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Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
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5
Lipids

Lipids are organic compounds with limited solubility in water. They are present in biologic systems mainly as energy stores within cells or as components of cell membranes. The nonpolar lipids occur mainly as esters of fatty acids that are virtually insoluble in water and enter metabolic pathways only after hydrolysis. The triacylglycerols (also called triglycerides or fats) are composed of three fatty acids esterified to glycerol. Cholesteryl esters are composed of a single fatty acid esterified to cholesterol. The polar or amphipathic lipids include fatty acids, in which the polar component is a negatively charged carboxyl ion; cholesterol, in which the polar component is an alcohol; sphingolipids, in which the polar group is phosphorylcholine (sphingomyelin) or a carbohydrate (glycosphingolipid); and glycerophosphatides (mainly lecithins), in which the polar component is a phosphate-containing aminoalcohol or polyalcohol. The term phospholipids encompasses glycerophosphatides and sphingomyelins.

The fatty acid components of lipids are classified as short-chain (less than 6 carbons), medium-chain (6 to 10 carbons), or long-chain (12 or more carbons). More than 90% of the fatty acids have an even number of carbon atoms. Fatty acids are also classified as saturated (lacking double bonds), monounsaturated (containing a single double bond), or polyunsaturated (containing more than one double bond). The polyunsaturated fatty acids are subdivided into those whose first double bond occurs either three carbon atoms from the methyl carbon (n-3 or w-3) or six carbon atoms from the methyl carbon (n-6

Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
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or w-6). The major saturated fatty acids in foods are palmitic acid (16 carbons) and stearic acid (18 carbons). The major monounsaturated fatty acid is oleic acid (18 carbons). The major polyunsaturated fatty acids in plant foods are linoleic acid, an n-6 fatty acid with 18 carbons and two double bonds, and linolenic acid, an n-3 fatty acid with 18 carbons and 3 double bonds. The major polyunsaturated fatty acids in fish are eicosapentaenoic acid (EPA), an n-3 fatty acid with 20 carbons and 5 double bonds, and docosahexaenoic acid (DHA), an n-3 fatty acid with 22 carbons and 6 double bonds.

Triglycerides are the principal lipid component of foods and the most concentrated source of energy among the macrocomponents of the diet (9 kcal/g). They can enhance palatability by absorbing and retaining flavors and by influencing the texture of foods. When fats are digested, emulsified, and absorbed, they facilitate the intestinal absorption (and perhaps also the transport) of the fat-soluble vitamins A, E, and D. Saturated and monounsaturated fatty acids and cholesterol can be readily synthesized from acetyl coenzyme A and thus are not essential dietary components. Small amounts of polyunsaturated fatty acids, which cannot be synthesized, are essential in the diet. They are precursors of important structural lipids (e.g., phospholipids in cell membranes) and of eicosanoids. Eicosanoids include prostaglandins (e.g., PGEs, PGFs, prostacyclin), thromboxanes, and leukotrienes.

Digestion of food fats and other lipids liberates free fatty acids, monoglycerides, and lesser amounts of monoacylphospholipids, which are then absorbed. The efficiency of fatty acid and monoglyceride absorption in healthy adults is high, ranging from 95 to 99%, whereas that of cholesterol ranges from 30 to 70%.

Fatty acids can be directly utilized as a source of energy by most body cells, with the exception of erythrocytes and cells of the central nervous system. Oxidative metabolism of long-chain fatty acids requires a carrier system (carnitine transferase) for mitochondrial transport. The central nervous system normally uses glucose as its major energy source, but the brain can utilize ketones that are produced during fatty acid catabolism when the supply of glucose is limited. Excess energy is stored principally as triglycerides within adipose tissue.

Cholesterol and phospholipids are major components of all cell membranes and of myelin. Cholesterol is also the precursor of the steroid hormones produced in the adrenal cortex and gonads, and of the bile acids produced in the liver.

Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
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DIETARY SOURCES AND USUAL INTAKES

More than one-third of the calories consumed by most people in the United States are provided by fat. Animal products in particular—red meats (beef, veal, pork, lamb), poultry, fish and shellfish, separated animal fats (such as tallow and lard), milk and milk products, and eggs—contribute more than half of the total fat to U.S. diets, three-fourths of the saturated fat, and all the cholesterol (NRC, 1988). In the U.S. Department of Agriculture (USDA) 1977-1978 Nationwide Food Consumption Survey, red meats were found to provide the major source of fat to Americans of all age groups other than infants (USDA, 1984). In the NHANES II survey, ground beef was found to be the single largest contributor of fat to the U.S. diet; mayonnaise, salad dressings, and margarine were the chief sources of linoleic acid; and eggs supplied the most cholesterol (Block et al., 1985).

Food supply disappearance data suggest that per capita consumption of fat in the United States has increased since the late 1970s. Although animal fats still predominate, the greater fat consumption can be attributed to vegetable products, reflecting increased use of margarines, vegetable shortenings, and edible oils (Bailey et al., 1988). Factors fostering the increased use of edible oils include the rapid growth of fast-food restaurants, in which many foods are cooked in oil, and the greater use of convenience foods that are fried or contain added oil (Raper and Marston, 1986).

Disappearance data, however, do not indicate the amount of fat actually consumed, because they are not adjusted for waste, spoilage, trimming, or cooking losses (NRC, 1988). Periodic surveys in which actual food consumption by individuals is measured indicate that people in the United States in fact have decreased the fat content of their diets. USDA surveys show that adults decreased their fat intake from 41% of total kcal in 1977 to 36.4% of total kcal in 1985-1986 (USDA, 1986, 1987). Although some of the decrease may reflect methodological differences, the results reflect changes in food selection as well. Since 1970, for example, consumption of red meat has declined, whereas consumption of poultry has increased and more low-fat milk than whole milk is being consumed (NRC, 1989).

ESSENTIAL FATTY ACIDS

Small amounts of linoleic acid must be present in the diet to maintain health. The inability of animals to produce linoleic acid is at-

Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
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Page 47

tributable to the lack of a 8-12 dehydrogenase to introduce a second double bond in its monounsaturated precursor (oleic acid). Once linoleic acid is available, however, it can be desaturated and elongated further to form arachidonic acid, a 20-carbon n-6 fatty acid with four double bonds. Thus, arachidonic acid is also considered an essential fatty acid, but only when linoleic acid deficiency exists. The third fatty acid traditionally classified as essential is the n-3 polyunsaturated fatty acid, a-linolenic acid. The role of linolenic acid in human nutrition is becoming clarified (Bivins et al., 1983; Neuringer and Connor, 1986). One possible case of deficiency has been described (Holman et al., 1982), and experiments in monkeys and rats have shown visual impairment and behavior differences after consumption of diets deficient in n-3 fatty acids (Neuringer and Connor, 1986). The retina and brain membranes are especially rich in docosahexaenoic acid. DHA and EPA can be synthesized from linolenic acid in the body or obtained directly in the diet from seafood. DHA and EPA are also synthesized by phytoplankton and algae and thus are abundant in fish and shellfish.

Linoleic and arachidonic acid, present in phospholipids, are important for maintaining the structure and function of cellular and subcellular membranes. In addition, n-6 and n-3 polyunsaturated fatty acids have been shown to be the precursors of eicosanoids (Glomset, 1985), which are important in the regulation of widely diverse physiological processes. A growing body of evidence indicates that nutritional status with respect to polyunsaturated fatty acids alters the production of eicosanoids. Consumption of fish rich in EPA can thereby modify platelet function and inflammatory responses.

Linoleic acid deficiency can be identified biochemically by analysis of plasma lipids. The characteristic abnormalities are low linoleic and arachidonic acid levels and elevated levels of 5,8,11-eicosatrienoic acid, a polyunsaturated, n-9 fatty acid produced from oleic acid. Studies in animals have shown that linoleic acid deficiency produces a variety of metabolic disturbances (Alfin-Slater and Aftergood, 1968). In infants fed formulas deficient in linoleic acid, drying and flaking of the skin have been observed (Wiese et al., 1958). Biochemical evidence of linoleic acid deficiency has also been found in premature infants whose fat intake is delayed (Friedman et al., 1976). Linoleic acid deficiency in adult humans was not reported until the early 1970s, when several investigators described such deficiency associated with scaly skin, hair loss, and impaired wound healing in hospitalized patients fed exclusively with intravenous fluids containing no fat (Collins et al., 1971; Paulsrud et al., 1972; Richardson and

Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
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Page 48

Sgoutas, 1975). In addition, patients with malabsorption due to biliary atresia and cystic fibrosis may be deficient in linoleic acid (Farrell et al., 1985; Gourley et al., 1982).

