Description
The dietary approach for the treatment of disorders of lipid metabolism, which include both hypercholesterolemia and hypertriglyceridemia, is a progressive reduction in total fat, saturated fat, trans fat, and cholesterol, coordinated in a plan to obtain or maintain reasonable body weight.  The diet follows the recommendations of the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III of the National Institutes of Health and the American Heart Association (AHA) (1-4).

Indications
Medical nutrition therapy (MNT) is recommended as the primary treatment and management tool for disorders of lipid metabolism.  MNT is recommended before administration of cholesterol-lowering medication in lower risk cases or in combination with drug therapy in higher risk cases. Recommended therapeutic lifestyle changes and target goals for low-density lipoprotein (LDL) cholesterol levels are based on risk factor assessment.  Major independent risk factors (exclusive of LDL cholesterol) that predict the 10-year risk for coronary heart disease (CHD) are based on Framingham risk evaluation scores (1).  These risk factors include (1):

• cigarette smoking
• hypertension (blood pressure greater than 140/90 mm Hg and/or receiving antihypertensive medication)
• low level of high-density lipoprotein (HDL) cholesterol (less than 40 mg/dL)
• family history of premature CHD (CHD in male first-degree relative younger than 55 years; CHD in female first-degree relative younger than 65 years)
• age (men, 45 years or older; women, 55 years or older)

    The high-risk category consists of persons who have existing CHD, persons who have CHD risk equivalents that confer a 10-year risk of CHD greater than 20%, and persons with diabetes.  The target LDL cholesterol level for these individuals is less than 100 mg/dL.  A subcategory of high risk, very high risk, contains persons with existing cardiovascular disease and diabetes and persons with cardiovascular disease and severe or poorly controlled multiple risk factors (4).  The very high-risk category has a therapeutic option to target the LDL cholesterol to less than 70 mg/dL (4).  Persons with more than one risk factor and a 10-year risk of CHD of 20% or less have an LDL cholesterol target goal of less than 130 mg/dL.  Persons with one or no risk factors and a 10-year risk of CHD less than 10% have an LDL target goal of less than 160 mg/dL.  Primary intervention using therapeutic lifestyle changes and drug therapy should begin after evaluation of the patient’s fasting lipid profile, consisting of levels of LDL cholesterol, total cholesterol, HDL cholesterol, and triglycerides and consideration of the risk factor assessment (1,4).  LDL cholesterol is the primary target for risk reduction intervention (1,4).  Targeting lower LDL goals, in combination with initiating cholesterol-lowering drug therapy at lower thresholds, is based on evidence from five randomized controlled trials demonstrating significant risk reduction for cardiac events at the recommended lower thresholds (4).  The NCEP recommends pharmacologic therapy that is sufficient to achieve a 30% to 40% reduction in baseline LDL cholesterol levels in all high risk and moderately high risk patients (4).

For patients hospitalized due to a cardiac event, LDL cholesterol levels begin to decline in the first few hours after an event and are significantly decreased within the first 24 to 48 hours.  These levels may remain low for up to 3 months.  Thus, the initial LDL cholesterol level obtained in the hospital may be substantially lower than is usual for the patient (1).  The NCEP ATP III emphasizes the need to begin drug therapy for high-risk patients (Refer to Table C-4: LDL Cholesterol Goals) in addition to the Therapeutic Lifestyle Changes Diet to reach the goal for LDL cholesterol.  When drugs are prescribed, the Therapeutic Lifestyle Changes Diet should always be maintained and reinforced (1).

    Clinical trials demonstrate that lowering LDL cholesterol reduces total mortality, coronary mortality, major coronary events, coronary artery procedures, and strokes in persons with established CHD (1,4).  The ATP III specifies LDL cholesterol less than 100 mg/dL as the goal of therapy in secondary prevention.  The ATP III recognizes that the risk of CHD is influenced by other factors not included among the major, independent risk factors listed previously.  Life-habit risk factors include obesity, physical inactivity, and atherogenic diet (1).  Emerging risk factors, for which scientific evidence demonstrates varying degrees of contribution to CHD risk in select persons, include lipoprotein, homocysteine, prothrombotic and proinflammatory factors, and impaired fasting blood glucose levels (more than 110 mg/dL) (1).  At this time, the evidence does not support specific modifications to target LDL cholesterol based on these risks.

Metabolic Syndrome
Metabolic syndrome is a clustering of three or more risk factors that include abdominal obesity, atherogenic dyslipidemia (elevated triglycerides level and low HDL cholesterol), hypertension, and insulin resistance (with or without glucose intolerance) (1).  The NCEP ATP III recognizes the need to address metabolic syndrome as a secondary target of risk-reduction therapy, after the primary target of LDL cholesterol lowering (1).  Management of metabolic syndrome primarily focuses on reducing underlying causes (eg, obesity and physical inactivity) and to treat associated nonlipid and lipid risk factors.  Physical activity at any level (light, moderate, or vigorous) as well as food patterns emphasizing a diet high in fruits, vegetables, and whole grains is associated with reduced incidence of metabolic syndrome (Grade II)* (5).  In the metabolic syndrome patient, a cardioprotective dietary pattern (low in saturated fat, trans fat, and cholesterol; limited in simple sugar intake; and increased in consumption of fruits, vegetables, and whole grains) provides the background for modifying the energy balance to achieve weight loss (Grade IV) (5).  Extremes in intakes of carbohydrates or fats should be avoided (Grade IV) (5). Restricted energy intake combined with at least 30 minutes of physical activity on most days of the week should be used recommended for individuals with metabolic syndrome (Grade II) (5).  Weight loss of 7% to 10% of body weight should be encouraged if indicated (Grade II) (5).

