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8 Dietary Fats: Total Fat and Fatty Acids SUMMARY Fat is a major source of fuel energy for the body and aids in the absorption of fat-soluble vitamins and carotenoids. Neither an Adequate Intake (AI) nor Recommended Dietary Allowance (RDA) is set for total fat because there are insufficient data to determine a defined level of fat intake at which risk of inadequacy or prevention of chronic disease occurs. An Acceptable Macronutrient Distribu- tion Range (AMDR), however, has been estimated for total fat—it is 20 to 35 percent of energy (see Chapter 11). A Tolerable Upper Intake Level (UL) is not set for total fat because there is no defined intake level of fat at which an adverse effect occurs. Saturated fatty acids are synthesized by the body to provide an adequate level needed for their physiological and structural func- tions; they have no known role in preventing chronic diseases. Therefore, neither an AI nor RDA is set for saturated fatty acids. There is a positive linear trend between total saturated fatty acid intake and total and low density lipoprotein (LDL) cholesterol concentration and increased risk of coronary heart disease (CHD). A UL is not set for saturated fatty acids because any incremental increase in saturated fatty acid intake increases CHD risk. It is neither possible nor advisable to achieve 0 percent of energy from saturated fatty acids in typical whole-food diets. This is because all fat and oil sources are mixtures of fatty acids, and consuming 0 percent of energy would require extraordinary changes in pat- terns of dietary intake. Such extraordinary adjustments may intro- duce undesirable effects (e.g., inadequate intakes of protein and 422

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423 D IETARY FATS: TOTAL FAT AND FATTY ACIDS certain micronutrients) and unknown and unquantifiable health risks. The AMDR for total fat is set at 20 to 35 percent of energy. It is possible to have a diet low in saturated fatty acids by following the dietary guidance provided in Chapter 11. n-9 cis Monounsaturated fatty acids are synthesized by the body and have no known independent beneficial role in human health and are not required in the diet. Therefore, neither an AI nor an RDA is set. There is insufficient evidence to set a UL for n-9 cis monounsaturated fatty acids. Linoleic acid is the only n-6 polyunsaturated fatty acid that is an essential fatty acid; it serves as a precursor to eicosanoids. A lack of dietary n-6 polyunsaturated fatty acids is characterized by rough and scaly skin, dermatitis, and an elevated eicosatrienoic acid:arachidonic acid (triene:tetraene) ratio. The AI for linoleic acid is based on the median intake in the United States where an n-6 fatty acid deficiency is nonexistent in healthy individuals. The AI is 17 g/d for young men and 12 g/d for young women. While intake levels much lower than the AI occur in the United States without the presence of a deficiency, the AI can provide the ben- eficial health effects associated with the consumption of linoleic acid (see Chapter 11). There is insufficient evidence to set a UL for n-6 polyunsaturated fatty acids. n-3 Polyunsaturated fatty acids play an important role as structural membrane lipids, particularly in nerve tissue and the retina, and are precursors to eicosanoids. A lack of α-linolenic acid in the diet can result in clinical symptoms of a deficiency (e.g., scaly dermatitis). An AI is set for α-linolenic acid based on median intakes in the United States where an n-3 fatty acid deficiency is nonexistent in healthy individuals. The AI is 1.6 and 1.1 g/d for men and women, respectively. While intake levels much lower than the AI occur in the United States without the presence of a deficiency, the AI can provide the beneficial health effects associated with the consumption of n-3 fatty acids (see Chapter 11). There is insufficient evidence to set a UL for n-3 fatty acids. Trans fatty acids are not essential and provide no known benefit to human health. Therefore, no AI or RDA is set. As with saturated fatty acids, there is a positive linear trend between trans fatty acid intake and LDL cholesterol concentration, and therefore increased risk of CHD. A UL is not set for trans fatty acids because any incre- mental increase in trans fatty acid intake increases CHD risk. Because trans fatty acids are unavoidable in ordinary, nonvegan diets, consuming 0 percent of energy would require significant changes in patterns of dietary intake. As with saturated fatty acids, such adjustments may introduce undesirable effects (e.g., elimina-

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424 DIETARY REFERENCE INTAKES tion of commercially prepared foods, dairy products, and meats that contain trans fatty acids may result in inadequate intakes of protein and certain micronutrients) and unknown and unquanti- fiable health risks. Nevertheless, it is recommended that trans fatty acid consumption be as low as possible while consuming a nutri- tionally adequate diet. Dietary guidance in minimizing trans fatty acid intake is provided in Chapter 11. BACKGROUND INFORMATION Total Fat Fat is a major source of fuel energy for the body. It also aids in the absorption of the fat-soluble vitamins A, D, E, and K and carotenoids. Dietary fat consists primarily (98 percent) of triacylglycerol, which is com- posed of one glycerol molecule esterified with three fatty acid molecules, and smaller amounts of phospholipids and sterols. Fatty acids are hydro- carbon chains that contain a methyl (CH3-) and a carboxyl (-COOH) end. The fatty acids vary in carbon chain length and degree of unsaturation (number of double bonds in the carbon chain). The fatty acids can be classified into the following categories: • Saturated fatty acids • Cis monounsaturated fatty acids • Cis polyunsaturated fatty acids — n-6 fatty acids — n-3 fatty acids • Trans fatty acids Dietary fat derives from both animal and plant products. 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 (oils); this is explained by their high content of unsaturated fatty acids. Exceptions to this rule are the seed 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 generally resembling saturated fatty acids and their presence tends to harden fats. In the discussion below, total fat intake refers to the intake of all forms of triacylglycerol, regardless of fatty acid composition, in terms of percentage of total energy intake. In addition to the functions of fat and fatty acids described above, fatty acids also function in cell signaling and alter expression of specific genes

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425 D IETARY FATS: TOTAL FAT AND FATTY ACIDS involved in lipid and carbohydrate metabolism (Jump and Clarke, 1999; Sessler and Ntambi, 1998). Fatty acids may themselves be ligands for, or serve as precursors for, the synthesis of unknown endogenous ligands for nuclear peroxisome proliferator activating receptors (Kliewer et al., 1997; Latruffe and Vamecq, 1997). These receptors are important regulators of adipogenesis, inflammation, insulin action, and neurological function. Phospholipids Phospholipids are a form of fat that contains one glycerol molecule that is esterified with two fatty acids and either inositol, choline, serine, or ethanolamine. Phospholipids are primarily located in the membranes of cells in the body and the globule membranes in milk. A very small amount of dietary fat occurs as phospholipid. The metabolism of phospholipids is described below for total fat. The various fatty acids that are contained in phospholipids are the same as those present in triglycerides. Saturated Fatty Acids The majority of dietary saturated fatty acids come from animal products such as meat and dairy products (USDA, 1996). The remaining comes from plant sources. These sources provide a series of saturated fatty acids for which the major dietary fatty acids range in chain length from 8 to 18 carbon atoms. These are: • 8:0 Caprylic acid • 10:0 Caproic acid • 12:0 Lauric acid • 14:0 Myristic acid • 16:0 Palmitic acid • 18:0 Stearic acid The saturated fatty acids are not only a source of body fuel, but are also structural components of cell membranes. Various saturated fatty acids are also associated with proteins and are necessary for their normal function. Saturated fatty acids can be synthesized by the body. Fats in general, including saturated fatty acids, play a role in providing desirable texture and palatability to foods used in the diet. Palmitic acid is particularly useful for enhancing the organoleptic properties of fats used in commercial products. Stearic acid, in contrast, has physical properties that limit the amount that can be incorporated into dietary fat.

