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TABLE 1 Dietary Reference Intakes for Dietary Fat: Total Fat and Fatty Acids by Life Stage Group DRI Values (g/day) a-Linolenic Acid/AI Total Fat/AIa Linoleic Acid/AI Life stage group Males and Female 0 through 6 mo 31 4.4 0.5 7 through 12 mo 30 4.6 0.5 NDb 1 through 3 y 7 0.7 4 through 8 y ND 10 0.9 Males 9 through 13 y ND 12 1.2 14 through 18 y ND 16 1.6 19 through 30 y ND 17 1.6 31 through 50 y ND 17 1.6 51 through 70 y ND 14 1.6 > 70 y ND 14 1.6 Females 9 through 13 y ND 10 1.0 14 through 18 y ND 11 1.1 19 through 30 y ND 12 1.1 31 through 50 y ND 12 1.1 51 through 70 y ND 11 1.1 > 70 y ND 11 1.1 Pregnancy All ages ND 13 1.4 Lactation All ages ND 13 1.3 a AI = Adequate Intake. If sufficient scientific evidence is not available to establish an EAR, and thus calculate an RDA, an AI is usually developed. For healthy breast-fed infants, the AI is the mean intake. The AI for other life stage and gender groups is believed to cover the needs of all healthy individuals in the group, but a lack of data or uncertainty in the data prevents being able to specify with confidence the percentage of individuals covered by this intake. b ND = Not determined.

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PART II: DIETARY FAT 123 DIETARY FAT: TOTAL FAT AND FATTY ACIDS A major source of energy for the body, fat also aids in the absorption of fat-soluble vitamins A, D, E, K, and other food components, such as carotenoids. Dietary fat consists mainly (98 percent) of triacylglycerol (which is made up of one glycerol molecule esterified with three fatty acid molecules) and small amounts of phospholipids and sterols. In this publi- cation, total fat refers to all forms of triacylglycerol, regardless of fatty acid composition. Neither an Estimated Average Requirement (EAR), and thus a Recommended Dietary Allowance (RDA), nor an Adequate Intake (AI) was set for total fat for individuals aged 1 year and older because data were insufficient to determine a defined intake level at which risk of inadequacy or prevention of chronic dis- ease occurs. However, AIs were set for infants aged 0 through 12 months based on observed mean fat intake of infants who were principally fed human milk. Since there is no defined intake level of fat at which an adverse effect occurs, a Tolerable Upper Intake Level (UL) was not set for total fat. An Acceptable Macro- nutrient Distribution Range (AMDR) has been estimated for total fat at 20–35 percent of energy for adults and children ages 4 and older and 30–40 percent for children ages 1 through 3. Main food sources of total fat are butter, marga- rine, vegetable oils, visible fat on meat and poultry products, whole milk, egg yolk, nuts, and baked goods, such as cookies, doughnuts, pastries and cakes and various fried foods. Fatty acids are the major constituents of triglycerides and fall into the fol- lowing categories: saturated fatty acids, cis monounsaturated fatty acids, cis polyunsaturated fatty acids (n-6 fatty acids and n-3 fatty acids), and trans fatty acids. Saturated fatty acids can be synthesized by the body, where they perform structural and metabolic functions. Neither an EAR (and thus an RDA) nor an AI was set for saturated fatty acids because they are not essential (meaning that they can be synthesized by the body) and have no known role in preventing chronic disease. There is a positive linear trend between saturated fatty acid intake and total and low density lipoprotein (LDL) cholesterol levels and an increased risk of coronary heart disease (CHD). However, a UL was not set for saturated fatty