*The American Dietetic Association has assigned grades, ranging from Grade I (good/strong) to Grade V (insufficient evidence), to evidence and conclusion statements. The grading system is described in Clinical Nutrition Management A Reference Guide.

Nutritional Adequacy
The Therapeutic Lifestyle Changes Diet is planned to meet the Dietary Reference Intakes as outlined in the Statement on Nutritional Adequacy.

    The National Institutes of Health maintain that the Therapeutic Lifestyle Changes Diet is consistent with good nutrition, and the aim of this diet is to achieve healthy eating patterns consistent with the Dietary Guidelines for Americans and American Heart Association Diet and Lifestyle Recommendations 2006 (1,3).  A diet low in saturated fat, trans fats, cholesterol, and total fat is recommended for all healthy persons 2 years of age and older (1,3). 

How to Order the Diet
Specify all that apply:

• Indicate Therapeutic Lifestyle Changes Diet (preferred) or Low-Fat, Low-Cholesterol Diet.  The registered dietitian will determine the specific approaches used to implement the Therapeutic Lifestyle Changes Diet and medical nutrition goals based on individualized assessment and target treatment objectives to reduce CHD risk.
• Further reduction in total fat intake may be implemented.  This additional reduction depends on the dietitian’s assessment and the patient’s compliance.
• If required, sodium control or other dietary modification should be specifically ordered.
• If weight reduction is desired, the dietitian should set the weight loss goal with the patient and determine the appropriate weight loss regimen.

Planning the Cardioprotective Diet
The Therapeutic Lifestyle Changes Diet stresses reductions in intake of saturated and trans fat (less than 7%) and cholesterol (less than 200 mg/dL) as the primary dietary modifications to lower LDL cholesterol in patients requiring primary and secondary prevention (1).  Based on the response to a low-saturated fat, low-cholesterol diet, additional therapeutic options, such as plant stanols/sterols (2 g/day) and increased viscous (soluble) fiber (10 to 25 g/day), can be implemented as part of MNT self-management training (1).  Refer to Disorders in Lipid Metabolism Evidence-Based Nutrition Practice Guideline (5).  When metabolic syndrome or its associated lipid risk factors (elevated triglycerides level or low HDL cholesterol level) are present, therapeutic lifestyle changes also should include weight reduction and increased physical activity (1,5).

Cardioprotective Dietary Approaches in Managing Disorders in Lipid Metabolism
Total fat and saturated fatty acids: Elevated LDL cholesterol is an independent risk factor for CHD (1).  Saturated fat is the principal dietary determinant of LDL cholesterol levels (6).  The reduction of dietary saturated fat directly decreases clearance of LDL and very-low-density lipoprotein (VLDL) remnants (1).  The recommendations for saturated fat are based on existing cardiovascular disease, risk factors, and LDL cholesterol value.  A diet consisting of 25% to 35% total fat, <7% saturated and trans fat, and <200 mg cholesterol lowers serum total cholesterol and LDL cholesterol by 9% to 16% and decreases the risk of CHD (Grade I) (5).  Sources of saturated fatty acids include: butter, lard, vegetable shortening, baked and pastry products, fat in meat, poultry, whole dairy products, palm oil, palm kernel oil, and cocoa butter.  Moderate reduction of total fat (25% to 30% of total energy) facilitates a decrease in saturated fatty acids and may also help in weight reduction in overweight patients (1,7).  The recommendations for total fat intake are based on the percentage of the patient’s total daily energy intake, metabolic profile, and need for weight loss.  The AHA does not recommend very-low-fat diets (less than 15% of total energy) (3).  Very-low-fat diets may lead to inadequate intake of essential fatty acids.  In addition, very-low-fat diets are often associated with the use of processed low-fat foods that are energy dense, compounding the metabolic abnormalities found in persons with high triglycerides levels, low HDL cholesterol levels, or insulin resistance (8,9).

    Polyunsaturated fatty acids (PUFA): The two major categories of PUFA are omega-6 and omega-3 fatty acids.  Linoleic acid is the primary omega-6 fatty acid and predominates in the American diet.  The AHA recommends that less than 10% of total fat energy come from PUFA.  The latest World Health Organization’s guidelines set a range of 4% to 10% for PUFA intake (10).  Isocalorically replacing saturated fatty acids with monounsaturated fatty acids (MUFA) and PUFA is associated with reductions in LDL cholesterol (Grade I) (5).  Studies have demonstrated that intakes of greater than 10% PUFA are associated with decreasing HDL cholesterol level, an independent predictor for CHD (10).  Sources of omega-6 fatty acids include corn oil, safflower oil, sunflower oil, soybean oil, nuts, and seeds.