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426 DIETARY REFERENCE INTAKES Cis Monounsaturated Fatty Acids Cis monounsaturated fatty acids are characterized by having one double bond with the hydrogen atoms present on the same side of the double bond. Typically, plant sources rich in cis monounsaturated fatty acids (e.g., canola oil, olive oil, and the high oleic safflower and sunflower oils) are liquid at room temperature. Monounsaturated fatty acids are present in foods with a double bond located at 7 (n-7) or 9 (n-9) carbon atoms from the methyl end. Monounsaturated fatty acids that are present in the diet include: • 18:1n-9 Oleic acid • 14:1n-7 Myristoleic acid • 16:1n-7 Palmitoleic acid • 18:1n-7 Vaccenic acid • 20:1n-9 Eicosenoic acid • 22:1n-9 Erucic acid Oleic acid accounts for about 92 percent of dietary monounsaturated fatty acids. Monounsaturated fatty acids, including oleic acid and nervonic acid (24:1n-9), are important in membrane structural lipids, particularly nervous tissue myelin. Other monounsaturated fatty acids, such as palmitoleic acid, are present in minor amounts in the diet. n-6 Polyunsaturated Fatty Acids The primary n-6 polyunsaturated fatty acids are: • 18:2 Linoleic acid γ-Linolenic acid • 18:3 Dihomo-γ-linolenic acid • 20:3 • 20:4 Arachidonic acid • 22:4 Adrenic acid • 22:5 Docosapentaenoic acid Linoleic acid cannot be synthesized by humans and a lack of it results in adverse clinical symptoms, including a scaly rash and reduced growth. Therefore, linoleic acid is essential in the diet. Linoleic acid is the precursor to arachidonic acid, which is the substrate for eicosanoid production in tissues, is a component of membrane structural lipids, and is also impor- tant in cell signaling pathways. Dihomo-γ-linolenic acid, also formed from linoleic acid, is also an eicosanoid precursor. n-6 Polyunsaturated fatty acids also play critical roles in normal epithelial cell function (Jones and

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427 D IETARY FATS: TOTAL FAT AND FATTY ACIDS Kubow, 1999). Arachidonic acid and other unsaturated fatty acids are involved with regulation of gene expression resulting in decreased expres- sion of proteins that regulate the enzymes involved with fatty acid synthesis (Ou et al., 2001). This may partly explain the ability of unsaturated fatty acids to influence the hepatic synthesis of fatty acids. n-3 Polyunsaturated Fatty Acids n-3 Polyunsaturated fatty acids tend to be highly unsaturated with one of the double bonds located at 3 carbon atoms from the methyl end. This group includes: α-Linolenic acid • 18:3 • 20:5 Eicosapentaenoic acid • 22:5 Docosapentaenoic acid • 22:6 Docosahexaenoic acid α-Linolenic acid is not synthesized by humans and a lack of it results in adverse clinical symptoms, including neurological abnormalities and poor growth. Therefore, α-linolenic acid is essential in the diet. It is the precursor for synthesis of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are formed in varying amounts in animal tissues, espe- cially fatty fish, but not in plant cells. EPA is the precursor of n-3 eicosanoids, which have been shown to have beneficial effects in preventing coronary heart disease, arrhythmias, and thrombosis (Kinsella et al., 1990). Trans Fatty Acids Trans fatty acids are unsaturated fatty acids that contain at least one double bond in the trans configuration. The trans double-bond configura- tion results in a larger bond angle than the cis configuration, which in turn results in a more extended fatty acid carbon chain more similar to that of saturated fatty acids rather than that of cis unsaturated, double-bond– containing fatty acids. The conformation of the double bond impacts on the physical properties of the fatty acid. Those fatty acids containing a trans double bond have the potential for closer packing or aligning of acyl chains, resulting in decreased mobility; hence fluidity is reduced when compared to fatty acids containing a cis double bond. Partial hydrogena- tion of polyunsaturated oils causes isomerization of some of the remaining double bonds and migration of others, resulting in an increase in the trans fatty acid content and the hardening of fat. Hydrogenation of oils, such as corn oil, can result in both cis and trans double bonds anywhere between carbon 4 and carbon 16. A major trans fatty acid is elaidic acid (9-trans 18:1).

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428 DIETARY REFERENCE INTAKES During hydrogenation of polyunsaturated fatty acids, small amounts of several other trans fatty acids (9-trans,12-cis 18:2; 9-cis,12-trans 18:2) are produced. In addition to these isomers, dairy fat and meats contain 9-trans 16:1 and conjugated dienes (9-cis,11-trans 18:2). The trans fatty acid content in foods tends to be higher in foods containing hydrogenated oils (Emken, 1995). Conjugated Linoleic Acid Conjugated linoleic acid (CLA) is a collective term for a group of geometric and positional isomers of linoleic acid in which the trans/cis double bonds are conjugated; that is, the double bonds occur without an intervening carbon atom not part of a double bond. At least nine different isomers of CLA have been reported as minor constituents of food (Ha et al., 1989), but only two of the isomers, cis-9,trans-11 and trans-10,cis-12, possess biological activity (Pariza et al., 2001). There is limited evidence to suggest that the trans-10,cis-12 isomer reduces the uptake of lipids by the adipocyte, and that the cis-9,trans-11 isomer is active in inhibiting carcino- genesis. Similarly, there are limited data to show that cis-9,trans-11 and trans-10,cis-12 isomers inhibit atherogenesis (Kritchevsky et al., 2000). CLA is naturally present in dairy products and ruminant meats as a consequence of biohydrogenation in the rumen. Butyrivibrio fibrisolvens, a ruminant microorganism, is responsible for the production of the cis-9, trans -11 CLA isomer that is synthesized as a result of the bio- hydrogenation of linoleic acid (Noble et al., 1974). The cis-9,trans-11 CLA isomer may be directly absorbed or further metabolized to trans-11 octadecenoic acid (vaccenic acid) (Pariza et al., 2001). After absorption, vaccenic acid can then be converted back to cis-9,trans-11 CLA within mammalian cells by ∆9 desaturase (Adlof et al., 2000; Chin et al., 1994; Griinari et al., 2000; Santora et al., 2000). Additionally, the biohydrogenation of several other polyunsaturated fatty acids has been shown to produce vaccenic acid as an intermediate (Griinari and Bauman, 1999), thus pro- viding additional substrate for the endogenous production of cis-9,trans-11 CLA. Griinari and coworkers (2000) estimate that approximately 64 per- cent of the CLA in cow’s milk is of endogenous origin. Verhulst and coworkers (1987) isolated a microorganism, Propioni- bacterium acnes, that appears to have the ability to convert linoleic acid to trans-10,cis-12 CLA, an isomer of CLA that is found in rumen digesta (Fellner et al., 1999). Trans-10 octadecenoic acid is formed in the rumen via biohydrogenation of trans-10,cis-12 CLA, and both have been reported to be found in cow’s milk (Griinari and Bauman, 1999). However, endogenous production of trans-10,cis-12 CLA from trans-10 octadecenoic acid does not occur because mammalian cells do not possess the ∆12 desaturase enzyme (Adlof et al., 2000; Pariza et al., 2001). Therefore, any trans-10,cis-12 CLA

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429 D IETARY FATS: TOTAL FAT AND FATTY ACIDS isomer that is reported in mammalian tissue or sera would likely originate from gastrointestinal absorption. Physiology of Absorption, Metabolism, and Excretion Total Fat Absorption. Dietary fat undergoes lipolysis by lipases in the gastro- intestinal tract prior to absorption. Although there are lipases in the saliva and gastric secretion, most lipolysis occurs in the small intestine. The hydrolysis of triacylglycerol is achieved through the action of pancreatic lipase, which requires colipase, also secreted by the pancreas, for activity. In the intestine, fat is emulsified with bile salts and phospholipids secreted into the intestine in bile, hydrolyzed by pancreatic enzymes, and almost completely absorbed. Pancreatic lipase has high specificity for the sn-1 and sn-3 positions of dietary triacylglycerols, resulting in the release of free fatty acids from the sn-1 and sn-3 positions and 2-monoacylglycerol. These products of digestion are absorbed into the enterocyte, and the triacyl- glycerols are reassembled, largely via the 2-monoacylglycerol pathway. This pathway conserves the fatty acid at the sn-2 position. The triacylglycerols are then assembled together with cholesterol, phospholipid, and apoproteins into chylomicrons. Following absorption, fatty acids of carbon chain length 12 or less may be transported as unesterified fatty acids bound to albumin directly to the liver via the portal vein, rather than acylated into triacylglycerols. Dietary phospholipids are hydrolyzed by pancreatic phospholipase A2 and cholesterol esters by pancreatic cholesterol ester hydrolase. The lyso- phospholipids are re-esterified and packaged together with cholesterol and triacylglycerols in intestinal lipoproteins or transported as lysophospholipid via the portal system to the liver. Chylomicrons enter the circulation through the thoracic duct. These particles enter the circulation and within the capillaries of muscle and adipose tissue. Chylomicrons come into contact with the enzyme lipo- protein lipase, which is located on the surface of capillaries. Activation of lipoprotein lipase apolipoprotein CII, an apoprotein present on chylo- microns, results in the hydrolysis of the chylomicron triacylglycerol fatty acids. Most of the fatty acids released in this process are taken up by adipose tissue and re-esterified into triacylglycerol for storage. Triacylglycerol fatty acids also are taken up by muscle and oxidized for energy or are released into the systemic circulation and returned to the liver.