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 124 acids because any incremental increase in intake increases the risk of CHD. It is recommended that individuals maintain their saturated fatty acid consumption as low as possible, while consuming a nutritionally adequate diet. Food sources of saturated fatty acids tend to be animal-based foods, including whole milk, cream, butter, cheese, and fatty meats. Coconut oil, palm oil, and palm kernel oil are also high in saturated fatty acids. Monounsaturated fatty acids (n-9) can be synthesized by the body and confer no known independent health benefits. Neither an EAR (and thus an RDA) nor an AI was set. Evidence was insufficient to set a UL for c is monounsaturated fatty acids. Foods high in monounsaturated fatty acids in- clude canola oil, olive oil, high-oleic sunflower oil, high-oleic safflower oil, and animal products, primarily meat fat. Animal products provide about 50 percent of dietary monounsaturated fatty acids. Cis polyunsaturated acids include the n-6 fatty acids and n-3 fatty acids. The parent acid of the n-6 fatty acid series is linoleic acid, the only n-6 fatty acid that is an essential fatty acid (EFA), meaning that it cannot be made by the body and must be obtained through the diet. Linoleic acid acts as a precursor for arachidonic acid, which in turn serves as the precursor for eicosanoids (e.g., prostaglandins, thromboxanes, and leukotrienes). Alpha-linolenic (a-linolenic) acid, the parent acid of the n-3 fatty acid series is the only n-3 fatty acid that is an essential fatty acid meaning that it cannot be made by the body and must be obtained through the diet. The n-3 fatty acids play an important role as a struc- tural membrane lipid, particularly in the nerve tissue and retina. The n-3 fatty acids also compete with the n-6 fatty acids for enzymes responsible for the production of the long-chain n-3 fatty acids and thereby influence the balance of n-3 and n-6 fatty acid-derived eicosanoids. The AIs for linoleic acid are based on the median intake of linoleic acid by different life stage and gender groups in the United States, where the presence of n-6 polyunsaturated fatty acid deficiency is nonexistent in healthy individu- als. Evidence was insufficient to set a UL for this and other n-6 polyunsaturated fatty acids. Foods rich in n-6 polyunsaturated fatty acids include nuts, seeds, and vegetable oils, such as sunflower, safflower, corn, and soybean oils. The AIs for a-linolenic acid are based on the median intakes of a-linolenic acid in the United States, where the presence of n-3 polyunsaturated fatty acid deficiency is basically nonexistent in healthy individuals. Evidence was insuffi- cient to set a UL for this and other n-3 fatty acids. Major food sources include certain vegetable oils and fish. Flaxseed, canola, and soybean oils contain high amounts of a-linolenic acid. Fatty fish, fish oils, and products fortified with fish oils contain longer chain n-3 fatty acids. Trans fatty acids are not essential and confer no known health benefits. Therefore, no EAR (and thus an RDA) or AI was set. As with saturated fatty

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PART II: DIETARY FAT 125 acids, there is a positive linear trend between trans fatty acid intake and LDL cholesterol concentration and therefore an increased risk of coronary heart dis- eases. It is recommended that individuals maintain their trans fatty acid con- sumption as low as possible without compromising the nutritional adequacy of their diet. Foods that contain trans fatty acids include traditional stick marga- rine and vegetable shortenings subjected to partial hydrogenation and various bakery products and fried foods prepared using partially hydrogenated oils. Milk, butter, and meats also contain trans fatty acids but at lower levels. A lack of either of the two essential fatty acids (EFAs), linoleic or a-linolenic acid, will result in symptoms of deficiency that include scaly skin, dermatitis, and reduced growth. Such deficiency is very rare in healthy popula- tions in the United States and Canada. Certain types of fatty acids, such as trans and saturated, have been shown to heighten the risk of heart disease in some people by boosting the level of LDL cholesterol in the bloodstream. DRI values are listed by life stage group in Table 1. FAT, FATTY ACIDS, AND THE BODY Background Information Dietary fat consists mainly of triacylglycerol (98 percent) and small amounts of phospholipids and sterols. Triacylglycerols are made up of one glycerol mol- ecule esterified with three fatty acid molecules. In this publication, total fat refers all to forms of triacylglycerol, regardless of fatty acid composition. Fatty acids are hydrocarbon chains that contain a methyl (CH3—) and a carboxyl (—COOH) end. Table 2 shows the major fatty acids found in the diet. Fatty acids vary in their carbon chain length and degree of unsaturation (the number of double bonds in the carbon chain) and can be classified as follows: • saturated fatty acids • cis monounsaturated fatty acids • cis polyunsaturated fatty acids — n-6 fatty acids — n-3 fatty acids • trans fatty acids A very small amount of dietary fat occurs as phospholipids, a form of fat that contains one glycerol molecule that is esterified with two fatty acids and either inositol, choline, serine, or ethanolamine. In the body, phospholipids are mainly located in the cell membranes and the globule membranes of milk.