    Omega-3 fatty acids: Studies have demonstrated beneficial effects of increased intake of omega-3 fatty acids in patients with coronary artery disease (11-14).  Most of these studies used supplements containing long-chain omega-3 fatty acids (eg, eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA] or fish oil) at daily dosages ranging from 850 mg to 2.9 g.  Studies that demonstrate a reduction in plasma triglycerides level provide higher dosages (3 to 4 g/day) (15).  The GISSI trial demonstrated that high doses of omega-3 fatty acids provide benefits in preventing  recurrent myocardial infarction events (1,14).  Epidemiological studies indicate that regular consumption of an average of two servings of fatty fish per week (about 3.5 oz) high in long chain omega-3 fatty acids is associated with a 30% to 40% reduced risk of death from cardiac events in subjects with prior disease (Grade II) (5).  One serving of fatty fish can provide approximately 1,000 mg of EPA and DHA (3).  This amount from a supplement or fish reduces CHD mortality rates in patients with CHD (Grade II) (5).  Because of the benefits of omega-3 fatty acids, the AHA Dietary Guidelines 2006 recommends consumption of more than two fish meals per week for the general population. Epidemiological studies indicate that inclusion of vegetable oils and food sources high in alpha-linolenic acid, resulting in a total intake of more than 1.5 g/day, is associated with a 40% to 65% reduced risk of death from cardiac events(Grade III) (5).  This amount is equivalent to consuming ½ to 1 tablespoon ground flaxseed meal, 1 teaspoon flaxseed oil, or 1 tablespoon of canola or walnut oil.   The 2006 AHA recommendations advise patients with documented CHD to consume approximately 1 g/day of EPA plus DHA, preferably from oily fish.  EPA plus DHA supplements could be considered in consultation with a physician (3).  For individuals with hypertriglyceridemia, 2 to 4 g/day of EPA plus DHA, provided as capsules under a physician’s care, are recommended (3).  Sources of omega-3 fatty acids include cold-water fish (salmon, mackerel, Atlantic herring, lake trout, albacore tuna, sardines, swordfish) tofu, soybean and canola oils, flaxseed, and English walnuts. 

    MUFA: Oleic acid is the primary MUFA.  Evidence indicates that oleic acid may cause as great a decrease in LDL cholesterol levels as does linoleic acid when substituted for saturated fatty acids in the diet.  Substitution of MUFA for saturated fat lowers LDL cholesterol levels without decreasing HDL cholesterol levels (Grade I)(5,16).Evidence supports that a diet high in MUFA (up to 30% of total energy) can improve specific dyslipidemias compared with diets of equal energy value that replace fat with carbohydrate.  A diet relatively high in unsaturated fat can prevent a decrease in HDL cholesterol levels and an increase in triglycerides levels that can occur in some individuals consuming a high-carbohydrate (more than 60% total energy), low-fat diet (17).  Sources of MUFA include canola oil, olive oil, peanut oil, and avocados.

    Trans fatty acids: Trans fatty acids are created through hydrogenation, a process in which vegetable oils are heated in the presence of metal catalysts to produce vegetable shortening and margarine.  Trans fatty acids increase LDL cholesterol levels and decrease HDL cholesterol levels.  Because saturated fats increase LDL cholesterol levels but do not decrease HDL cholesterol levels, trans fatty acids can produce a greater increase in the ratio of LDL cholesterol to HDL cholesterol (Grade I) (5). Population and cohort studies show that a high trans fatty acid intake increases risk of CHD events (Grade II) (5).  It is estimated that 5% to 6% of the fat in the American diet is composed of trans fatty acids (16).  Sources of trans fatty acids include hardened vegetable fat, stick margarine, shortening, and baked products made with these fats.  Public concern has been raised about the use of margarine and whether other options, including butter, might be a better choice.  The AHA Nutrition Committee recommends margarine as a preferable substitute for butter.  Soft margarine with no more than 2 g of saturated and trans fat per tablespoon and with liquid oil as the first ingredient is recommended in place of stick margarine.  According to the 2005 ADA guidelines, a diet consisting of <7% saturated and trans fat combined should be the therapeutic goal for saturated and trans fat intake(Grade I) (5). According to the 2006 guidelines from the AHA, a diet should consist of <7% saturated fat and <1% trans fat(3).

    Cholesterol: Dietary cholesterol is found only in animal products, especially those foods that are high in saturated fatty acids (eg, meats and whole dairy products).  There is some evidence that dietary cholesterol enhances the serum cholesterol-raising action of saturated fatty acids, although to a lesser extent than saturated fat (1,3).  Most foods high in saturated fat are also sources of dietary cholesterol.  Reduced intake of foods high in saturated fat provides the additional benefit of limiting cholesterol intake. Cholesterol-rich foods that are relatively low in saturated fatty acids, notably eggs and, to a lesser extent, shellfish, have smaller effects on LDL cholesterol (3).  Therefore, periodic consumption of eggs and shellfish can be integrated into the Therapeutic Lifestyle Changes Diet meal plan.