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430 DIETARY REFERENCE INTAKES Metabolism. Most newly absorbed fatty acids enter adipose tissue for storage as triacylglycerol. However, in the postabsorptive state or during exercise when fat is needed for fuel, adipose tissue triacylglycerol under- goes lipolysis and free fatty acids are released into the circulation. Hydrolysis occurs via the action of the adipose tissue enzyme hormone-sensitive lipase. The activity of this lipase is suppressed by insulin. When plasma insulin concentrations fall in the postabsorptive state, hormone-sensitive lipase is activated to release more free fatty acids into the circulation. Thus, in the postabsorptive state, free fatty acid concentrations in plasma are high; conversely, in the postprandial state, hormone-sensitive lipase activity is suppressed and free fatty acid concentrations in plasma are low. Free fatty acids circulate in the blood bound to albumin. The major site of fatty acid oxidation is skeletal muscle. When free fatty acid concen- trations are relatively high, muscle uptake of fatty acids is also high. As in liver, fatty acids in the muscle are transported via a carnitine-dependent pathway into mitochondria where they undergo β-oxidation, which involves removal of two carbon fragments. These two carbon units enter the citric acid cycle as acetyl coenzyme A (CoA), through which they are completely oxidized to carbon dioxide with the generation of large quantities of high- energy phosphate bonds, or they condense to form ketone bodies. Muscle can oxidize both fatty acids and glucose for energy. However, the uptake of fatty acids in excess of the needs for oxidation for energy by muscle does result in temporary storage as triacylglycerol (Bessesen et al., 1995). High uptake of fatty acids by skeletal muscle also reduces glucose uptake by muscle and glucose oxidation (Pan et al., 1997; Roden et al., 1996). Fatty acids released from adipose tissue or to a lesser extent during hydrolysis of chylomicron and very low density lipoprotein (VLDL) triacylglycerols are also taken up and oxidized by the liver. Oxidation of fatty acids containing up to 18 carbon atoms occurs mainly in the mito- chondria. Oxidation of excess fatty acids in the liver, which occurs in pro- longed fasting and with high intakes of medium-chain fatty acids, results in formation of large amounts of acetyl CoA that exceed the capacity for entry to the citric acid cycle. These 2-carbon acetyl CoA units condense to form ketone bodies (e.g., acetoacetate and β-hydroxybutyrate) that are released into the circulation. During starvation or prolonged low carbohy- drate intake, ketone bodies can become an important alternate energy substrate to glucose for the brain and muscle. High dietary intakes of medium-chain fatty acids also result in the generation of ketone bodies. This is explained by the carnitine-independent influx of medium-chain fatty acids into the mitochondria, thus by-passing this regulatory step of fatty acid entry into β-oxidation. Fatty acids of greater than 18 carbon atoms require chain shortening in peroxisomes prior to mitochondrial β-oxidation.

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431 D IETARY FATS: TOTAL FAT AND FATTY ACIDS Fatty acids that do not enter into oxidative pathways can be re-esterified into triacylglycerols or other lipids. The major pathway for triacylglycerol synthesis in liver is the 3-glycerophosphate pathway, which shows a high degree of specificity for saturated fatty acids at the sn-1(3) position and for unsaturated fatty acids at the sn-2 position. In the liver, triacylglycerols can either be stored temporarily or incorporated into triacylglycerol-rich VLDL and released into the plasma. The triacylglycerol fatty acids of VLDL have the same fate as chylomicron triacylglycerol fatty acids. When VLDL triacylglycerols undergo lipolysis, the remaining triacylglycerol-depleted particle is called a VLDL remnant. These remnants are either removed directly by the liver or they are further metabolized in the vascular com- partment to form low density lipoproteins (LDL). Excretion. Fatty acids are generally catabolized entirely by oxidative processes from which the only excretion products are carbon dioxide and water. Small amounts of ketone bodies produced by fatty acid oxidation are excreted in urine. Fatty acids are present in the cells of the skin and intestine, thus small quantities are lost when these cells are sloughed. Saturated Fatty Acids Absorption. When saturated fatty acids are ingested along with fats con- taining appreciable amounts of unsaturated fatty acids, they are absorbed almost completely by the small intestine. In general, the longer the chain length of the fatty acid, the lower will be the efficiency of absorption. However, unsaturated fatty acids are well absorbed regardless of chain length. Studies with human infants have shown the absorption to be 75, 62, 92, and 94 percent of palmitic acid, stearic acid, oleic acid, and linoleic acid, respectively, from vegetable oils (Jensen et al., 1986). The absorption of palmitic acid and stearic acid from human milk is higher than from cow milk and vegetable oils (which are commonly used in infant formulas) because of the specific positioning of these long-chain saturated fatty acids at the sn-2 position of milk triacylglycerols (Carnielli et al., 1996a; Jensen, 1999). The intestinal absorption of palmitic acid and stearic acid from vegetable oils was 75 to 78 percent compared with 91 to 97 percent from fats with these fatty acids in the sn-2 position (Carnielli et al., 1996a). Still, absorption of stearic acid was over 90 percent complete in healthy adults when contained in triacylglycerols of mixed fatty acids (Bonanome and Grundy, 1989). Long-chain saturated fatty acids released into the lumen through the action of pancreatic lipase are less readily solubilized into mixed micelles than are unsaturated fatty acids; in the alkaline pH of the intestine they can form insoluble soaps with calcium and other divalent

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432 DIETARY REFERENCE INTAKES cations and can be excreted (Carnielli et al., 1996a; Lucas et al., 1997; Tomarelli et al., 1968). 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 (C8:0 and C10:0) are absorbed and transported bound to albumin as free fatty acids in the portal circulation and cleared by the liver. About two-thirds of lauric acid (C12:0) is transported with chylomicron triacylglycerols, whereas the remaining one-third enters the portal circulation as free fatty acids. Metabolism. Pathways of oxidation of saturated fatty acids are similar to those for other types of fatty acids (see earlier section, “Total Fat”). Unoxidized stearic acid (9 to 14 percent) is rapidly desaturated and con- verted to the monounsaturated fatty acid, oleic acid (Emken, 1994; Rhee et al., 1997). For this reason, dietary stearic acid has metabolic effects that are closer to those of oleic acid rather than those of other long-chain saturated fatty acids. The saturated fatty acids, in contrast to cis mono- or polyunsaturated fatty acids, have a unique property in that they suppress the expression of LDL receptors (Spady et al., 1993). Through this action, dietary saturated fatty acids raise serum LDL cholesterol concentrations (Mustad et al., 1997). Excretion. Saturated fatty acids, like other fatty acids, are generally com- pletely oxidized to carbon dioxide and water. cis-Monounsaturated Fatty Acids Absorption. The absorption of cis-monounsaturated fatty acids (based on oleic acid data) is in excess of 90 percent in adults and infants (Jensen et al., 1986; Jones et al., 1985). The pathways of cis-monounsaturated fat digestion and absorption are similar to those of other fatty acids (see earlier section, “Total Fat”). Metabolism. Oleic acid, the major monounsaturated fatty acid in the body, is derived mainly from the diet. Small amounts also come from desaturation of stearic acid. Stable isotope tracer methods have shown that approximately 9 to 14 percent of dietary stearic acid is converted to oleic acid in vivo (Emken, 1994; Rhee et al., 1997). Based on the amount of stearic acid in the average diet (approximately 3 percent of energy), desaturation of dietary stearic acid is not a main source of oleic acid in the body. Oleic acid is oxidized, as are all other fatty acids, by β-oxidation. However, there is some evidence that oxidation of chylomicron-derived oleic acid is significantly greater than for palmitic acid (Schmidt et al.,