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 126 TABLE 2 Major Dietary Fatty Acids Category of Fatty Acid Specific Fatty Acids Found in the Diet caprylic acid, 8:0a Saturated fatty acids • • caproic acid, 10:0 • lauric acid, 12:0 • myristic acid, 14:0 • palmitic acid, 16:0 • stearic acid, 18:0 Cis monounsaturated fatty acids • myristoleic acid, 14:1 n-7 • palmitoleic acid, 16:1 n-7 • oleic acid, 18:1 n-9 (account for 92% of monounsaturated dietary fatty acids) • cis-vaccenic acid, 18:1 n-7 • eicosenoic acid, 20:1 n-9 • erucic acid, 22:1 n-9 Cis polyunsaturated fatty acids linoleic acid,b 18:2 n-6 polyunsaturated fatty acid • g-linoleic acid, 18:3 • dihomo-g-linolenic acid, 20:3 • • arachidonic acid, 20:4 • adrenic acid, 22:4 • docosapentaenoic acid, 22:5 a-linolenic acid,b 18:3 n-3 polyunsaturated fatty acid • • eicosapentaenoic acid, 20:5 • docosapentaenoic acid, 22:5 • docosahexaenoic acid, 22:6 Trans fatty acid • 9-trans, 18:1; 9-trans, 16:1; 9-cis,11-trans, 18:2; 9-trans,12-cis, 18:2; 9-cis,12-trans, 18:2 a The first value refers to chain length or number of carbon atoms and the second value refers to the number of double bonds. b Linoleic acid and a-linolenic acid cannot be synthesized in the body and are therefore essential in the diet. Function A major source of energy for the body, fat aids in the absorption of fat-soluble vitamins A, D, E, K, and other food components, such as carotenoids. Fatty acids function in cell signaling and alter the expression of specific genes in-

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PART II: DIETARY FAT 127 TABLE 3 The Functions of Fat and Fatty Acids Fat and Fatty Acids Function Total fata • Major source of energy • Aids in absorption of the fat-soluble vitamins and carotenoids Saturated fatty acids • Sources of energy • Structural components of cell membranes • Enable normal function of proteins Cis monounsaturated fatty acids • Key components of membrane structural lipids, particularly nervous tissue myelin Cis polyunsaturated fatty acids n-6 polyunsaturated fatty acids • Substrates for eicosanoid production, including prostaglandins • Precursors of arachidonic acid • Components of membrane structural lipids • Important in cell signaling pathways • Vital for normal epithelial cell function • Involved in the regulation of genes for proteins that regulate fatty acid synthesis n-3 polyunsaturated fatty acids • Precursors for synthesis of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). EPA is the precursor for n-3 eicosanoids Phospholipids • Major constituents of cell membranes a Total fat refers to all forms of triacylglycerol, regardless of fatty acid composition. volved in lipid and carbohydrate metabolism. Fatty acids, the major constitu- ents of triglycerides, may also serve as precursors or ligands for receptors that are important regulators of adipogenesis, inflammation, insulin action, and neu- rological function. Table 3 summarizes the functions of fat and fatty acids. Absorption, Metabolism, Storage, and Excretion TOTAL FAT In the intestine, dietary fat is emulsified with bile salts and phospholipids (se- creted into the intestine by the liver), hydrolyzed by pancreatic enzymes, and

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 128 almost completely absorbed. Following absorption, the fats are reassembled together with cholesterol, phospholipids, and apoproteins into chylomicrons, which enter the circulation through the thoracic duct. Chylomicrons come into contact with the enzyme lipoprotein lipase (LPL) (located on the surface of capillaries of muscle and adipose tissue) and LPL hydrolyzes the chylomicron triacylglycerol fatty acids. Most of the fatty acids released in this process are taken up by adipose tissue and re-esterfied into triacylglycerol for storage. When fat is needed for fuel, free fatty acids from the liver and muscle are released into the circulation to be taken up by various tissues, where they are oxidized to provide energy. Muscle, which is the main site of fatty acid oxida- tion, uses both fatty acids and glucose for energy. Fatty acids released from fat tissue can also be oxidized by the liver. As fatty acids are broken down through oxidation, carbon dioxide and water are released. Small amounts of ketone bodies are also produced and ex- creted in the urine. The cells of the skin and intestine also contain fatty acids. Thus, small quantities are lost when these cells are sloughed. SATURATED FATTY ACIDS When absorbed along with fats containing appreciable amounts of unsaturated fatty acids, saturated fatty acids are absorbed almost completely by the small intestine. In general, the longer the chain length of the fatty acid, the lower the efficiency of absorption. Following absorption, long-chain saturated fatty acids are re-esterified along with other fatty acids into triacylglycerols and released in chylomicrons. Medium-chain saturated fatty acids are absorbed, bound to al- bumin, transported as free fatty acids in the portal circulation, and cleared by the liver. Oxidation of saturated fatty acids is similar to oxidation of other types of fatty acids (see “Total Fat” above). A unique feature of saturated fatty acids is that they suppress expression of LDL receptors, thus raising blood LDL cholesterol levels. Like other fatty acids, saturated fatty acids tend to be completely oxidized to carbon dioxide and wa- ter. Saturated fatty acids also increase HDL cholesterol. CIS MONOUNSATURATED FATTY ACIDS Absorption of cis monounsaturated fatty acids is in excess of 90 percent (based on oleic acid data) in adults and infants, and the pathways of digestion, absorp- tion, metabolism, and excretion are similar to those of other fatty acids (see “Total Fat” above).