    Carbohydrates: Complex carbohydrates should make up the majority of digestible carbohydrates.  When fat intake is reduced and nutrient replacement is required to maintain energy balance, the replacement should be complex carbohydrates.  Recommended sources include whole grains, legumes, fruits, vegetables, nuts, and low-fat dairy products.  Data on the ideal isocaloric substitution of carbohydrate for fat to maximize LDL-cholesterol lowering are presently not available (Grade V) (5).

    Total protein and soy protein: Approximately 15% of total energy should be provided as protein.  Currently there is no scientific evidence to support the concepts that high-protein diets result in sustained weight loss, significant changes in metabolism, or improved health (7,18).  Recent randomized, controlled trials have demonstrated that consumption of 20 to 50 g of soy protein daily may reduce LDL cholesterol levels (5,19-22).  Studies vary greatly in their estimation of the effect of diets low in saturated fat and cholesterol containing 26 to 50 g of soy protein, either as food or as a soy supplement with 0 to 165 mg of isoflavones (Grade II), and effects may vary based on initial cholesterol level (Grade III) (5).  If consistent with patient preference and not contraindicated by risks or harms, then soy (eg, isolated soy protein, textured soy, tofu) may be included as part of a cardioprotective diet.  Consuming 26 to 50 g/day of soy protein in place of animal protein can reduce total cholesterol by 0% to 20% and LDL cholesterol by 4% to 25% (Grade II) (5).  Evidence is insufficient to establish a beneficial role for isoflavones as an independent component (Grade III) (5).  Soy protein concentrates that remove isoflavones during processing may not be as effective (21).  In October 1999, the Food and Drug Administration approved a health claim that allows food label claims for reduced risk of heart disease on foods that contain more than 6.25 g of soy protein per serving (3).  The claim states that 25 g of soy protein per day, as part of a diet low in saturated fat and cholesterol, may reduce the risk of heart disease.  Sources of soy protein include soy milk, soybeans, tofu, soy-based meat and cheese substitutes, and alfalfa sprouts.  Soy protein may not be recommended in some individuals with breast cancer.  Individuals with breast cancer or at high risk for breast cancer should speak with their physician (5).  Consumption of greater than 50 g of soy protein with isoflavones may cause gastrointestinal distress in some individuals (5).  Additionally, care should be taken when introducing soy into a patient’s diet, because some individuals have an undiagnosed allergy to soy protein (5).

    Total energy: Maintaining a balance between energy intake and expenditure is a goal of MNT.  Some patients with high LDL cholesterol levels are sensitive to energy intake.  Weight reduction and attainment of a reasonable  body weight will completely correct their elevated LDL cholesterol concentrations.  In many people, weight reduction will also reduce plasma triglycerides levels and raise HDL cholesterol levels (3).

    Fiber: A high intake of total dietary fiber (eg, 25 to 35 g/day) is recommended for adults and is associated with decreased risk for CHD and cardiovascular disease (Grade II) (3,5,23).  Increased intake of foods rich in soluble fiber correlates with decreased serum cholesterol levels (Grade I) (3,5,23).  Consuming diets high in total fiber (17 to 30 g/day) and soluble fiber (7 to 13 g/day) as part of a diet low in saturated fat and cholesterol can further reduce total cholesterol levels by 2% to 3% and LDL cholesterol levels by up to 7% (Grade I) (5).  Choosing soluble fibers (notably beta glucan and pectin) found in oats, barley, and pectin-containing fruits and vegetable provides adjunctive lipid-lowering benefits beyond those achieved through the reduction of total and saturated fat alone (3,23).  The AHA recommends the intake of more than 25 g/day of soluble fiber from a variety of sources, including grains, vegetables, fruits, legumes, and nuts (3).

Other Dietary Factors Influencing Blood Lipid Levels and Risk Factors
Antioxidants: Oxidative processes are involved in the development and clinical expression of cardiovascular disease, and dietary antioxidants may contribute to disease resistance (3).  Epidemiological data suggest that intake of foods rich in vitamin E, C, and beta carotene as part of a cardioprotective dietary pattern is associated with decreased risk for coronary artery disease (Grade III) (5,24-29).  Most studies have involved the consumption of antioxidant-rich foods, such as fruits, vegetables, and whole grains, from which antioxidants were derived (29).  Because so many nutrients are contained in these foods, it is difficult to directly link the antioxidant nutrients to the reduction in CHD risk.  Antioxidants such as vitamin E, vitamin C, and beta carotene (or carotenoids) should be specifically planned into a cardioprotective dietary pattern (Grade III) (5).  The AHA recommends increased consumption of antioxidant-rich fruits, vegetables, and whole grains, which is associated with reduced disease risk (Grade III) (5,29).  There is limited evidence to support the use of antioxidant supplements for disease prevention, even though this topic has been an issue of considerable debate (29).  Vitamin E, vitamin C, and beta carotene supplements should not be recommended to reduce the risk of cardiovascular disease because they have shown no protection for cardiovascular disease events or mortality (Grade II) (5).  The observation that adequate consumption of vitamin E may be difficult to achieve by dietary means leads the debate regarding vitamin E supplementation (26,27).  Recent trials provide stronger evidence that vitamin E supplementation does not reduce cardiovascular disease or all-cause mortality; in some cases, vitamin E supplementation may lead to negative health outcomes including increased risk of death from hemorrhagic stroke (30-34).  The Cambridge Heart Antioxidant Study (32) demonstrated a benefit of vitamin E in secondary prevention; however, the GISSI trial (14) and Heart Outcomes Prevention Evaluation Study (33) showed no beneficial effects of vitamin E at doses of 300 mg and 400 mg, respectively.  Supplemental vitamin E, vitamin C, beta carotene, and selenium should not be taken with the simvastatin/niacin drug combination because of possible blunting of HDL2 (the HDL subfraction that is thought to be most protective) and an increased percentage of stenosis demonstrated in one study (Grade III) (5).  Supplemental beta carotene cannot be recommended for individuals who smoke because of an increased risk for lung cancer in these individuals (Grade III) (5,28,29,34).