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531 D IETARY FATS: TOTAL FAT AND FATTY ACIDS Martinez M. 1992. Tissue levels of polyunsaturated fatty acids during early human development. J Pediatr 120:S129–S138. Martinez M, Ballabriga A, Gil-Gibernau JJ. 1988. Lipids of the developing human retina: I. Total fatty acids, plasmalogens, and fatty acid composition of ethanolamine and choline phosphoglycerides. J Neurosci Res 20:484–490. Mascioli EA, Smith MF, Trerice MS, Meng HC, Blackburn GL. 1979. Effect of total parenteral nutrition with cycling on essential fatty acid deficiency. J Parenter Enteral Nutr 3:171–173. Mascioli EA, Lopes SM, Champagne C, Driscoll DF. 1996. Essential fatty acid defi- ciency and home total parenteral nutrition patients. Nutrition 12:245–249. McGee DL, Reed DM, Yano K, Kagan A, Tillotson J. 1984. Ten-year incidence of coronary heart disease in the Honolulu Heart Program. Relationship to nutrient intake. Am J Epidemiol 119:667–676. Meng HC. 1983. A case of human linolenic acid deficiency involving neurological abnormalities. Am J Clin Nutr 37:157–159. Mensink RP, Hornstra G. 1995. The proportion of trans monounsaturated fatty acids in serum triacylglycerols or platelet phospholipids as an objective indicator of their short-term intake in healthy men. Br J Nutr 73:605–612. Mensink RP, Katan MB. 1990. Effect of dietary trans fatty acids on high-density and low-density lipoprotein cholesterol levels in healthy subjects. N Engl J Med 323:439–445. Mensink RP, Katan MB. 1992. Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials. Arterioscler Thromb 12:911–919. Mensink RP, de Louw MHJ, Katan MB. 1991. Effects of dietary trans fatty acids on blood pressure in normotensive subjects. Eur J Clin Nutr 45:375–382. Mensink RP, Zock PL, Katan MB, Hornstra G. 1992. Effect of dietary cis and trans fatty acids on serum lipoprotein[a] levels in humans. J Lipid Res 33:1493–1501. Mensink RP, Temme EH, Hornstra G. 1994. Dietary saturated and trans fatty acids and lipoprotein metabolism. Ann Med 26:461–464. Meydani SN, Endres S, Woods MM, Goldin BR, Soo C, Morrill-Labrode A, Dinarello CA, Gorbach SL. 1991. Oral (n-3) fatty acid supplementation suppresses cytokine production and lymphocyte proliferation: Comparison between young and older women. J Nutr 121:547–555. Meydani SN, Lichtenstein AH, Cornwall S, Meydani M, Goldin BR, Rasmussen H, Dinarello CA, Schaefer EJ. 1993. Immunologic effects of National Cholesterol Education Panel Step-2 Diets with and without fish-derived n -3 fatty acid enrichment. J Clin Invest 92:105–113. Michels K, Sacks F. 1995. Trans fatty acids in European margarines. N Engl J Med 332:541–542. Miller WC, Niederpruem MG, Wallace JP, Lindeman AK. 1994. Dietary fat, sugar, and fiber predict body fat content. J Am Diet Assoc 94:612–615. Mohrhauer H, Holman RT. 1963. The effect of dose level of essential fatty acids upon fatty acid composition of the rat liver. J Lipid Res 4:151–159. Mølvig J, Pociot F, Worsaae H, Wogensen LD, Baek L, Christensen P, Mandrup- Poulsen T, Andersen K, Madsen P, Dyerberg J, Nerup J. 1991. Dietary supple- mentation with ω-3-polyunsaturated fatty acids decreases mononuclear cell proliferation and interleukin-1β c ontent but not monokine secretion in healthy and insulin-dependent diabetic individuals. Scand J Immunol 34:399–410. Moore SA, Yoder E, Murphy S, Dutton GR, Spector AA. 1991. Astrocytes, not neurons, produce docosahexaenoic acid (22:6ω-3) and arachidonic acid (20:4ω-6). J Neurochem 56:518–524.

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532 DIETARY REFERENCE INTAKES Morley R. 1998. Nutrition and cognitive development. Nutrition 14:752–754. Mortensen JZ, Schmidt EB, Nielsen AH, Dyerberg J. 1983. The effect of n-6 and n-3 fatty acids on hemostasis, blood lipids and blood pressure. Thromb Haemostas 50:543–546. Müller H, Jordal O, Seljeflot I, Kierulf P, Kirkhus B, Ledsaak O, Pedersen JI. 1998. Effect on plasma lipids and lipoproteins of replacing partially hydrogenated fish oil with vegetable fat in margarine. Br J Nutr 80:243–251. Murgatroyd PR, Van De Ven MLHM, Goldberg GR, Prentice AM. 1996. Alcohol and the regulation of energy balance: Overnight effects on diet-induced thermogenesis and fuel storage. Br J Nutr 75:33–45. Murgatroyd PR, Goldberg GR, Leahy FE, Gilsenan MB, Prentice AM. 1999. Effects of inactivity and diet composition on human energy balance. Int J Obes Relat Metab Disord 23:1269–1275. Mustad VA, Etherton TD, Cooper AD, Mastro AM, Pearson TA, Jonnalagadda SS, Kris-Etherton PM. 1997. Reducing saturated fat intake is associated with increased levels of LDL receptors on mononuclear cells in healthy men and women. J Lipid Res 38:459–468. Mutanen M, Aro A. 1997. Coagulation and fibrinolysis factors in healthy subjects consuming high stearic or trans fatty acid diets. Thromb Haemost 77:99–104. Neaton JD, Wentworth D. 1992. Serum cholesterol, blood pressure, cigarette smoking, and death from coronary heart disease. Overall findings and differences by age for 316,099 white men. Arch Intern Med 152:56–64. Nelson GJ, Schmidt PC, Corash L. 1991. The effect of a salmon diet on blood clotting, platelet aggregation and fatty acids in normal adult men. Lipids 26:87–96. Nelson GJ, Schmidt PC, Bartolini GL, Kelley DS, Kyle D. 1997. The effect of dietary docosahexaenoic acid on plasma lipoproteins and tissue fatty acid composi- tion in humans. Lipids 32:1137–1146. Nestel PJ, Noakes M, Belling GB, McArthur R, Clifton PM, Abbey M. 1992a. Plasma cholesterol-lowering potential of edible-oil blends suitable for commercial use. Am J Clin Nutr 55:46–50. Nestel PJ, Noakes M, Belling B, McArthur R, Clifton P, Janus E, Abbey M. 1992b. Plasma lipoprotein lipid and Lp[a] changes with substitution of elaidic acid for oleic acid in the diet. J Lipid Res 33:1029–1036. Nestel P, Clifton P, Noakes M. 1994. Effects of increasing dietary palmitoleic acid compared with palmitic and oleic acids on plasma lipids of hypercholes- terolemic men. J Lipid Res 35:656–662. Neuringer M, Connor WE, Van Petten C, Barstad L. 1984. Dietary omega-3 fatty acid deficiency and visual loss in infant rhesus monkeys. J Clin Invest 73:272– 276. Neuringer M, Connor WE, Lin DS, Barstad L, Luck S. 1986. Biochemical and functional effects of prenatal and postnatal ω3 fatty acid deficiency on retina and brain in rhesus monkeys. Proc Natl Acad Sci USA 83:4021–4025. Nielsen LB. 1999. Atherogenecity of lipoprotein(a) and oxidized low density lipo- protein: Insight from in vivo studies of arterial wall influx, degradation and efflux. Atherosclerosis 143:229–243. Niinikoski H, Lapinleimu H, Viikari J, Rönnemaa T, Jokinen E, Seppänen R, Terho P, Tuominen J, Välimäki I, Simell O. 1997a. Growth until 3 years of age in a prospective, randomized trial of a diet with reduced saturated fat and choles- terol. Pediatrics 99:687–694.