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PART II: DIETARY FAT 129 CIS-POLYUNSATURATED FATTY ACIDS • n-6 polyunsaturated fatty acids: Digestion and absorption of n-6 fatty ac- ids is efficient and occurs via the same pathways as those of other long- chain fatty acids (see “Total Fat” above). The parent fatty acid of the n-6 fatty acids series is linoleic acid. Humans can desaturate and elongate linoleic acid to form arachidonic acid. Arachidonic acid is the precursor to a number of eicosanoids (e.g., prostaglandins, thromboxanes, and leukotrienes) that are involved in platelet aggregation, hemodynamics, and coronary vascular tone. The n-6 fatty acids are almost completely absorbed and are either incorporated into tissue lipids, used in eicosanoid synthesis, or oxidized to carbon dioxide and water. Small amounts are lost via the sloughing of skin and other epithelial cells. • n-3 polyunsaturated fatty acids: Digestion and absorption is similar to that of other long-chain fatty acids (see “Total Fat” above). The body cannot synthesize a-linolenic acid, the parent fatty acid of the n-3 se- ries, and thus requires a dietary source of it. a-Linolenic acid is not known to have any specific functions other than to serve as a precursor for synthesis of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The n-3 fatty acids are almost completely absorbed and are ei- ther incorporated into tissue lipids, used in eicosanoid synthesis, or oxidized to carbon dioxide and water. Small amounts are lost via slough- ing of skin and other epithelial cells. TRANS FATTY ACIDS As with other fatty acids, absorption is about 95 percent. Trans fatty acids are transported similarly to other dietary fatty acids and are distributed within the cholesteryl ester, triacylglycerol, and phospholipid fractions of lipoprotein. Avail- able animal and human data indicate that the trans fatty acid content of tissues (except the brain) reflects diet content and that selective accumulation does not occur. Trans fatty acids are completely catabolized to carbon dioxide and water. DETERMINING DRIS Determining Requirements TOTAL FAT Neither an EAR (and thus an RDA) nor an AI was set for total fat for individuals aged 1 year and older because data were insufficient to determine an intake level at which risk of inadequacy or prevention of chronic disease occurs. How-

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 130 ever, because of the importance of fat to provide the energy needed for growth, AIs were set for infants aged 0 through 12 months. These AIs were based on the observed mean fat intake of infants who were principally fed human milk (0–6 months) and human milk and complementary foods (7–12 months). SATURATED FATTY ACIDS Neither an EAR (and thus an RDA) nor an RDA was set for saturated fatty acids because they are not essential and have no known role in preventing chronic disease. CIS MONOUNSATURATED FATTY ACIDS Cis monounsaturated fatty acids (n-9) confer no known independent health benefits. Since these fatty acids are not required in the diet, neither an EAR (and thus an RDA) nor an AI was set. CIS POLYUNSATURATED FATTY ACIDS • n-6 polyunsaturated fatty acids: In the absence of adequate information on the amount of linoleic acid required to correct the symptoms of an n- 6 polyunsaturated fatty acid deficiency, an EAR (and hence an RDA) could not be established. The AIs for linoleic acid are based on the me- dian intake of linoleic acid by different life stage and gender groups in the United States, where the presence of n-6 polyunsaturated fatty acid deficiency is basically nonexistent in healthy individuals. • n-3 polyunsaturated fatty acids: Because of the lack of evidence for deter- mining a requirement in healthy individuals, an EAR (and thus an RDA) could not be established. The AIs for a-linolenic acid are based on the median intakes of a-linolenic acid in the United States where the pres- ence of n-3 polyunsaturated fatty acid deficiency is basically nonexist- ent in healthy individuals. TRANS FATTY ACIDS Trans fatty acids confer no known health benefits. They are chemically classi- fied as unsaturated fatty acids, but behave more like saturated fatty acids in the body. Therefore, no EAR (and thus RDA) or AI was set. CONJUGATED LINOLEIC ACID There are no known requirements for conjugated linoleic acid (CLA) in the body. Therefore, no EAR (and thus RDA) or AI was set.