    Folic acid and vitamins B6 and B12: Homocysteine, an amino acid in the blood, appears to oxidize LDL cholesterol (16).  A high level of serum homocysteine, independent of other cardiac risk factors, is associated with increased risk for coronary artery disease.  Conversely, low homocysteine levels are associated with reduced risk. (Grade II) (5,16).  An increase in blood total homocysteine levels of 5 μmol/L elevates the risk of coronary artery disease as much as does a 20 mg/dL increase in total cholesterol (16).  Factors that influence blood homocysteine levels include: deficiencies of folate, B6, and B12; age; sex; menopausal status; renal function; and certain medications.  Folate is required for the conversion of homocysteine to methionine, an amino acid.  Serum folate levels have an inverse relationship with total homocysteine levels (35-37).  Although supplemental folate (0.5 to 2.5 mg) taken alone or in combination with B6 (10 to 25 mg) and B12 (0.4 mg) reduced homocysteine levels by 17% to 34%, it did not reduce the risk for coronary events after a period of 6 months to 2 years in stable coronary artery disease patients, post-stroke patients, or post-angioplasty patients that had normal baseline homocysteine levels and total cholesterol levels (Grade II) (5,38,39).  Folate, vitamin B6, and vitamin B12 should be included in the cardioprotective dietary pattern to meet the Dietary Reference Intakes.  If an individual has high serum homocysteine levels (usually greater than 13 μmol/L), these B vitamins may lower serum homocysteine levels by 17% to 34% (Grade II) (5).

    Alcohol: Alcohol does not affect LDL cholesterol concentrations, but it does increase serum triglycerides concentrations and HDL cholesterol levels in many individuals.  The mechanism for the rise in HDL cholesterol is not known.  It is also not known whether the higher level of HDL affords any protection against CHD.  Population and cohort studies, primarily of men, suggest that one or two drinks of alcohol-containing beverages per day are associated with reduced risk of cardiovascular disease, while excessive consumption of alcohol is associated with increased CHD (Grade II) (5,40-42 ).  The NCEP report and the AHA do not specifically recommend alcohol consumption for CHD prevention (1,5).  Most data do not support an association the between type of alcoholic beverage (wine, beer, or liquor) and protection against cardiovascular disease (Grade II) (5,40-42).  The cardiovascular disease benefits of alcohol may be realized when alcohol is consumed with meals (Grade III) (5,40-42).  Observational studies have found a relationship between high alcohol intake (more than three drinks per day) and elevated blood pressure (3,5).  The AHA Guidelines 2000 are consistent with the US Dietary Guidelines in recommending that daily alcohol consumption be limited to two drinks for men and one drink for women.

    Phytochemicals: Phytochemicals are nutritive substances found in plants.  Nuts, whole grains, fruits, and vegetables contain a variety of phytochemicals.  Epidemiologic studies show a relationship between the intake of phytochemicals, primarily plant sterols, flavonoids, and plant sulfur compounds, and CHD.  Plant sterols found in rice bran decrease cholesterol levels (43).  Flavonoids found in tea, onions, soy, and wine have antioxidant properties.  Plant sulfur substances found in garlic, onions, and leeks decrease serum cholesterol (44).  Studies are difficult to interpret because food sources containing phytochemicals have multiple compounds, and results distinguishing a specific cause and effect to the atherosclerotic process have been limited.  Studies are currently assessing the relationship of phytochemicals to CHD. 

    Nuts:  Nuts may enhance the cardioprotective dietary pattern because of their beneficial fatty acid profile as well as other favorable nutritional components (5,43).  The daily consumption of 50 to 113 g (½ to 1 cups) of nuts with a diet low in saturated fat and cholesterol decreased total cholesterol by 4% to 21% and LDL cholesterol by 6% to 29% when weight was not gained  (Grade II) (5,45,46).  Nuts (walnuts, almonds, peanuts, macadamia, pistachios, and pecans) may be isocalorically incorporated into a cardioprotective dietary pattern low in saturated fat and cholesterol (5).  Consuming 5 oz/week of nuts is associated with a reduced risk of CHD (5,45,46). 