OCR for page 422
533 D IETARY FATS: TOTAL FAT AND FATTY ACIDS Niinikoski H, Viikari J, Rönnemaa T, Helenius H, Jokinen E, Lapinleimu H, Routi T, Lagström H, Seppänen R, Välimäki I, Simell O. 1997b. Regulation of growth of 7- to 36-month-old children by energy and fat intake in the prospective, randomized STRIP baby trial. Pediatrics 100:810–816. Noakes M, Clifton PM. 1998. Oil blends containing partially hydrogenated or interesterified fats: Differential effects on plasma lipids. A m J Clin Nutr 68:242–247. Noble RC, Moore JH, Harfoot CG. 1974. Observations on the pattern of bio- hydrogenation of esterified and unesterified linoleic acid in the rumen. Br J Nutr 31:99–108. Nommsen LA, Lovelady CA, Heinig MJ, Lönnerdal B, Dewey KG. 1991. Determi- nants of energy, protein, lipid, and lactose concentrations in human milk during the first 12 mo of lactation: The DARLING Study. Am J Clin Nutr 53:457–465. Obarzanek E, Hunsberger SA, Van Horn L, Hartmuller VV, Barton BA, Stevens VJ, Kwiterovich PO, Franklin FA, Kimm SYS, Lasser NL, Simons-Morton DG, Lauer RM. 1997. Safety of a fat-reduced diet: The Dietary Intervention Study in Children (DISC). Pediatrics 100:51–59. Olsen SF, Hansen HS, Jensen B, Sørensen TIA. 1989. Pregnancy duration and the ratio of long-chain n-3 fatty acids to arachidonic acid in erythrocytes from Faroese women. J Intern Med 225:185–189. Olsen SF, Sørensen JD, Secher NJ, Hedegaard M, Henriksen TB, Hansen HS, Grant A. 1992. Randomised controlled trial of effect of fish-oil supplementa- tion on pregnancy duration. Lancet 339:1003–1007. O’Neill JA, Caldwell MD, Meng HC. 1977. Essential fatty acid deficiency in surgical patients. Ann Surg 185:535–542. Ou J, Tu H, Luk A, DeBose-Boyd RA, Bashmakov Y, Goldstein JL, Brown MS. 2001. Unsaturated fatty acids inhibit transcription of the sterol regulatory element- binding protein-1c (SREBP-1c) gene by antagonizing ligand-dependent activa- tion of the LXR. Proc Natl Acad Sci USA 98:6027–6032. Pan DA, Lillioja S, Kriketos AD, Milner MR, Baur LA, Bogardus C, Jenkins AB, Storlien LH. 1997. Skeletal muscle triglyceride levels are inversely related to insulin action. Diabetes 46:983–988. Pariza MW, Park Y, Cook ME. 2001. The biologically active isomers of conjugated linoleic acid. Prog Lipid Res 40:283–298. Parker DR, Weiss ST, Troisi R, Cassano PA, Vokonas PS, Landsberg L. 1993. Relationship of dietary saturated fatty acids and body habitus to serum insulin concentrations: The Normative Aging Study. Am J Clin Nutr 58:129–136. Paulsrud JR, Pensler L, Whitten CF, Stewart S, Holman RT. 1972. Essential fatty acid deficiency in infants induced by fat-free intravenous feeding. Am J Clin Nutr 25:897–904. Pedersen HS, Mulvad G, Seidelin KN, Malcom GT, Boudreau DA. 1999. n-3 Fatty acids as a risk factor for haemorrhagic stroke. Lancet 353:812–813. Pietinen P, Ascherio A, Korhonen P, Hartman AM, Willett WC, Albanes D, Virtamo J. 1997. Intake of fatty acids and risk of coronary heart disease in a cohort of Finnish men. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Am J Epidemiol 145:876–887. Ponder DL, Innis SM, Benson JD, Siegman JS. 1992. Docosahexaenoic acid status of term infants fed breast milk or infant formula containing soy oil or corn oil. Pediatr Res 32:683–688.

OCR for page 422
534 DIETARY REFERENCE INTAKES Putnam JC, Carlson SE, DeVoe PW, Barness LA. 1982. The effect of variations in dietary fatty acids on the fatty acid composition of erythrocyte phosphatidyl- choline and phosphatidylethanolamine in human infants. Am J Clin Nutr 36:106–114. Raben A, Andersen HB, Christensen NJ, Madsen J, Holst JJ, Astrup A. 1994. Evi- dence for an abnormal postprandial response to a high-fat meal in women predisposed to obesity. Am J Physiol 267:E549–E559. Ratnayake WMN, Hollywood R, O’Grady E, Pelletier G. 1993. Fatty acids in some common food items in Canada. J Am Coll Nutr 12:651–660. Ratnayake WM, Chardigny JM, Wolff RL, Bayard CC, Sebedio JL, Martine L. 1997. Essential fatty acids and their trans geometrical isomers in powdered and liquid infant formulas sold in Canada. J Pediatr Gastroenterol 25:400–407. Rhee SK, Kayani AJ, Ciszek A, Brenna JT. 1997. Desaturation and interconversion of dietary stearic and palmitic acids in human plasma and lipoproteins. Am J Clin Nutr 65:451–458. Richardson TJ, Sgoutas D. 1975. Essential fatty acid deficiency in four adult patients during total parenteral nutrition. Am J Clin Nutr 28:258–263. Riella MC, Broviac JW, Wells M, Scribner BH. 1975. Essential fatty acid deficiency in human adults during total parenteral nutrition. Ann Intern Med 83:786–789. Ritzenthaler KL, McGuire MK, Falen R, Shultz TD, Dasgupta N, McGuire MA. 2001. Estimation of conjugated linoleic acid intake by written dietary assess- ment methodologies underestimates actual intake evaluated by food duplicate methodology. J Nutr 131:1548–1554. Roche HM, Zampelas A, Jackson KG, Williams CM, Gibney MJ. 1998. The effect of test meal monounsaturated fatty acid:saturated fatty acid ratio on postprandial lipid metabolism. Br J Nutr 79:419–424. Roden M, Price TB, Perseghin G, Petersen KF, Rothman DL, Cline GW, Shulman GI. 1996. Mechanism of free fatty acid-induced insulin resistance in humans. J Clin Invest 97:2859–2865. Rodriguez A, Sarda P, Nessmann C, Boulot P, Poisson J-P, Leger CL, Descomps B. 1998. Fatty acid desaturase activities and polyunsaturated fatty acid composi- tion in human fetal liver between the seventeenth and thirty-sixth gestational weeks. Am J Obstet Gynecol 179:1063–1070. Rogers S, James KS, Butland BK, Etherington MD, O’Brien JR, Jones JG. 1987. Effects of a fish oil supplement on serum lipids, blood pressure, bleeding time, haemostatic and rheological variables. A double blind randomised con- trolled trial in healthy volunteers. Atherosclerosis 63:137–143. Rosenthal MD, Doloresco MA. 1984. The effects of trans fatty acids on fatty acyl ∆5 desaturation by human skin fibroblasts. Lipids 19:869–874. Rudel LL, Haines J, Sawyer JK, Shah R, Wilson MS, Carr TP. 1997. Hepatic origin of cholesteryl oleate in coronary artery atherosclerosis in African green monkeys. J Clin Invest 100:74–83. Russell RM. 1992. Changes in gastrointestinal function attributed to aging. Am J Clin Nutr 55:1203S–1207S. Ruttenberg H, Davidson LM, Little NA, Klurfeld DM, Kritchevsky D. 1983. Influ- ence of trans unsaturated fats on experimental atherosclerosis in rabbits. J Nutr 113:835–844. Ryan AS, Montalto MB, Groh-Wargo S, Mimouni F, Sentipal-Walerius J, Doyle J, Siegman JS, Thomas AJ. 1999. Effect of DHA-containing formula on growth of preterm infants to 59 weeks postmenstrual age. Am J Hum Biol 11:457–467.

