Fats: Total fat & fatty acids
Fats are the most concentrated form of energy for the body (37 kJ/g). They also aid in the absorption of the fat-soluble vitamins, A, D, E and K and other fat-soluble biologically-active components. Chemically, most of the fats in foods are triglycerides, made up of a unit of glycerol combined with three fatty acids which may be the same or different. The differences between one triglyceride and another are largely due to the fatty acids content. Other dietary fats include phospholipids, phytosterols and cholesterol.
There are three major types of naturally-occurring fatty acids - saturated, cis-monounsaturated and cis-polyunsaturated. A fourth form, the trans fatty acids, are produced by partial hydrogenation of polyunsaturated oils in food processing and they also occur naturally in ruminant animal foods. Saturated fats are found mainly in animal-based foods and polyunsaturates and monounsaturates predominate in plant-based foods.
Saturated fatty acids contain no double bond; they are fully saturated with hydrogen. They are the main type of fatty acids found in milk, cream, butter and cheese, meats from most of the land animals, palm oil and coconut oil as well as in products such as pies, biscuits, cakes and pastries. Saturated fatty acids have both physiological and structural functions. They can be synthesised by the body so are not required in the diet.
The main monounsaturated fatty acid is oleic acid with one double bond. Olive, canola and peanut oils are rich in oleic acid. The monounsaturates are also synthesised by the body and are thus not required in the diet.
Polyunsaturated fatty acids contain two or more double bonds. The most common is linoleic acid (LA, 18:2). It is described as 'n-6' due to the position of the double bonds and occurs in seed oils, eg sunflower, safflower and corn. Other n-6 fatty acids include ?-linolenic (18:3), dihomo-?-linolenic (20:3), arachidonic acid (20:4) and adrenic acid (22:4). LA is the precursor of arachidonic acid, a substrate for eicosanoid production which is also involved in the regulation of gene expression (Ou et al 2001). LA is also found as a structural component of cell membranes and is important in cell signalling. High intakes of n-6 polyunsaturated fats have been associated with blood lipid profiles associated with a lower risk of coronary heart disease (eg lower total and LDL cholesterol, increased HDL cholesterol and reduced triacylglycerol) (Arntzenius et al 1985, Becker et al 1983, Sonnenberg et al 1996).
Smaller amounts of polyunsaturated fatty acids with double bonds in the n-3 position also occur in the diet. These are sometimes referred to as omega fatty acids. Humans are unable to insert a double bond at the n-3 position of a fatty acid and thus require a dietary source. The parent fatty acid of the n-3 series is a-linolenic (ALA, 18:3). ALA is found in legumes, canola oils and margarines, linseed oils and products, certain nuts such as walnuts, and in small amounts in leafy vegetables. Canola oils and margarines and linseed oils are rich sources and legumes contribute some. A second group of n-3 fatty acids are the long chain (LC) acids eicosapentaenoic acid (EPA, 20:5), docosahexaenoic acid (DHA, 22:6) and docosapentaenoic acid (DPA, 22:5) that are found predominantly in oily fish such as mackerel, herrings, sardines, salmon and tuna and other seafood. Whilst a-linolenic acid predominates in western diets, the fish oils, DHA, EPA and DPA predominate in other communities consuming their traditional diet, such as the Inuit (Holman et al 1982).
ALA primarily functions as a precursor for the synthesis of EPA which in turn forms DHA but may also have an independent role in protection against coronary heart disease via different mechanisms (Crawford et al 2000). Conversion of ALA to EPA and DHA is limited and varies according to the intakes of other fatty acids (Burdge et al 2003, Emken 2003, Pawlosky et al 2001). Thus, a typical intake of ALA may be less able to satisfy the physiological requirements for LC n-3 fatty acids than the smaller and often more variable intakes of pre-formed LC n-3 fatty acids.
DHA plays an important role as a structural membrane lipids, particularly in nerve tissue and the retina, and can also act as a precursor to certain eicosanoids. EPA is the precursor of the 3 series of prostaglandins and the 5 series of leukotrienes. In recent years, research has shown both cardiovascular and anti-inflammatory benefits of LC n-3 fatty acids (Albert et al 1998, 2002, Burr et al 1989, Dallongeville et al 2003, Djousse et al 2001, Dolecek 1992, GISSI-Prevenzione Investigators 1999, Hu et al 1999, Pischon et al 2003, WHO 2003). Early on, because of the nature of the fish oils used in studies, these benefits were attributed to EPA and its impact on eicosanoid production (Simopoulos 1991) but recent studies suggest that DHA is the primary mediator of cardiovascular benefits, influencing gene expression of key metabolic regulators, particularly in endothelial cells (Mori et al 1999). The potential role of DPA, as a very minor component of fish oil, has been largely ignored, despite the fact that recent research shows DPA contributes almost 30% of total LC n-3 in our diet (Howe et al 2003, 2005).