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PART II: DIETARY FAT 131 Criteria for Determining Fat Requirements, by Life Stage Group TOTAL FAT Life stage groupa Criterion 0 through 6 mo Average consumption of total fat from human milk 7 through 12 mo Average consumption of total fat from human milk and complementary foods LINOLEIC ACID Life stage group Criterion 0 through 6 mo Average consumption of total n-6 fatty acids from human milk 7 through 12 mo Average consumption of total n-6 fatty acids from human milk and complementary foods Median intake from CSFIIb 1 through 18 y 19 through 50 y Median intake from CSFII for 19 to 30 y group 51 y and through 70 y Median intake from CSFII > 70 y Median intake from CSFII for 51 through 70 y group Pregnancy Median intake from CSFII for all pregnant women Lactation Median intake from CSFII for all lactating women ALPHA-LINOLENIC ACID Life stage group Criterion 0 through 6 mo Average consumption of total n-3 fatty acids from human milk 7 through 12 mo Average consumption of total n-3 fatty acids from human milk and complementary foods Median intake from CSFIIb 1 through 18 y 19 y and older Median intake from CSFII for all adult age groups Pregnancy Median intake from CSFII for all pregnant women Lactation Median intake from CSFII for all lactating women a A DRI value for total fat was not set for any life stage group other than infants. b Continuing Survey of Food Intake by Individuals (1994–1996, 1998).

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 132 The AMDR An AMDR has been estimated for total fat at 20–35 percent of energy for adults and children aged 4 and older and 30–40 percent for children ages 1 through 3. The AMDRs for n-6 polyunsaturated fatty acids (linoleic acid) and n-3 poly- unsaturated fatty acids (a-linolenic acid) are 5–10 percent and 0.6–1.2 per- cent, respectively (see Part II, “Macronutrients, Healthful Diets, and Physical Activity”). The UL TOTAL FAT The Tolerable Upper Intake Level (UL) is the highest level of daily nutrient intake that is likely to pose no risk of adverse effects for almost all people. Since there is no defined intake level of total fat at which an adverse effect occurs, a UL was not set for total fat. SATURATED FATTY ACIDS AND TRANS FATTY ACIDS There is a positive linear trend between saturated fatty acid intake and total and LDL cholesterol levels and a positive linear trend between trans fatty acid and LDL cholesterol concentration. Any incremental increases in saturated and trans fatty acid intakes increase CHD risk, therefore a UL was not set for saturated or trans fatty acids. It is neither possible nor advisable to achieve zero percent of energy from saturated fatty acids or trans fatty acids in typical diets, since this would require extraordinary dietary changes that may lead to inadequate protein and micronutrient intake, as well as other undesirable effects. It is recommended that individuals maintain their saturated and trans fatty acid consumption as low as possible while following a nutritionally adequate diet. CIS MONOUNSATURATED AND CIS POLYUNSATURATED FATTY ACIDS Evidence was insufficient to set a UL for cis monounsaturated fatty acids, and cis polyunsaturated (n-6 and n-3) fatty acids. DIETARY SOURCES Foods Dietary fat intake is primarily (98 percent) in the form of triacylglycerols and is derived from both animal- and plant-based products. The principal foods that contribute to fat intake are butter, margarine, vegetable oils, visible fat on meat

