Medical Nutrition Therapy for Disorders of Lipid MetabolismManual of Clinical Nutrition Management C- 43 Copyright © 20 13 Compass Group, Inc.
(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 (> 200 mg/dL), 2 to 4 g/day of EPA
plus DHA, provided as capsules under a physician’s care, are recommended as a therapeutic option (Grade II) (3,5).
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