OCR for page 422
535 D IETARY FATS: TOTAL FAT AND FATTY ACIDS Rywik SL, Manolio TA, Pajak A, Piotrowski W, Davids CE, Broda GB, Kawalec E. 1999. Association of lipids and lipoprotein level with total mortality and mor- tality caused by cardiovascular and cancer diseases (Poland and United States collaborative study on cardiovascular epidemiology). Am J Cardiol 84:540–548. Salem N, Wegher B, Mena P, Uauy R. 1996. Arachidonic and docosahexaenoic acids are biosynthesized from their 18-carbon precursors in human infants. Proc Natl Acad Sci USA 93:49–54. Salem N, Litman B, Kim H-Y, Gawrisch K. 2001. Mechanisms of action of docosa- hexaenoic acid in the nervous system. Lipids 36:945–959. Salmerón J, Hu FB, Manson JE, Stampfer MJ, Colditz GA, Rimm EB, Willett WC. 2001. Dietary fat intake and risk of type 2 diabetes in women. Am J Clin Nutr 73:1019–1026. Sanders TAB, Reddy S. 1992. The influence of a vegetarian diet on the fatty acid composition of human milk and the essential fatty acid status of the infant. J Pediatr 120:S71–S77. Sanders TAB, Vickers M, Haines AP. 1981. Effect of blood lipids and haemostasis of a supplement of cod-liver oil, rich in eicosapentaenoic and docosahexaenoic acids, in healthy young men. Clin Sci 61:317–324. Sanders TAB, de Grassi T, Miller GJ, Morrissey JH. 2000. Influence of fatty acid chain length and cis/trans isomerization on postprandial lipemia and factor VII in healthy subjects (postprandial lipids and factor VII). A therosclerosis 149:413–420. Sanjurjo P, Matorras R, Ingunza N, Alonso M, Rodriguez-Alarcón J, Perteagudo L. 1993. Cross-sectional study of percentual changes in total plasmatic fatty acids during pregnancy. Horm Metab Res 25:590–592. Santora JE, Palmquist DL, Roehrig KL. 2000. Trans-vaccenic acid is desaturated to conjugated linoleic acid in mice. J Nutr 130:208–215. Sauerwald TU, Hachey DL, Jensen CL, Chen H, Anderson RE, Heird WC. 1996. Effect of dietary α-linolenic acid intake on incorporation of docosahexaenoic and arachidonic acids into plasma phospholipids of term infants. L ipids 31:S131–S135. Sauerwald TU, Hachey DL, Jensen CL, Chen H, Anderson RE, Heird WC. 1997. Intermediates in endogenous synthesis of C22:6ω3 and C20:4ω6 by term and preterm infants. Pediatr Res 41:183–187. Schakel SF, Buzzard IM, Gebhardt SE. 1997. Procedures for estimating nutrient values for food composition databases. J Food Comp Anal 10:102–114. Schmidt DE, Allred JB, Kien CL. 1999. Fractional oxidation of chylomicron-derived oleate is greater than that of palmitate in healthy adults fed frequent small meals. J Lipid Res 40:2322–2332. Schmidt EB, Pedersen JO, Ekelund S, Grunnet N, Jersild C, Dyerberg J. 1989. Cod liver oil inhibits neutrophil and monocyte chemotaxis in healthy males. Athero- sclerosis 77:53–57. Schmidt EB, Varming K, Ernst E, Madsen P, Dyerberg J. 1990. Dose–response studies on the effect of n -3 polyunsaturated fatty acids on lipids and haemostasis. Thromb Haemost 63:1–5. Schmidt EB, Lervang H-H, Varming K, Madsen P, Dyerberg J. 1992. Long-term supplementation with n-3 fatty acids. I: Effect on blood lipids, haemostasis and blood pressure. Scand J Clin Lab Invest 52:221–228. Schutz Y. 2000. Role of substrate utilization and thermogenesis on body-weight control with particular reference to alcohol. Proc Nutr Soc 59:511–517.

OCR for page 422
536 DIETARY REFERENCE INTAKES Scott DT, Janowsky JS, Carroll RE, Taylor JA, Auestad N, Montalto MB. 1998. Formula supplementation with long-chain polyunsaturated fatty acids: Are there developmental benefits? Pediatrics 102:E59. Seppänen-Laakso T, Vanhanen H, Laakso I, Kohtamäki H, Viikari J. 1993. Replace- ment of margarine on bread by rapeseed and olive oils: Effects on plasma fatty acid composition and serum cholesterol. Ann Nutr Metab 37:161–174. Sessler AM, Ntambi JM. 1998. Polyunsaturated fatty acid regulation of gene expres- sion. J Nutr 128:923–926. Sevak L, McKeigue PM, Marmot MG. 1994. Relationship of hyperinsulinemia to dietary intake in South Asian and European men. Am J Clin Nutr 59:1069–1074. Shea S, Basch CE, Stein AD, Contento IR, Irigoyen M, Zybert P. 1993. Is there a relationship between dietary fat and stature or growth in children three to five years of age? Pediatrics 92:579–586. Shekelle RB, Missell L, Paul O, Shyrock AM, Stamler J. 1985. Fish consumption and mortality from coronary heart disease. N Engl J Med 313:820. Sherwood NE, Jeffery RW, French SA, Hannan PJ, Murray DM. 2000. Predictors of weight gain in the Pound of Prevention Study. Int J Obes Relat Metab Disord 24:395–403. Shetty PS, Prentice AM, Goldberg GR, Murgatroyd PR, McKenna APM, Stubbs RJ, Volschenk PA. 1994. Alterations in fuel selection and voluntary food intake in response to isoenergetic manipulation of glycogen stores in humans. Am J Clin Nutr 60:534–543. Shimp JL, Bruckner G, Kinsella JE. 1982. The effects of dietary trilinoelaidin on fatty acid and acyl desaturases in rat liver. J Nutr 112:722–735. Shintani TT, Beckham S, Brown AC, O’Connor HK. 2001. The Hawaii Diet: Ad libitum high carbohydrate, low fat multi-cultural diet for the reduction of chronic disease risk factors: Obesity, hypertension, hypercholesterolemia, and hyperglycemia. Hawaii Med J 60:69–73. Siguel EN, Lerman RH. 1993. Trans-fatty acid patterns in patients with angio- graphically documented coronary artery disease. Am J Cardiol 71:916–920. Siguel EN, Blumberg JB, Caesar J. 1986. Monitoring the optimal infusion of intra- venous lipids. Arch Pathol Lab Med 110:792–797. Sinclair AJ. 1975. Incorporation of radioactive polyunsaturated fatty acids into liver and brain of developing rat. Lipids 10:175–184. Sinclair AJ, Murphy KJ, Li D. 2000. Marine lipids: Overview “news insights and lipid composition of Lyprinol™” Allerg Immunol (Paris) 32:261–271. Slattery ML, Potter JD, Duncan DM, Berry TD. 1997. Dietary fats and colon cancer: Assessment of risk associated with specific fatty acids. Int J Cancer 73:670–677. Smith P, Arnesen H, Opstad T, Dahl KH, Eritsland J. 1989. Influence of highly concentrated n-3 fatty acids on serum lipids and hemostatic variables in survi- vors of myocardial infarction receiving either oral anticoagulants or matching placebo. Thromb Res 53:467–474. Song JH, Miyazawa T. 2001. Enhanced level of n-3 fatty acid in membrane phospho- lipids induces lipid peroxidation in rats fed dietary docosahexaenoic acid oil. Atherosclerosis 155:9–18. Sørensen NS, Marckmann P, Høy C-E, van Duyvenvoorde W, Princen HMG. 1998. Effect of fish-oil-enriched margarine on plasma lipids, low-density-lipoprotein particle composition, size, and susceptibility to oxidation. A m J Clin Nutr 68:235–241.