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PART II: DIETARY FAT 133 and poultry products, whole milk, egg yolk, nuts, and baked goods, such as cookies, doughnuts, and cakes. In general, animal fats have higher melting points and are solid at room temperature, which is a reflection of their high content of saturated fatty acids. Plant fats (oils) tend to have lower melting points and are liquid at room tem- perature because of their high content of unsaturated fatty acids. Exceptions to this rule are some tropical oils (e.g., coconut oil and palm kernel oil), which are high in saturated fat and solid at room temperature. Trans fatty acids have physical properties that generally resemble saturated fatty acids, and their presence tends to harden fats. Food sources for the various fatty acids that are typically consumed in North American diets are listed in Table 4. Dietary Supplements This information was not provided at the time the DRI values for total fat and fatty acids were set. INADEQUATE INTAKE AND DEFICIENCY Total Fat Inadequate intake of dietary fat may result in impaired growth and an increased risk of chronic disease. If fat intake, along with carbohydrate and protein in- take, is too low to meet energy needs, an individual will be in negative energy balance. Depending on the severity and duration of the deficit, this may lead to malnutrition or starvation. If the diet contains adequate energy, carbohydrate can replace fat as an energy source. However, fat restriction is of particular concern during infancy, childhood, and pregnancy, during which there are relatively high energy re- quirements for both energy expenditure and fetal development. Imbalanced intake can also be of concern. Compared with higher fat diets, low-fat and high-carbohydrate diets may alter metabolism in a way that in- creases the risk of chronic diseases, such as coronary heart disease and diabetes. These changes include a reduction in high density lipoprotein (HDL) choles- terol concentration, an increase in serum triacylglycerol concentration, and higher responses in glucose and insulin concentrations following food consumption. This metabolic pattern has been associated with an increased risk of CHD and Type II diabetes, although strong evidence does not exist that low-fat diets actu- ally predispose an individual to either CHD or diabetes. Some populations that consume low-fat diets, and in which habitual en- ergy intake is relatively high, have a low prevalence of these chronic diseases.

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 134 TABLE 4 Commonly Consumed Food Sources of Fatty Acids Fatty Acid Food Sources Saturated fatty acids Sources tend to be animal-based foods, including whole milk, cream, butter, cheese, and fatty meats such as pork and beef. Coconut, palm, and palm kernel oils also contain relatively high amounts of saturated fatty acids. Saturated fatty acids provide approximately 20–25 percent of energy in human milk. Cis monounsaturated fatty acids Animal products, primarily meat fat, provide about 50 percent of monounsaturated fatty acids in a typical North American diet. Oils that contain monounsaturated fatty acids include canola and olive oil. Monounsaturated fatty acids provide approximately 20 percent of energy in human milk. Cis polyunsaturated fatty acids: n-6 polyunsaturated fatty acids Nuts, seeds, and vegetable oils such as sunflower, safflower, corn, and soybean oils. g-Linolenic acid is found in black currant seed oil and evening primrose oil. Arachidonic acid is found in small amounts in meat, poultry, and eggs. n-3 polyunsaturated fatty acids Major sources include certain vegetable oils and fish. Flaxseed, canola, and soybean contain high amounts of a-linolenic acid. Fatty fish are major dietary sources of EPA and DHA. Trans fatty acids Traditional stick margarine and vegetable shortenings subjected to partial hydrogenation, milk, butter, and meats. Pastries, fried foods, doughnuts, and french fries are also contributors of trans fatty acid intake. Human milk contains approximately 1–5 percent of total energy as trans fatty acids and, similarly, infant formulas contain approximately 1–3 percent.

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PART II: DIETARY FAT 135 Similarly, populations that consume high-fat diets (i.e., ≥ 40 percent of energy) and experience a low prevalence of chronic diseases often include people who engage in heavy physical labor, are lean, and have a low family history of chronic diseases. Conversely, in sedentary populations, such as those in the United States and Canada where overweight and obesity are common, high-carbohydrate, low-fat diets induce changes in lipoprotein and glucose/insulin metabolism in ways that could raise the risk for chronic diseases. Available prospective studies have not concluded whether high-carbohydrate, low-fat diets present a health risk in the North American population. n-6 Polyunsaturated Fatty Acids Because adipose tissue lipids in free-living healthy adults contain about 10 per- cent of total fatty acids as linoleic acid, the biochemical and clinical signs of essential fatty acid deficiency do not appear during dietary fat restriction or malabsorption when they are accompanied by an energy deficit. In this situa- tion, the release of linoleic acid and small amounts of arachidonic acid from adipose tissue reserves may prevent the development of essential fatty acid de- ficiency. However, during total parenteral nutrition (TPN) with dextrose solu- tions, insulin concentrations are high and mobilization of adipose tissue is pre- vented. This results in the characteristic signs of essential fatty acid deficiency. When n-6 fatty acid intake is inadequate or absorption is impaired, tissue concentrations of arachidonic acid decrease, inhibition of the desaturation of oleic acid is reduced, and synthesis of eicosatrienoic acid from oleic acid in- creases. A lack of dietary n-6 polyunsaturated fatty acids is characterized by rough scaly skin, dermatitis, and an elevated eicosatrienoic acid:arachidonic acid (triene:tetraene) ratio. n-3 Polyunsaturated Fatty Acids A lack of a-linolenic acid in the diet can result in clinical symptoms of a defi- ciency (e.g., scaly dermatitis). Unlike essential fatty acid deficiency (of both n-6 and n-3 fatty acids), plasma eicosatrienoic acid (20:3 n-9) remains within nor- mal ranges, and skin atrophy and scaly dermatitis are absent when the diet is only deficient in n-3 fatty acids. Because of their function, growing evidence suggests that dietary n-3 poly- unsaturated fatty acids (EPA and DHA) may reduce the risk of many chronic diseases including CHD, stroke, and diabetes. For example, n-3 fatty acids may reduce CHD risk through a variety of mechanisms, such as by preventing arrhythmias, reducing atherosclerosis, decreasing platelet aggregation and plasma

