3g per 1 oz serving), 1 percent fat cottage cheese or imitation cheeses made from vegetable oils, and fat-free or low-fat yogurt are good choices. It should be noted that 2 percent fat dairy products are still rich in saturated fat. Evaporated fat-free milk can be used in recipes calling for heavy cream. Low-fat or fat-free yogurt, 1 percent fat cottage cheese, and fat-free sour cream substitutes can replace sour cream in dips and salad dressings.
  
• Lean meats (beef, pork, and lamb), poultry, and fish (up to 5 oz per day). Lean cuts of beef include sirloin tip, round steak, rump roast, arm roast and, for pork, center-cut ham, loin chops, and tenderloin. All visible fat should be trimmed before cooking. Ground meat should be extra-lean and drained well after cooking. Meat can be ground at home or a butcher can grind very lean, well trimmed cuts of meat such as those that come from the round. Ground turkey, which can be seasoned and used like ground beef, is very lean if it does not contain turkey skin and fat. Both lean ground meat and ground turkey can be incorporated into soups, stews, and casseroles that contain grain products and vegetables. Special reduced-fat ground meat products (e.g., with carrageenan) may be selected. It is not necessary to eliminate or drastically reduce lean red meat consumption. Lean meat is rich in protein, contains a highly absorbable iron (Fe⁺⁺), and is a good source of zinc and vitamin B₁₂. Lean meat can contribute to maintenance of iron stores in premenopausal women.
  
  • Soy products. Foods containing soy-based meat analogues can be substituted in part for meat products.
    
  • Processed meats. Processed meats, such as lunch meat, bacon, bologna, salami, sausage, and frankfurters generally have a high content of saturated fat and sodium. Several new processed meat products are lower in saturated fat, total fat, and cholesterol. Read the Nutrition Facts food label to choose foods low in saturated fat, cholesterol, and sodium.
    
  • Organ meats. Liver, sweetbreads, kidneys, and brain have a high cholesterol content and should be used only occasionally.
    
  • Chicken and turkey. These are good sources of lean protein. Removing the skin and underlying fat layers substantially reduces the fat content. Chicken and turkey can be substituted for some of the lean red meat in the diet, but they do not contain as much iron. Chicken and other poultry should be prepared in ways that minimize the addition of saturated fat.
    
  • Fish. Fish are low in saturated fat, some are high in n-3 fatty acids (see Diet Appendix C), and they are a good source of lean protein. The preparation of fish is important. Like chicken and turkey, it should be prepared to limit additional saturated fat.
    
  • Shellfish. Shellfish are low in saturated fat. The cholesterol content of shellfish is variable (see Diet Appendix C). Shrimp are relatively high in cholesterol, but can be eaten occasionally.
    
  
  About 5 ounces of fish, poultry, or meat per day can be included on the TLC Diet as 2 servings, each serving about the size of a deck of playing cards. A serving of meat in a restaurant often exceeds 5 ounces. (The saturated fat, total fat, and cholesterol content of various cooked meats are presented in Diet Appendix C).
  
• Fats and oils (including fats and oils used in food preparation). Fats high in saturated fat, trans fat, and cholesterol must be limited. This includes lard and meat fat. Some vegetable fats—coconut oil, palm kernel oil, and palm oil—are high in saturated fat and should be avoided; they often are used in bakery goods, processed foods, popcorn oils, and nondairy creamers. The Nutrition Facts food label is a guide for choosing fats and oils lowest in saturated fat. Hydrogenated shortenings and hard margarines are sources of trans fat and should be reduced. Vegetable oils and fats high in unsaturated fat do not raise blood cholesterol, but they have a high caloric density. These include canola oil, corn oil, olive oil, safflower oil, soybean oil, and sunflower oil. Margarine contains some trans fat but has less cholesterol-raising potential than butter, and thus is preferable to butter. In general, the softer the margarine, the less LDL-cholesterol-raising potential it has. Hydrogenated shortening contains trans fat, resembles hard margarines, and should be limited. Hydrogenated shortenings are found in many commercially prepared baked foods, such as crackers, cookies, doughnuts, and desserts. There are many reduced fat margarines, vegetable oil spreads, and low-fat and fat-free salad dressings on the market. The Nutrition Facts food label provides the amount of fat and saturated fat per serving.
  
• Nuts. Nuts are high in fat, but in most nuts the predominant fats are unsaturated. The intake of nuts should fit within the calorie and fat goal.
  
• Eggs. Egg yolks are high in cholesterol (215 mg/egg) and should be limited to no more than two egg yolks per week. Egg yolks often are found in cooked and processed foods. Egg whites contain no cholesterol, and they can be eaten often. Egg whites or commercial egg substitutes or reduced-cholesterol egg products can replace whole eggs in many recipes.
  

e) Other eating tips

• Snacks. Some choices for snacks that are low in saturated fat are graham crackers, rye crisp, melba toast, pretzels, low-fat or fat-free crackers, bread sticks, bagels, English muffins, fruit, ready-to-eat cereals, and vegetables; fat-free corn chips and potato chips can be made at home or purchased in some stores. Popcorn should be air popped or cooked in small amounts of vegetable oil. Low-fat cookies include animal crackers, fig and other fruit bars, ginger snaps, and molasses cookies.
  
• Desserts and sweets. Moderate amounts of sweets and modified-fat desserts (low in saturated fat) may be chosen. For example, fruits, low-fat or fat-free fruit yogurt, fruit ices, sherbet, angel food cake, jello, frozen low-fat or fat-free yogurt, and low-fat ice cream. Cookies, cakes, and pie crusts can be made using unsaturated oil or soft margarines, egg whites or egg substitutes, and fat-free milk. Candies with little or no fat include hard candy, gumdrops, jelly beans, and candy corn. Read the Nutrition Facts food label to choose those products lowest in saturated fat and calories.
  