Until dose-response relationships have been established, the relative efficacy of EPA, DPA and DHA remains uncertain. Moreover, the extent of their interconversion is also uncertain. Hence it is not possible to differentiate between intake requirements for EPA, DPA and DHA at this stage.
A lack of dietary n-6 or n-3 polyunsaturated fatty acids is characterised by rough, scaly skin, dermatitis, increased transepidermal water loss, reduced growth and a high triene: tetraene ratio (Goodgame et al 1978, Holman et al 1982, Jeppersen et al 2000, Mascioli et al 1996, O'Neill et al 1977). They cannot be formed in the body and is therefore essential in the diet. Studies on patients given fat-free parenteral feeding have provided insight into the levels at which essential fatty acid deficiency occurs but are not sufficient to establish an average requirement. (Fleming et al 1976, Goodgame et al 1978, Jeppersen et al 1998, Riella et al 1975).
There is some evidence that the ratio of n-6 to n-3 fatty acids may be important. Jensen et al (1997) reported that infants fed formulas containing an LA:ALA ratio of 4.8:1 had lower arachidonic acid concentrations and impaired growth compared to infants fed ratios of 9.7:1 or above. However, more recent large trials of ratios of 5:12 and 10:1 found no evidence of reduced growth or other problems (Simmer 2002). Various authorities have recommended ratios of LA:ALA or n-6:n-3 ratios ranging from 5:1, to 10:1 or 5:1 to 15:1 or 6:1 to 16:1 for infant formula (ESPGAN, Committee on Nutrition 1991, ISSFAL 1994, LSRO 1998).
A number of studies have looked at the n-6:n-3 ratio in relation to heart disease with inconsistent results (Dolecek & Graditis 1991, Ezaki et al 1999, Hu et al 1999, Kromhout et al 1985, Lands et al 1990, 1992, Nelson et al 1991, Shekelle et al 1985). However, on the basis of these results, the FAO:WHO Consultation on Fats and Oils (1994) recommended that the ratio of LA to ALA in the diet should be between 5:1 and 10:1 and suggested that individuals with a ratio greater than 10:1 should be encouraged to consume more n-3-rich foods. In contrast, an expert workshop in the Netherlands (de Deckere 1998) concluded that setting an n-6:n-3 ratio would not be helpful. They also proposed that there should be separate recommendations for plant (18:3) and marine (20:5, 22:5, 22:6) n-3 fatty acids.
Based on the concept of essentiality and given the lack of dose-response data to derive EARs for those components considered essential, AIs have been set for LA (n-6 in infants), ALA and the combined LC n-3 fatty acids, DHA:EPA:DPA. The AIs are based on median population intakes in Australia.
For children, adolescents and adults an EAR, RDI or AI for total fat was not set as it is the type of fats consumed that relate to essentiality and to many of the physiological and health outcomes. A suggested range of per cent energy as fat in relation to chronic disease prevention is addressed in the 'Chronic disease' section. In infancy, as fat is the major single source of energy in breast milk, an AI recommendation for total fat has been made based on breast milk composition. Recommendations for fatty acids in infancy are also based on total n-6 or n-3 derived from the composition of breast milk.