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 136 triacylglycerol concentration, slightly increasing HDL concentration, modulat- ing endothelial function, and decreasing proinflammatory eicosanoids. ADVERSE EFFECTS OF OVERCONSUMPTION As mentioned earlier, there is no defined level of fat intake at which an adverse effect, such as obesity, can occur. An AMDR for fat intake, however, has been estimated based on potential adverse effects occurring from consuming low-fat and high-fat diets (see Part II, “Macronutrients, Healthful Diets, and Physical Activity”). High-fat diets in excess of energy needs can cause obesity. Several studies have shown associations between high-fat intakes and an increased risk of CHD, cancer, and insulin resistance. However, the type of fatty acid con- sumed is very important in defining these associations. The potential adverse effects of overconsuming fatty acids are summarized in Table 5. Special Considerations Individuals sensitive to n-3 polyunsaturated fatty acids: People who take hy- poglycemic medications should consume n-3 fatty acids with caution. Because n-3 fatty acids may excessively prolong bleeding time, DHA and EPA supple- ments should be taken with caution by people who take anticoagulants, includ- ing aspirin and warfarin. Exercise: High-fat diets may result in a positive energy balance and therefore in weight gain under sedentary conditions. Active people can probably consume relatively high-fat diets while maintaining their body weight. Athletes may not be able to train as effectively on short-term (fewer than 6 days) high-fat diets as they could on high-carbohydrate diets. It is important to note that physical activity may account for a greater percentage of the variance in weight gain than does dietary fat. Genetic factors: Some data indicate that genes may affect the relationship be- tween diet and obesity. Some people with relatively high metabolic rates appear to be able to eat high-fat diets (44 percent of energy from fat) without becoming obese. Intervention studies have shown that people susceptible to weight gain and obesity appear to have an impaired ability to oxidize more fat after eating high-fat meals. Alcohol: Significant alcohol intake (23 percent of energy) can depress fatty acid oxidation. If the energy derived from alcohol is not used, the excess is stored as fat.

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PART II: DIETARY FAT 137 TABLE 5 Potential Adverse Effects of Fatty Acid Overconsumption Fatty Acid Potential Adverse Effects of Overconsumption Saturated fatty acids In general, the higher the saturated fatty acid intake, the higher the serum total and LDL cholesterol concentrations. There is a positive linear relationship between serum total and LDL cholesterol concentrations and the risk of CHD or mortality from CHD. Cis monounsaturated fatty acids Overconsumption of energy related to a high-fat, high-monounsaturated fatty acid diet is one risk associated with excess monounsaturated fatty acid intake. High intakes can also cause an increased intake of saturated fatty acids, since many animal fats that contain one have the other. Cis polyunsaturated fatty acids: n-6 polyunsaturated fatty acids An AMDR was estimated based on the adverse effects from consuming a diet too high or low in n-6 polyunsaturated fatty acids (see Part II, “Macronutrients, Healthful Diets, and Physical Activity”). n-3 polyunsaturated fatty acids Data on the effects of EPA and DHA intakes on bleeding times are mixed. Until more information is available, supplemental forms of EPA and DHA should be taken with caution. An AMDR was estimated based on the adverse effects from consuming a diet too high or low in n-3 polyunsaturated fatty acids (see Part II, “Macronutrients, Healthful Diets, and Physical Activity”). Trans fatty acids There is a positive linear trend between trans fatty acid intake and LDL concentration, and therefore an increased risk of CHD. Recent data have shown a dose-dependent relationship between trans fatty acid intake and the LDL:HDL ratio. The combined results of numerous studies have indicated that the magnitude of this effect is greater for trans fatty acids, compared with saturated fatty acids.