    Stanol and sterol ester–containing foods: Plant sterols occur naturally and are isolated from soybean oils (3).  Plant sterols are generally esterified, forming sterol esters, to increase solubility; in some cases, plant sterols are saturated to form stanol esters (3).  Esterified forms of plant sterols and stanols are potent hypercholesterolemic agents, and the daily consumption of 2 to 3 g (in the form of margarine, lowfat yogurt, orange juice, breads, and cereals) lowers total cholesterol concentrations in a dose-dependent manner by 4% to 11% and LDL cholesterol concentrations by 7% to 15% (Grade I) (5,47,48). The efficacy of the two forms, plant stanol esters and plant sterol esters, is comparable (Grade II) (5, 47, 48).  In addition, non-esterified forms of sterols and stanols are equally effective (Grade III) (5,49).  The total cholesterol and LDL-cholesterol lowering effects of stanols and sterols are evident even when sterols and stanols are consumed as part of a cholesterol-lowering diet (Grade I) (5,47,48).  For patients receiving statin therapy, plant stanols further reduce LDL cholesterol and total cholesterol (Grade III) (5).  A limited effect of plant stanols and sterols on HDL cholesterol and triglycerides has been reported.  If consistent with patient preference and not contraindicated by risks or harms, then plant sterol ester– and stanol ester–enriched foods may be consumed two or three times per day, for a total of 2 or 3 g/day, in addition to a cardioprotective diet to further lower total cholesterol and LDL cholesterol levels (Grade I) (5).  For maximal effectiveness, foods containing plant sterols and stanols (spreads, juices, and yogurts) should be eaten with other foods (5).  To prevent weight gain, isocalorically substitute stanol- and sterol-enriched foods for other foods (5).  Plant stanols and sterols are effective in people who take statin drugs.  Plant sterol and stanol products should not be used in individuals with sitosterolemia (5). 

Other Diet Approaches
Very-low-fat, high-carbohydrate (VLFHC) diets: Very-low-fat (up to 15% of total energy), high-carbohydrate (greater than or equal to 60% of total energy) diets have been implemented with patients who are not responsive to diets with more moderate fat intake (eg, 25% to 30%).  Progression of coronary atherosclerosis was delayed among patients who consumed a VLFHC diet and engaged in regular exercise (50,51).  Replacing both saturated fat and unsaturated fat with carbohydrates can lower total cholesterol and LDL cholesterol levels.  In addition, carbohydrate increases VLDL concentrations by adding triglycerides to VLDL particles, a characteristic unfavorable to individuals who have preestablished characteristics of metabolic syndrome.  A VLFHC diet also decreases HDL cholesterol levels (1).  However, the VLFHC diet–induced lowering of HDL cholesterol concentrations has not been associated with the increased risk of atherosclerosis seen with low HDL cholesterol levels that are associated with a high-fat diet (52).  Decreases in total cholesterol and HDL cholesterol levels with VLFCH diet plans may result in a more favorable total cholesterol–to-HDL ratio.  This finding was observed in participants in the Lifestyle Heart Trial who demonstrated angiographic regression of their CHD while also demonstrating diet-induced lowering of HDL cholesterol levels (51).

    The VLFCH diet plans include the Pritikin program and the Ornish meal plans (50,51).  These meal plans limit total fat intake to less than 10% of total energy and encourage the consumption of whole grains, fruits, and vegetables in addition to increased physical activity and reduced stress.  In certain individuals under a physician’s supervision, very-low-fat diets may lead to weight loss and improved lipid profiles.  However, these diets are not recommended by the AHA, as previously mentioned, especially for persons who exhibit characteristics of metabolic syndrome or who have hypertriglyceridemia (3). See Total fat and saturated fatty acids.

    Mediterranean diet: The traditional Mediterranean diet has been investigated based on favorable effects on the lipid profile and decreased CHD risk in persons who live in Mediterranean countries.  The Mediterranean diet is a plant-based diet that emphasizes fruits, vegetables, breads and other cereal grains, potatoes, beans, nuts, and seeds (53).  Olive oil is the principal fat source.  Cheese and yogurt are the key dairy products consumed daily.  Fish, poultry, and eggs are consumed in moderate amounts.  Desserts consist of fresh fruit, and concentrated sugars are eaten only a few times per week.  Little red meat is eaten, and moderate amounts of red wine can be consumed with meals (53).  Total fat content of the diet ranges from 25% to 35% of total energy, and saturated fat contributes less than 8% of total energy.  Few studies have examined the Mediterranean diet plan.  In one study, recurrent myocardial infarction, all cardiovascular events, and cardiac and other deaths were reduced by 70% in the group consuming a Mediterranean diet (54).  Further research is needed to investigate the impact of this diet plan on cholesterol lowering and to determine if it is the specific dietary components (eg, omega-3 fatty acid), increases in specific fatty acid consumption (eg, oleic acid or linolenic acid), or increased antioxidant consumption (eg, vitamins C and E) that cause the cholesterol-lowering effect (54).

    Cardiovascular risk (1,3,4): Increased blood cholesterol levels or, more specifically, increased levels of LDL cholesterol are related to increased risk of CHD.  Coronary risk rises progressively with an increase in cholesterol levels, particularly when cholesterol levels are greater than 200 mg/dL.  Patients with established CHD are at high risk of subsequent myocardial infarction or CHD death, a risk five to seven times higher than without established CHD.