Linoleic acid intake at levels from 1 to 2% of total dietary calories is sufficient to prevent both biochemical and clinical evidence of deficiency in several animal species and in humans (Holman, 1970). For infants consuming 100 kcal/kg body weight per day, this would correspond to a daily intake of approximately 0.2 g/kg. The American Academy of Pediatrics (AAP, 1985) has recommended that infant formulas provide at least 2.7% of energy as linoleic acid. For the average adult, a minimally adequate intake of linoleic acid is 3 to 6 g/day. This level is more than met by diets in the United States, since most vegetable oils are particularly rich sources of linoleic acid. In several studies, linoleic acid has been found to range from 5 to 10% of calories in diets providing 25 to 50% of energy as fat (Bieri and Evarts, 1973; Witting and Lee, 1975). As discussed in the section on vitamin E (see Chapter 7), large amounts of polyunsaturated fatty acids may increase the need for this fat-soluble, antioxidant nutrient. The Committee on Diet and Health of the Food and Nutrition Board recently recommended that the average population intake of n-6 polyunsaturated fatty acids remain at the current level of about 7% of calories and that individual intakes not exceed 10% of calories because of lack of information about the long-term consequences of a higher intake (NRC, 1989).

For many reasons, especially because essential fatty acid deficiency has been observed exclusively in patients with medical problems affecting fat intake or absorption, the subcommittee has not established an RDA for n-3 or n-6 polyunsaturated fatty acids. The rapid developments in the field of fat-soluble dietary factors, and their physiologic role in eicosanoid production, will require periodic reappraisal of their significance in nutrition and the regulation of metabolic functions. The possibility of establishing RDAs for these fatty acids should be considered in the near future. For example, Neuringer et al. (1988) proposed that the consumption of n-3 fatty acids in humans should be 10 to 25% that of linoleic acid, particularly during pregnancy, lactation, and infancy. Synthetic infant formulas generally contain only vegetable oils as their lipid sources and thus contain only 18carbon polyunsaturates. Even when these formulas supply ample linolenic acid, DHA levels in the infants' erythrocyte membrane phospholipids are much lower than in those infants receiving either human milk or formulas supplemented with sources of longer-chain n-3 fatty acids (Carlson et al., 1986; Crawford et al., 1977). Also, the ratio of dietary linoleic acid to EPA and DHA can affect platelet

Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
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Page 49

function and inflammatory responses, and may thereby influence the development of certain chronic diseases, such as coronary heart disease and rheumatoid arthritis (Leaf and Weber, 1988).

OTHER CONSIDERATIONS

It has long been recognized that the amount and nature of fat ingested affects plasma cholesterol concentration, and that high blood cholesterol levels are strongly related to the incidence and risk of atherosclerotic vascular disease, especially coronary heart disease. Several types of evidence, including clinical dietary and drug trials, show that the cholesterol contained in the plasma's low-density lipoprotein (LDL) fraction is the principal detrimental component, whereas high levels of cholesterol in high-density lipoproteins (HDL) are associated with a reduced risk of coronary heart disease. Other factors, such as genetic background, cigarette smoking, hypertension, and obesity, also increase the risk of coronary artery disease (NRC, 1989). The strongest dietary determinant of blood cholesterol level is the saturated fatty acid content (NRC, 1989). The cholesterol content of the diet has an appreciable, but usually lesser influence. Increased intake of both these nutrients decreases LDL receptor activity in liver cells and increases LDL cholesterol levels in the blood (Spady and Dietschy, 1988).

In the past decade, considerable attention has been given to the potential role of dietary factors in the etiology and prevention of cancer. This subject has recently been reviewed in depth, and several organizations have proposed dietary guidelines toward lowering the risk of certain cancers. These guidelines have included the suggestion that total fat intake should be reduced (DHHS, 1988; NRC, 1982; NRC, 1989).