OCR for page 422
537 D IETARY FATS: TOTAL FAT AND FATTY ACIDS Sorkin JD, Andres R, Muller DC, Baldwin HL, Fleg JL. 1992. Cholesterol as a risk factor for coronary heart disease in elderly men. The Baltimore Longitudinal Study of Aging. Ann Epidemiol 2:59–67. Spady DK, Woolett LA, Dietschy JM. 1993. Regulation of plasma LDL-cholesterol levels by dietary cholesterol and fatty acids. Annu Rev Nutr 13:355–361. Sperling RI, Benincaso AI, Knoell CT, Larkin JK, Austen KF, Robinson DR. 1993. Dietary ω-3 polyunsaturated fatty acids inhibit phosphoinositide formation and chemotaxis in neutrophils. J Clin Invest 91:651–660. Sprecher H. 1992. Interconversions between 20- and 22-carbon n-3 and n-6 fatty acids via 4-desaturase independent pathways. In: Sinclair AJ, Gibson R, eds. Essential Fatty Acids and Eicosanoids: Invited Papers from the Third International Congress. Champaign, IL: American Oil Chemists’ Society. Pp. 18–22. Sprecher H, Luthria DL, Mohammed BS, Baykousheva SP. 1995. Reevaluation of the pathways for the biosynthesis of polyunsaturated fatty acids. J Lipid Res 36:2471–2477. Stacpoole PW, Alig J, Ammon L, Crockett SE. 1989. Dose–response effects of dietary marine oil on carbohydrate and lipid metabolism in normal subjects and patients with hypertriglyceridemia. Metabolism 38:946–956. Stamler J, Wentworth D, Neaton JD. 1986. Is relationship between serum choles- terol and risk of premature death from coronary heart disease continuous and graded? Findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT). J Am Med Assoc 256:2823–2828. Sugano M, Ikeda I. 1996. Metabolic interactions between essential and trans-fatty acids. Curr Opin Lipidol 7:38–42. Sundram K, Ismail A, Hayes KC, Jeyamalar R, Pathmanathan R. 1997. Trans (elaidic) fatty acids adversely affect the lipoprotein profile relative to specific saturated fatty acids in humans. J Nutr 127:514S–520S. Suter PM, Schutz Y, Jequier E. 1992. The effect of ethanol on fat storage in healthy subjects. N Engl J Med 326:983–987. Tavani A, Negri E, D’Avanzo B, La Vecchia C. 1997. Margarine intake and risk of nonfatal acute myocardial infarction in Italian women. Eur J Clin Nutr 51:30–32. Thompson PJ, Misso NLA, Passarelli M, Phillips MJ. 1991. The effect of eicosa- pentaenoic acid consumption on human neutrophil chemiluminescence. Lipids 26:1223–1226. Thomsen C, Rasmussen O, Lousen T, Holst JJ, Fenselau S, Schrezenmeir J, Hermansen K. 1999. Differential effects of saturated and monounsaturated fatty acids on postprandial lipemia and incretin responses in healthy subjects. Am J Clin Nutr 69:1135–1143. Thorngren M, Gustafson A. 1981. Effects of 11-week increase in dietary eicosa- pentaenoic acid on bleeding time, lipids, and platelet aggregation. Lancet 2:1190–1193. Tomarelli RM, Meyer BJ, Weaber JR, Bernhart FW. 1968. Effect of positional distri- bution on the absorption of the fatty acids of human milk and infant formulas. J Nutr 95:583–590. Troiano RP, Briefel RR, Carroll MD, Bialostosky K. 2000. Energy and fat intakes of children and adolescents in the United States: Data from the National Health and Nutrition Examination Surveys. Am J Clin Nutr 72:1343S–1353S. Troisi R, Willett WC, Weiss ST. 1992. Trans-fatty acid intake in relation to serum lipid concentrations in adult men. Am J Clin Nutr 56:1019–1024.

OCR for page 422
538 DIETARY REFERENCE INTAKES Turpeinen AM, Wübert J, Aro A, Lorenz R, Mutanen M. 1998. Similar effects of diets rich in stearic acid or trans-fatty acids on platelet function and endothelial prostacyclin production in humans. Arterioscler Thromb Vasc Biol 18:316–322. Tuyns AJ, Kaaks R, Haelterman M. 1988. Colorectal cancer and the consumption of foods: A case-control study in Belgium. Nutr Cancer 11:189–204. Uauy R, Mena P, Wegher B, Nieto S, Salem N. 2000a. Long chain polyunsaturated fatty acid formation in neonates: Effect of gestational age and intrauterine growth. Pediatr Res 47:127–135. Uauy R, Mize CE, Castillo-Duran C. 2000b. Fat intake during childhood: Metabolic responses and effects on growth. Am J Clin Nutr 72:1354S–1360S. Umegaki K, Hashimoto M, Yamasaki H, Fujii Y, Yoshimura M, Sugisawa A, Shinozuka K. 2001. Docosahexaenoic acid supplementation-increased oxida- tive damage in bone marrow DNA in aged rats and its relation to antioxidant vitamins. Free Radic Res 34:427–435. USDA (U.S. Department of Agriculture). 1996. The Food Guide Pyramid. Home and Garden Bulletin No. 252. Washington, DC: U.S. Government Printing Office. USDA/HHS (U.S. Department of Health and Human Services). 2000. Nutrition and Your Health: Dietary Guidelines for Americans, 5th ed. Home and Garden Bulletin No. 232. Washington, DC: U.S. Government Printing Office. Valenzuela A, Morgado N. 1999. Trans fatty acid isomers in human health and in the food industry. Biol Res 32:273–287. van Dam RM, Huang Z, Giovannucci E, Rimm EB, Hunter DJ, Colditz GA, Stampfer MJ, Willett WC. 2000. Diet and basal cell carcinoma of the skin in a prospec- tive cohort of men. Am J Clin Nutr 71:135–141. van den Brandt PA, van’t Veer P, Goldbohm RA, Dorant E, Volovics A, Hermus RJJ, Sturmans F. 1993. A prospective cohort study on dietary fat and the risk of postmenopausal breast cancer. Cancer Res 53:75–82. van Erp-baart M-A, Couet C, Cuadrado C, Kafatos A, Stanley J, van Poppel G. 1998. Trans f atty acids in bakery products from 14 European countries: The TRANSFAIR Study. J Food Comp Anal 11:161–169. van Houwelingen AC, Hornstra G. 1994. Trans fatty acids in early human develop- ment. World Rev Nutr Diet 75:175–178. van Houwelingen AC, Sørensen JD, Hornstra G, Simonis MMG, Boris J, Olsen SF, Secher NJ. 1995. Essential fatty acid status in neonates after fish-oil supple- mentation during late pregnancy. Br J Nutr 74:723–731. van Poppel G, van Erp-baart M-A, Leth T, Gevers E, Van Amelsvoort J, Lanzmann- Petithory D, Kafatos A, Aro A. 1998. Trans fatty acids in foods in Europe: The TRANSFAIR Study. J Food Comp Anal 11:112–136. Veierød MB, Laake P, Thelle DS. 1997. Dietary fat intake and risk of lung cancer: A prospective study of 51,452 Norwegian men and women. Eur J Cancer Prev 6:540–549. Velie E, Kulldorff M, Schairer C, Block G, Albanes D, Schatzkin A. 2000. Dietary fat, fat subtypes, and breast cancer in postmenopausal women: A prospective cohort study. J Natl Cancer Inst 92:833–839. Verhulst A, Janssen G, Parmentier G, Eyssen H. 1987. Isomerization of polyunsatu- rated long chain fatty acids by propionibacteria. Syst Appl Microbiol 9:12–15. Vermunt SHF, Mensink RP, Simonis MMG, Hornstra G. 2000. Effects of dietary α-linolenic acid on the conversion and oxidation of 13C-α-linolenic acid. Lipids 35:137–142.