    Substantial evidence indicates that lowering total cholesterol and LDL cholesterol levels (often combined with drug interventions) will decrease the incidence of CHD in both primary and secondary prevention settings (eg, patients with and without evidence of CHD, respectively) (3,4).

    Short-term clinical trials support the projection that for individuals with serum cholesterol levels initially in the 250 to 300 mg/dL range, each 1% reduction in serum cholesterol level yields approximately a 2% reduction in CHD rates.  Epidemiologic studies suggest that the reduction in CHD rates achievable by a long-term cholesterol-lowering regimen amounts to as much as 3% for each 1% reduction in serum cholesterol level.  Thus, it is reasonable to estimate that the 10% to 15% reduction in serum cholesterol level resulting from MNT should reduce CHD risk by 20% to 30%. 

Patient-Centered vs Population Approaches (1,3)
The patient-centered and population approaches are complimentary and together represent a coordinated strategy aimed at reducing cholesterol levels and coronary risk.

    Patient-centered approach: A clinical or patient-based approach seeks to identify individuals at high risk who will benefit from intensive intervention efforts.  Criteria define the candidates for medical intervention.   Guidelines describe how to detect hypercholesterolemia, how to set goals for patients, and how to treat and monitor these patients.

    Population approach: The population or public health approach attempts to lower blood cholesterol levels in the whole population by promoting healthful changes in dietary habits and physical activity levels.  The AHA and the NCEP III take the position that a generalized reduction in cholesterol levels in Americans should decrease the prevalence of CHD.  It is widely assumed that the eating habits of Americans are primarily responsible for high cholesterol levels.  For this reason, the AHA and the NCEP III recommend that the population at large adopt an eating pattern designed to maintain plasma cholesterol levels near the desirable range.

Special Groups
Older adults: According to the AHA, advanced age does not preclude the need to follow the Therapeutic Lifestyle Changes Diet or heart-healthy guidelines (3,4).  Postmenopausal women and older men with elevated LDL cholesterol are at increased risk of developing cardiovascular disease and therefore should be managed based on risk assessment (1,3,4).  When older individuals follow a reduced saturated fat and cholesterol diet, LDL cholesterol levels decrease (1,3,55).  In addition, drug therapy (eg, statins) can be a beneficial adjunct in high-risk patients and is the preferred therapy in place of hormone-replacement therapy in postmenopausal women (1,4).  Because older adults have decreasing total energy needs, they have the added challenge of requiring education on the need for nutrient-dense foods within various food groups to meet nutritional needs (56).

    Pregnant women with preexisting lipid disorders: Elevations in blood cholesterol and triglycerides levels may occur during pregnancy, with maximal levels in the third trimester and a return to normal levels after delivery.  Generally, the MNT previously prescribed for the preexisting lipid disorder should be continued during pregnancy.  If MNT is very restrictive, careful consideration should be given to ensure adequate nutrient intake.  Drug therapy should be discontinued during pregnancy, since the effect of lipid-lowering drugs on the fetus has not been carefully studied (1,3).

    Children and adolescents: The AHA Guidelines 2000 are indicated for all healthy individuals older than 2 years (3).  However, according to the AHA, it should not be assumed that a diet for adults is also appropriate for children.  Individual growth and nutritional requirements need to be considered at each stage of development.  Studies have demonstrated that diets low in saturated fat can support adequate growth and development in children and adolescents (57,58).  The prevalence of obesity and type 2 diabetes mellitus is increasing in the pediatric population (3).  Nutrition strategies for this population should focus on appropriate nutritional intake, balancing energy intake, and increasing physical activity (3).

    Racial and ethnic populations: African Americans have the highest overall CHD mortality rate and the highest out-of-hospital coronary death rates of any ethnic group in the Unites States, particularly at younger ages (1).  The increased incidence is partly attributed to increased prevalence of coronary risk factors, including hypertension, ventricular hypertrophy, diabetes mellitus, cigarette smoking, obesity, and physical inactivity.  Other high-risk ethnic groups and minority populations in the United States include Hispanics, Native Americans, Asian and Pacific Islanders, and South Asians.  The NCEP ATP III recommends intervention for cholesterol management consistent with recommendations outlined for all other populations (1). 

ATP III Guidelines
Criteria that define candidates for MNT intervention and the Therapeutic Lifestyle Changes Diet and lifestyle modifications have been established by the NCEP ATP III, which builds on the previous recommendations of ATP II and ATP I (1).  These guidelines emphasize the importance of MNT provided by a registered dietitian in facilitating the behavior changes needed to follow the recommended diet and lifestyle changes before initiating therapy with cholesterol-lowering medications or in adjunct with this therapy.  The guidelines are expected to substantially increase the number of Americans being treated for high cholesterol.  The number of people receiving dietary treatment is expected to increase from 52 million to 65 million, and the number of people receiving prescribed cholesterol-lowering drugs is expected to increase from 13 million to 36 million (1).