Additional research is needed to clarify the role of diet in carcinogenesis and to determine the proportion of energy that should be provided by dietary fats relative to other macrocomponents to reduce the risks of heart disease and cancer. However, a decrease in the average consumption of fat by Americans from its present level of approximately 36% of calories appears to be desirable. An additional benefit of reducing the fat content of the diet may be lower caloric intakes and hence a reduced prevalence of obesity and its adverse effects on health. After a comprehensive evaluation of the evidence, the Food and Nutrition Board's Committee on Diet and Health recommended that the fat content of the U.S. diet not exceed 30% of caloric intake, that less than 10% of calories should be provided from

Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
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saturated fatty acids, and that dietary cholesterol should be less than 300 mg/day (NRC, 1989).

REFERENCES

AAP (American Academy of Pediatrics). 1985. Appendix K: Composition of human milk: normative data. Pp. 363-368 in G.B. Forbes, ed. Pediatric Nutrition Handbook. American Academy of Pediatrics, Elk Grove Village, Il1.

Alfin-Slater, R.B., and L. Aftergood. 1968. Essential fatty acids reinvestigated. Physiol. Rev. 48:758-784.

Bailey, L., L. Duewer, F. Gray, R. Hoskin, J. Putnam, and S. Short. 1988. Food consumption. Natl. Food Rev. 11:1-10.

Bieri, J.G., and R.P. Evarts. 1973. Tocopherols and fatty acids in American diets. The recommended allowance for vitamin E. J. Am. Diet. Assoc. 62:147-151.

Bivins, B.A., R.M. Bell, R.P. Rapp, and W.O. Griffen, Jr. 1983. Linoleic acid versus linolenic acid: what is essential? J. Parent. Ent. Nutr. 7:473-478.

Block, G., C.M. Dresser, A.M. Hartman, and M.D. Carroll. 1985. Nutrient sources in the American diet: quantitative data from the NHANES II survey. II. Macronutrients and fats. Am. J. Epidemiol. 122:27-40.

Carlson, S.E., P.G. Rhodes, and M.G. Ferguson. 1986. Docosahexaenoic acid status of preterm infants at birth and following feeding with human milk or formula. Am. J. Clin. Nutr. 44:798-804.

Collins, F.D., A.J. Sinclair, J.B. Royle, D.A. Coats, A.T. Maynard, and F.L.. Leonard. 1971. Plasma lipids in human linoleic acid deficiency. Nutr. Metab. 13:150-167.

Crawford, M.A., A.G. Hassam, and B.M. Hall. 1977. Metabolism of essential fatty acids in the human fetus and neonate. Nutr. Metab. 21, Suppl. 1:187-188.

DHHS (U.S. Department of Health and Human Services). 1988. The Surgeon General's Report on Nutrition and Health. U.S. Government Printing Office, Washington, D.C. 727 pp.

Farrell, P.M., E.H. Mischler, M.J. Engle, D.J. Brown, and S.-M. Lau. 1985. Fatty acid abnormalities in cystic fibrosis. Pediatr. Res. 19:104-109.

Friedman, Z., A. Danon, M.T. Stahlman, and J.A. Oates. 1976. Rapid onset of essential fatty acid deficiency in the newborn. Pediatrics 58:640-649.

Glomset, J.A. 1985. Fish, fatty acids, and human health. N. Engl. J. Med. 312:12531254.

Gourley, G.R., P.M. Farrell, and G.B. Odell. 1982. Essential fatty acid deficiency after hepatic portoenterostomy for biliary atresia. Am. J. Clin. Nutr. 36:1194-1199.

Holman, R.T. 1970. Biological activities of and requirements for polyunsaturated acids. Pp. 607-682 in Progress in the Chemistry of Fats and Other Lipids, Vol. 9. Pergamon Press, New York.

Holman, R.T., S.B. Johnson, and T.F. Hatch. 1982. A case of human linolenic acid deficiency involving neurological abnormalities. Am. J. Clin. Nutr. 35:617-623.

Leaf, A., and P.C. Weber. 1988. Cardiovascular effects of n-3 fatty acids. N. Engl. J. Med. 318:549-557.

Neuringer, M.D., and W.E. Connor. 1986. N-3 fatty acids in the brain and retina: evidence for their essentiality. Nutr. Rev. 44:285-294.

Neuringer, M., G.J. Anderson, and W.E. Connor. 1988. The essentiality of N-3 fatty acids for the development and function of the retina and brain. Annu. Rev. Nutr. 8:517-541.

Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
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NRC (National Research Council). 1982. Diet, Nutrition, and (Cancer. Report of the Committee on Diet, Nutrition, and Cancer, Assemly of Life Sciences. National Academy Press, Washington, D.C. 478 pp.

NRC (National Research Council). 1988. Designing Foods: Animal Product Options in the Marketplace. Report of the Committee on Technological Options to Improve the Nutritional Attributes of Animal Products, Board on Agriculture. National Academy Press, Washington, D.C. 367 pp.

NRC (National Research Council). 1989. Diet and Health: Implications for Reducing Chronic Disease Risk. Report of the Comnittee on Diet and Health, Food and Nutrition Board. National Academy Press, Washington, D.C. 750 pp.

Paulsrud, J.R., L. Pensler, C.F. Whitten, S. Stewart, and R.T. Holman. 1972. Essential fatty acid deficiency in infants induced by fat-free intravenous feeding. Am. J. Clin. Nutr. 25:897-904.

Raper, N.R., and R.M. Marston. 1986. Levels and sources of flat in the U.S. food supply. Pp. 127-152 in C. Ip, D.F. Birt, A.E. Rogers, and C. Mettlin, eds. Dietary Fat and Cancer. Alan R. Liss, New York.

Richardson, T.J., and D. Sgoutas. 1975. Essential fatty acid  deficiency in four adult patients during total parenteral nutrition. Am. J. Clin. Nutr. 28:258-263.

Spady, D.K., and J.M. Dietschy. 1988. Interaction of dietary cholesterol and triglycerides in the regulation of hepatic low density lipoprotein transport in the hamster. J. Clin. Invest. 81:300-309.

USDA (U.S. Department of Agriculture). 1984. Nutrient Intakes: Individuals in 48 States, Year 1977-78. Nationwide Food Consumption Survey. Report No. 1-2. Consumer Nutrition Division, Human Nutrition Information Service, Hyattsville, Md.

USDA (U.S. Department of Agriculture). 1986. Nationwide Food Consumption Survey. Continuing Survey of Food Intakes of Individuals: Men 19-50 Years, 1 Day, 1985. Report No. 85-3. Nutrition Monitoring Division, Human Nutrition Information Service. U.S. Department of Agriculture, Hyattsville, Md. 94 pp.

USDA (U.S. Department of Agriculture). 1987. Nationwide Food Consumption Survey. Continuing Survey of Food Intakes of Individuals: Women 19-50 Years and Their Children 1-5 Years, 4 Days, 1985. Report No. 85-4. Nutrition Monitoring Division, Human Nutrition Information Service. U.S. Department of Agriculture, Hyattsville, Md. 182 pp.

Wiese, H.F., A.E. Hansen, and D.J.D. Adam. 1958. Essential fatty acids in infant nutrition. J. Nutr. 58:345-360.

Witting, L.A., and L. Lee. 1975. Dietary levels of vitamin E and polyunsaturated fatty acids and plasma vitamin E. Am. J. Clin. Nutr. 28:571-576.

Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
×
Page 44
Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
×
Page 45
Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
×
Page 46
Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
×
Page 47
Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
×
Page 48
Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
×
Page 49
Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
×
Page 50
Suggested Citation:"Lipids." National Research Council. 1989. Recommended Dietary Allowances: 10th Edition. Washington, DC: The National Academies Press. doi: 10.17226/1349.
×
Page 51
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Since its introduction in 1943 Recommended Dietary Allowances has become the accepted source of nutrient allowances for healthy people.

These Recommended Dietary Allowances (RDAs) are used throughout the food and health fields. Additionally, RDAs serve as the basis for the U.S. Recommended Daily Allowances, the Food and Drug Administration's standards for nutrition labeling of foods.

The 10th Edition includes research results and expert interpretations from years of progress in nutrition research since the previous edition and provides not only RDAs but also "Estimated Safe and Adequate Daily Dietary Intakes"—provisional values for nutrients where data were insufficient to set an RDA.

Organized by nutrient for ready reference, the volume reviews the function of each nutrient in the human body, sources of supply, effects of deficiencies and excessive intakes, relevant study results, and more.

The volume concludes with the invaluable "Summary Table of Recommended Dietary Allowances," a convenient and practical summary of the recommendations.

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