OCR for page 422
539 D IETARY FATS: TOTAL FAT AND FATTY ACIDS Vessby B, Uusitupa M, Hermansen K, Riccardi G, Rivellese AA, Tapsell LC, Nälsén C, Berglund L, Louheranta A, Rasmussen BM, Calvert GD, Maffetone A, Pedersen E, Gustafsson I-B, Storlien LH. 2001. Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU study. Diabetologia 44:312–319. Vidgren HM, Ågren JJ, Schwab U, Rissanen T, Hänninen O, Uusitupa MIJ. 1997. Incorporation of n-3 fatty acids into plasma lipid fractions, and erythrocyte membranes and platelets during dietary supplementation with fish, fish oil, and docosahexaenoic acid-rich oil among healthy young men. Lipids 32:697–705. Vidgren HM, Louheranta AM, Ågren JJ, Schwab US, Uusitupa MIJ. 1998. Divergent incorporation of dietary trans fatty acids in different serum lipid fractions. Lipids 33:955–962. Virella G, Fourspring K, Hyman B, Haskill-Stroud R, Long L, Virella I, La Via M, Gross AJ, Lopes-Virella M. 1991. Immunosuppressive effects of fish oil in normal human volunteers: Correlation with the in vitro effects of eicosapentanoic acid on human lymphocytes. Clin Immunol Immunopathol 61:161–176. Virtanen SM, Feskens EJM, Räsänen L, Fidanza F, Tuomilehto J, Giampaoli S, Nissinen A, Kromhout D. 2000. Comparison of diets of diabetic and non- diabetic elderly men in Finland, The Netherlands and Italy. Eur J Clin Nutr 54:181–186. Vobecky JS, Vobecky J, Normand L. 1995. Risk and benefit of low fat intake in childhood. Ann Nutr Metab 39:124–133. Vogel RA, Corretti MC, Plotnick GD. 2000. The postprandial effect of components of the Mediterranean diet on endothelial function. J Am Coll Cardiol 36:1455– 1460. Voss A, Reinhart M, Sankarappa S, Sprecher H. 1991. The metabolism of 7,10,13,16,19-docosapentaenoic acid to 4,7,10,13,16,19-docosahexaenoic acid in rat liver is independent of a 4-desaturase. J Biol Chem 266:19995–20000. Ward KD, Sparrow D, Vokonas PS, Willett WC, Landsberg L, Weiss ST. 1994. The relationships of abdominal obesity, hyperinsulinemia and saturated fat intake to serum lipid levels: The Normative Aging Study. Int J Obes Relat Metab Disord 18:137–144. Watts GF, Jackson P, Burke V, Lewis B. 1996. Dietary fatty acids and progression of coronary artery disease in men. Am J Clin Nutr 64:202–209. Weijenberg MP, Feskens EJM, Kromhout D. 1996. Total and high density lipo- protein cholesterol as risk factors for coronary heart disease in elderly men during 5 years of follow-up. The Zutphen Elderly Study. A m J Epidemiol 143:151–158. Wene JD, Connor WE, DenBesten L. 1975. The development of essential fatty acid deficiency in healthy men fed fat-free diets intravenously and orally. J Clin Invest 56:127–134. West DB, York B. 1998. Dietary fat, genetic predisposition, and obesity: Lessons from animal models. Am J Clin Nutr 67:505S–512S. Wetzel MG, Li J, Alvarez RA, Anderson RE, O’Brien PJ. 1991. Metabolism of linolenic acid and docosahexaenoic acid in rat retinas and rod outer seg- ments. Exp Eye Res 53:437–446. Wheeler TG, Benolken RM, Anderson RE. 1975. Visual membranes: Specificity of fatty acid precursors for the electrical response to illumination. S cience 188:1312–1314.

OCR for page 422
540 DIETARY REFERENCE INTAKES Wild SH, Fortmann SP, Marcovina SM. 1997. A prospective case-control study of lipoprotein(a) levels and apo(a) size and risk of coronary heart disease in Stanford Five-City Project participants. Arterioscler Thromb Vasc Biol 17:239–245. Willatts P, Forsyth JS, DiModugno MK, Varma S, Colvin M. 1998. Effect of long- chain polyunsaturated fatty acids in infant formula on problem solving at 10 months of age. Lancet 352:688–691. Willett WC, Stampfer MJ, Mason JE, Colditz GA, Speizer FE, Rosner BA, Sampson LA, Hennekens CH. 1993. Intake of trans fatty acids and risk of coronary heart disease among women. Lancet 341:581–585. Wojenski CM, Silver MJ, Walker J. 1991. Eicosapentaenoic acid ethyl ester as an antithrombotic agent: Comparison to an extract of fish oil. Biochim Biophys Acta 1081:33–38. Wong KH, Deitel M. 1981. Studies with a safflower oil emulsion in total parenteral nutrition. Can Med Assoc J 125:1328–1334. Wong S, Nestel PJ. 1987. Eicosapentaenoic acid inhibits the secretion of triacylglycerol and of apoprotein B and the binding of LDL in Hep G2 cells. Atherosclerosis 64:139–146. Wood R, Kubena K, O’Brien B, Tseng S, Martin G. 1993a. Effect of butter, mono- and polyunsaturated fatty acid-enriched butter, trans fatty acid margarine, and zero trans fatty acid margarine on serum lipids and lipoproteins in healthy men. J Lipid Res 34:1–11. Wood R, Kubena K, Tseng S, Martin G, Crook R. 1993b. Effect of palm oil, marga- rine, butter, and sunflower oil on the serum lipids and lipoproteins of normocholesterolemic middle-aged men. J Nutr Biochem 4:286–297. Yamashita N, Maruyama M, Yamazaki K, Hamazaki T, Yano S. 1991. Effect of eicosapentaenoic and docosahexaenoic acid on natural killer cell activity in human peripheral blood lymphocytes. Clin Immunol Immunopathol 59:335–345. Yao CH, Slattery ML, Jacobs DR, Folsom AR, Nelson ET. 1991. Anthropometric predictors of coronary heart disease and total mortality: Findings from the US Railroad Study. Am J Epidemiol 134:1278–1289. Yaqoob P, Pala HS, Cortina-Borja M, Newsholme EA, Calder PC. 2000. Encapsu- lated fish oil enriched in α-tocopherol alters plasma phospholipid and mono- nuclear cell fatty acid compositions but not mononuclear cell functions. Eur J Clin Invest 30:260–274. Yasuda S, Watanabe S, Kobayashi T, Hata N, Misawa Y, Utsumi H, Okuyama H. 1999. Dietary docosahexaenoic acid enhances ferric nitrilotriacetate-induced oxidative damage in mice but not when additional alpha-tocopherol is supple- mented. Free Radic Res 30:199–205. Yu S, Derr J, Etherton TD, Kris-Etherton PM. 1995. Plasma cholesterol-predictive equations demonstrate that stearic acid is neutral and monounsaturated fatty acids are hypocholesterolemic. Am J Clin Nutr 61:1129–1139. Zambon S, Friday KE, Childs MT, Fujimoto WY, Bierman EL, Ensinck JW. 1992. Effect of glyburide and ω3 fatty acid dietary supplements on glucose and lipid metabolism in patients with non-insulin-dependent diabetes mellitus. Am J Clin Nutr 56:447–454. Zevenbergen JL, Houtsmuller UMT, Gottenbos JJ. 1988. Linoleic acid require- ment of rats fed trans fatty acids. Lipids 23:178–186. Zock PL, Katan MB. 1992. Hydrogenation alternatives: Effects of trans fatty acids and stearic acid versus linoleic acid on serum lipids and lipoproteins in humans. J Lipid Res 33:399–410.

OCR for page 422
541 D IETARY FATS: TOTAL FAT AND FATTY ACIDS Zock PL, Mensink RP. 1996. Dietary trans-fatty acids and serum lipoproteins in humans. Curr Opin Lipidol 7:34–37. Zock PL, Blijlevens RAMT, de Vries JHM, Katan MB. 1993. Effects of stearic acid and trans fatty acids versus linoleic acid on blood pressure in normotensive women and men. Eur J Clin Nutr 47:437–444. Zock PL, Katan MB, Mensink RP. 1995. Dietary trans fatty acids and lipoprotein cholesterol. Am J Clin Nutr 61:617. Zucker ML, Bilyeu DS, Helmkamp GM, Harris WS, Dujovne CA. 1988. Effects of dietary fish oil on platelet function and plasma lipids in hyperlipoproteinemic and normal subjects. Atherosclerosis 73:13–22.