• Cooking methods. Methods that use little or no fat include steaming, baking, broiling, grilling, or stir frying in small amounts of fat. Cook foods in the microwave or in a nonstick pan without added fat. Foods may be pan fried with limited fat. Soups and stews should be chilled for a few hours, and the congealed fat removed. Salt should be limited in the preparation of soups, stews, and other dishes. Herbs and spices can often be used instead of salt to help prevent or control high blood pressure.
  
• Eating away from home. Choose entrees, potatoes, and vegetables prepared without sauces, cheese, or butter when eating away from home. Eat only a small portion of meat. Choose vegetable or fruit salads, with salad dressings on the side. Limit toppings, such as chopped eggs, crumbled bacon, and cheese. Request soft margarine instead of butter, and use it sparingly.
  

A reference work on food and nutrition may be useful to patients. One available reference is the USDA's Home and Garden Bulletin No. 72, Nutritive Value of Foods.⁷⁸³ In addition, a typical 1-day menu for TLC Diets for both men and women which displays different eating patterns is included in Diet Appendix B.

2) Role of the dietitian in management of the metabolic syndrome
After LDL cholesterol is controlled, medical nutrition therapy turns attention to the metabolic syndrome. Strategies for weight reduction described in the Obesity Education Initiative report (also see www.nhlbi.nih.gov) are helpful.^78,79 Weight reduction and dietary change introduced in medical nutrition therapy aim to achieve and maintain goals for LDL cholesterol as well as glucose and blood pressure. Hypocaloric diets, increased physical activity, and weight loss usually improve levels of LDL cholesterol, glycemic levels, and blood pressure and have the potential to improve long-term metabolic control. The distribution of calories from total fat and carbohydrate can vary (see Table V.2-2) and can be individualized based on the nutrition assessment and treatment goals.

	6. Improving patient adherence to life habit changes

Top 1. Population approach:... 2. General approach to... 3. Components of the... 4. Management of the... 5. Practical approach to... 6. Improving patient adherence...

 
Outpatient studies show that variability in lipoprotein responsiveness to diet is often due to poor compliance. Good compliance is hampered in part by increased consumption of foods prepared away from home. In 1995 about 40 percent of the food budget was spent on food prepared away from home, compared with 25 percent in 1970.⁷⁸⁴ The consumer has less knowledge of and less control over the nutritional content of food prepared away from home. Moreover, calories, saturated fat, and cholesterol tend to be higher in premade food than food prepared at home.⁷⁸⁴ Food prepared away from home usually does not carry nutrition labeling. Barriers to adherence to dietary therapy must be addressed and reasonable solutions provided. Physicans in general report little confidence in the patients' ability to adhere to dietary change. In one survey, 17 percent of physicians reported that most patients complied, 59 percent reported that some complied, and 22 percent estimated that few patients complied.

Lack of adequate nutrition education in medical schools has been a contributing factor to low adherence to dietary therapy that fortunately is now being addressed. The newly implemented NHLBI-funded Nutrition Academic Award Program is now underway in 21 U.S. medical schools. This program provides training in nutritional assessment and counseling for medical students and other health professionals in training.⁷⁸⁵ Other barriers, such as lack of time, lack of adequate referral strategies, lack of third party reimbursement, and competition with pharmacological intervention are also being addressed.⁷⁸⁶

Beyond these systemic problems, a validated methodology related to effective nutritional assessment and intervention is lacking. Ready access to a brief dietary assessment tool and accompanying follow up assessments are as yet not standard practice for most physicians. Advances have been made in the past decade regarding the combined use of behavioral strategies along with standardized diet assessment and intervention approaches.^776-782 (See Appendix A for an example of a validated assessment tool.)

There is growing evidence from the behavioral therapy literature that strategic approaches to lifestyle intervention can achieve better and more consistent long-term adherence.^787-789 These strategies are based on learning principles that address the need to overcome barriers to adherence with lifestyle change and reinforce newly adopted behaviors.^789-791 The vast majority of these studies appear in the weight management field.⁷⁹² The Obesity Guidelines panel reviewed 36 randomized clinical trial reports to determine potential benefits of behavioral therapy.^78,79 Key findings from these studies are summarized below:

• Multimodal strategies work better than a single approach.
  
• More frequent contact is associated with better adherence.
  
• Adherence declines with discontinued intervention or followup.
  
• Greater intensity of intervention, especially initially, is associated with faster and more sustained adherence.
  
• Motivation is enhanced when the patient sets achievable goals.
  

Further lessons learned from the behavioral literature emphasize the importance of baseline assessment of dietary intake, use of self-monitoring to improve adherence, and use of health messages that are matched to level of readiness to change, culturally sensitive, interactive, address prior knowledge, come from reliable sources, and recommend reasonable, gradual, and easily implemented change. Additional research is needed with measures of the efficacy and effectiveness of office-based dietary assessment methodology, especially as this relates to behavioral strategies enhancing dietary adherence.

Related Articles:

Diet Appendix A
Circulation 2002 106: 3283-3284. [Extract] [Full Text]

Diet Appendix B
Circulation 2002 106: 3287-3296. [Extract] [Full Text]

Diet Appendix C
Circulation 2002 106: 3299. [Extract] [Full Text]

References
Circulation 2002 106: 3373-3421. [Extract] [Full Text]

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