Management of Specific Dyslipidemias and Special Considerations
Because the LDL cholesterol level offers more precise risk assessment and is the primary target of medical interventions, treatment decisions are primarily based on LDL cholesterol levels.  However, the NCEP ATP III recommends the evaluation of a comprehensive lipoprotein panel that includes fasting blood LDL cholesterol, HDL cholesterol, triglycerides, and total cholesterol.  A comprehensive panel provides a more accurate picture so that the Therapeutic Lifestyle Changes Diet and drug therapy can be individualized based on a patient’s metabolic characteristics.

    Low HDL cholesterol (<40 mg/dL): Low HDL cholesterol levels are a significant risk factor for CHD, independent of LDL cholesterol levels and other risk factors (1).  A reduced serum level of HDL cholesterol is defined as a concentration less than 40 mg/dL.  For every 1 mg/dL decrease in HDL cholesterol level, the risk of CHD is increased by 2% to 3% (60).  Likewise, higher HDL cholesterol levels appear to afford a degree of protection against CHD.  This protection warrants considering a high HDL cholesterol level (>60 mg/dL) as a negative risk factor.  HDL cholesterol is measured as part of the lipoprotein analyses for primary prevention in adults without CHD.  For secondary prevention in adults with evidence of CHD, lipoprotein analysis is required in all patients, and classification is based on only LDL cholesterol.  Appropriate advice in treatment includes smoking cessation, weight reduction, and increased physical activity.  Avoidance of certain drugs that reduce HDL cholesterol, such as beta-adrenergic blocking agents (beta-blockers), anabolic steroids, and progestational agents, should also be considered (1).

    Very high LDL cholesterol (>190 mg/dL): Persons with very high LDL cholesterol levels usually have genetic forms of hypercholesterolemia (eg, familial hypercholesterolemia, familial defective apolipoprotein B, and polygenic hypercholesterolemia).  Early detection should be completed in young adults to prevent premature CHD.  These disorders often require combined drug therapy (statin and bile acid sequestrant) to achieve the goals of LDL-lowering therapy (1).

    Elevated serum triglycerides levels (>200 mg/dL): According to the NCEP ATP III, meta-analyses of prospective studies indicate that elevated triglycerides levels are an independent risk factor for CHD.  Factors that contribute to elevated triglycerides levels include obesity and overweight, physical inactivity, cigarette smoking, excess alcohol intake, high-carbohydrate diets (more than 60% of energy intake), certain diseases (eg, type 2 diabetes mellitus, chronic renal failure, and nephrotic syndrome), certain drugs (eg, corticosteroids, estrogens, retinoids, and higher doses of beta-adrenergic blocking agents), and genetic disorders (1).  Generally, elevated serum triglycerides levels are most often observed in persons with metabolic syndrome (1).  The NCEP ATP III adopts the following classification of serum triglycerides levels:

The VLDL level is the most readily available measure of atherogenic remnant lipoproteins.  The ATP III identifies the sum of LDL and VLDL cholesterol (termed non-HDL cholesterol, which can also be calculated by taking total cholesterol minus HDL cholesterol) as a secondary target of therapy in persons with high triglycerides levels (more than 200 mg/dL) (1).  The goal for non-HDL cholesterol in persons with high serum triglycerides levels can be set at 30 mg/dL higher than that for LDL cholesterol (eg, if LDL goal is less than 100 mg/dL, non-HDL goal would be less than 130 mg/dL) (1).

    The treatment for elevated triglycerides level depends on the causes and severity (1).  The primary aim of therapy is to achieve the target goal of LDL cholesterol.  Fibrates and nicotinic acid can be used in combination with LDL-lowering drugs to lower triglycerides and achieve lipid goals (1,4).

    When low HDL cholesterol (less than 40 mg/dL) is associated with a high triglycerides level (200 to 499 mg/dL), the secondary priority is achieving the non-HDL cholesterol goal (as previously described).  The HDL-raising drugs, which include fibrates and nicotinic acid, can be considered in persons with CHD and CHD risk equivalents.  Fibrates and nicotinic acid can be used in combination with LDL-lowering drugs to achieve lipid goals (1,4).

    An important adjunct to long-term change in eating habits and lifestyle is an increase in physical activity.  There is evidence that regular exercise alone reduces CHD mortality by increasing HDL cholesterol levels and, in some patients, lowering LDL cholesterol levels.  The exercise should emphasize aerobic activity, such as brisk walking, jogging, swimming, bicycling, and tennis.  Improvements in cardiovascular fitness result from exercising at moderate intensity for 30 to 45 minutes on most, if not all, days (Grade II) (1,5).  Vigorous, high-intensity exercise must be performed with caution in high-risk persons and only with the advice of a physician and under the supervision of trained personnel (1).

Self-Management Training for the Patient with Disorder of Lipid Metabolism
Once the patient’s risk assessment, clinical status, motivation, comprehension, and environmental support are assessed, the dietitian should set goals with the patient and/or caregiver and provide self-management training to meet the patient’s individualized needs.  Refer to the following evidence-based nutrition practice guidelines (5, 62) or a combination of treatment guidelines as needed for treatment and frequency of MNT intervention:

• Coronary artery bypass graft (CABG) medical nutrition therapy protocol (63)
• Disorders of Lipid Metabolism Evidence-Based Nutrition Practice Guideline (5) 

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