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DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 138 Interaction of n-6 and n-3 fatty acid metabolism: Many studies, primarily in animals, have suggested that the balance between linoleic and a-linolenic acids is important in determining the amounts of arachidonic acid, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) in tissue lipids. An inappropriate ratio may involve too high an intake of either linoleic acid or a-linolenic acid, too little of one fatty acid, or a combination leading to an imbalance between the two. The ratio between the two is likely to be of most importance in diets that are low in or devoid of arachidonic acid, EPA, and DHA. The importance of this ratio is unknown in diets that are high in these three fatty acids. n-6:n-3 polyunsaturated fatty acid ratio: The ratio of linoleic acid to a- linolenic acid in the diet is important because the two fatty acids compete for the same desaturase enzymes. Thus, a high ratio of linoleic acid to a-linolenic acid can inhibit the conversion of a-linolenic acid to DHA, while a low ratio will inhibit the desaturation of linoleic acid to arachidonic acid. Although limited, the available data suggest that linoleic to a-linolenic acid ratios below 5:1 may be associated with impaired growth in infants. Based on limited studies, the linoleic to a-linolenic acid or total n-3 to n-6 fatty acid ratios of 5:1–10:1, 5:1–15:1, and 6:1–16:1 have been recommended for infant formulas. Based on limited studies, a reasonable linoleic to a-linolenic acid ratio of 5:1–10:1 has been recommended for adults. KEY POINTS FOR FAT AND FATTY ACIDS A major source of energy for the body, fat aids in tissue 3 development and the absorption of the fat-soluble vitamins A, D, E, K, and other food components, such as carotenoids. Dietary fat contains fatty acids that fall into the following 3 categories: saturated fatty acids, cis monounsaturated fatty acids, cis polyunsaturated fatty acids (n-6 fatty acids and n-3 fatty acids), trans fatty acids, and conjugated linoleic acid. Neither an EAR (and thus RDA) nor an AI was set for total fat 3 for individuals aged 1 year and older because data were insufficient to determine an intake level at which risk of inadequacy or prevention of chronic disease occurs. A UL was not set for total fat. AIs for total fat were set for infants aged 0 through 12 months based on observed mean fat intake of infants who were principally fed human milk. An AMDR has been estimated for total fat at 20–35 percent of 3 energy for adults and children aged 4 and older and 30-40 percent for children ages 1 through 3.

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PART II: DIETARY FAT 139 ✓ The main food sources of total fat are butter, margarine, vegetable oils, visible fat on meat and poultry products, whole milk, egg yolk, nuts, and baked goods. ✓ Neither an EAR (and thus RDA) nor an AI was set for trans or saturated fatty acids because they are not essential and have no known role in preventing chronic disease. ✓ There is a positive linear trend between both trans and saturated fatty acid intake and LDL cholesterol levels, and thus increased risk of CHD. A UL was not set for trans or saturated fatty acids because any incremental increase in intake increases the risk of CHD. ✓ It is recommended that individuals maintain their trans and saturated fatty acid intakes as low as possible while consuming a nutritionally adequate diet. ✓ Food sources of saturated fatty acids tend to be meats, bakery items, and full-fat dairy products. Foods that contain trans fatty acids include traditional stick margarine and vegetable shortenings that have been partially hydrogenated, with lower levels in meats and dairy products. ✓ Cis monounsaturated fatty acids can be synthesized by the body and confer no known health benefits. Since they are not required in the diet, neither an AI nor an RDA was set. There was insufficient evidence to set a UL. ✓ Animal products, primarily meat fat, provide about 50 percent of dietary cis monounsaturated fatty acids intake. ✓ Linoleic and α-linolenic fatty acids are essential, and therefore must be obtained from foods. AIs were set based on intake of healthy individuals. There was insufficient evidence to set a UL for cis polyunsaturated (n-6 and n-3) fatty acids. ✓ Foods rich in n-6 polyunsaturated fatty acids include nuts, seeds, certain vegetables, and vegetable oils, such as sunflower, safflower, corn, and soybean oils. Major food sources of n-3 polyunsaturated fatty acids include certain vegetable oils (flaxseed, canola, and soybean oils) and fatty fish. ✓ High-fat diets in excess of energy needs can cause obesity. Several studies have shown associations between high-fat intakes and an increased risk of CHD, cancer, and insulin resistance. However, the type of fatty acid consumed is very important in defining these associations.