Recommendations by life stage and gender
|0-6 months||Total fat||31 g/day|
|n-6 polyunsaturated fats||4.4 g/day|
|n-3 polyunsaturated fats||0.5 g/day|
|7-12 months||Total fat||30 g/day|
|n-6 polyunsaturated fats||4.6 g/day|
|n-3 polyunsaturated fats||0.5 g/day|
Rationale: The AI for 0-6 months was set by multiplying together the average intake of breast milk (0.78 L/day) and the average concentration of fat, n-6 or n-3 in breast milk (40; 5.6 and 0.63 g/L, respectively) from nine studies reviewed by FNB:IOM (2002) and rounding. The AI for 7-12 months was set by multiplying together the average intake of breast milk (0.6 L/day) and the average concentration of fat, n-6 or n-3 in breast milk (40; 5.6 and 0.63 g/L respectively) from nine studies reviewed by FNB:IOM (2002) and adding the median intake from complementary foods (5.7, 1.2 and 0.11 g/day, respectively) from the US CSFII data for 1994-96 (FNB:IOM 2002)
Children, adolescents & adults
|Linoleic acid||a-linolenic acid||Total LC n-3
|Boys and girls|
|1-3 yr||5 g/day||0.5 g/day||40 mg/day|
|4-8 yr||8 g/day||0.8 g/day||55 mg/day|
|9-13 yr||10 g/day||1.0 g/day||70 mg/day|
|14-18 yr||12 g/day||1.2 g/day||125 mg/day|
|9-13 yr||8 g/day||0.8 g/day||70 mg/day|
|14-18 yr||8 g/day||0.8 g/day||85 mg/day|
|Adults 19+ yr|
|Men||13 g/day||1.3 g/day||160 mg/day|
|Women||8 g/day||0.8 g/day||90 mg/day|
Rationale: The AIs for LA and ALA were based on the highest median intakes of any of the gender-related age groups taken from an analysis of the National Nutrition Survey of Australia of 1995 (Howe et al 2003, 2005). For LC n-3, to overcome a marked gender disparity caused by particularly higher relative intakes in younger adult males (19-30 years), the AI was based on the median intake for all adults of the relevant gender. As national data were not available for New Zealand, similar values were assumed. The AIs do not necessarily reflect optimal intakes but are the values found in a population with no apparent essential fatty acid deficiency. (The 'Chronic disease prevention' section includes a suggested dietary target)
|Linoleic acid||a-linolenic acid||Total LC n-3
|14-18 yr||10 g/day||1.0 g/day||110 mg/day|
|19-50 yr||10 g/day||1.0 g/day||115 mg/day|
Rationale: Demand for n-6 and n-3 fatty acids for placental and foetal tissue must be met from maternal stores or by increased dietary intake, but there is a lack of data for assessing additional needs. The AIs for pregnancy were therefore based on that of the non-pregnant women, with an additional amount based on the increased average body weight in pregnancy (x 1.25).
|Linoleic acid||a-linolenic acid||Total LC n-3
|14-18 yr||12 g/day||1.2 g/day||140 mg/day|
|19-50 yr||12 g/day||1.2 g/day||145 mg/day|
Rationale: There is a lack of data about the requirements in pregnancy, so the AIs were based on that for non-pregnant, non-lactating women plus that of the infant. As the infant recommendation includes only an AI for total n-3 based on milk concentration, this amount was apportioned between ALA and LC omega-3 in the same ratio as in the maternal AI when assessing the additional requirement.
Upper level of intake
Linoleic acid: No UL was set because there is no known level at which adverse effects may occur.
a-linolenic acid: No UL was set because there is no known level at which adverse effects may occur. The longer chain DHA, EPA and DPA fatty acids derived from ALA are more biologically-potent than ALA itself.
LC n-3 fatty acids (DHA, EPA, DPA):
Infants 0-12 months Not possible to establish
Children, adolescents and adults 3,000 mg/day
Rationale: There is some evidence to suggest that high levels of these fatty acids may impair immune response and prolong bleeding time. However the immune function tests were performed in vitro and it is unclear how the results would translate to the in vivo situation. Prolonged bleeding times have been seen in the Inuit, but it is not known if they were caused by high LC n-3 consumption. The US Food and Drug Administration (DHHS 1997) has set a 'Generally Regarded as Safe' level of 3000 mg/day for LC n-3 which has been adopted here as the upper level of intake for children, adolescents and adults. (Note that is unlikely that this level of intake would be reached by consumption of seafood alone. If it were, then consideration would need to be given to the possible effects of concomitant intakes of other potential toxins such as mercury). It is not possible to estimate an upper level of intake for infants.
Albert CM, Campos H, Stampfer MJ, Ridker PM, Manson JE, Willett WC, Ma J. Blood levels of long-chain n-3 fatty acids and the risk of sudden death. N Engl J Med 2002;346:1113-8.
Albert CM, Hennekens CH, O'Donnell CJ, Ajani UA, Carey VJ, Willett WC, Ruskin JN, Manson JE. Fish consumption and risk of sudden cardiac death. JAMA 1998;279:23-8.
Arntzenius AC, Kromhout D, Barth JD, Reiber JHC, Brusschke AVG, Buis BM, van Gent CM, Kempen-Voogd N, Strikwerda S, van der Velde EA. Diet, lipoproteins and the progression of coronary atherosclerosis. The Leiden Intervention Trial. N Engl J Med 1985;312:805-11.
Becker N, Illingworth R, Alaupovic P, Connor WE, Sundberg EE. Effects of saturated, monounsaturated and ?-6 polyunsaturated fatty acids on plasma lipids, lipoproteins and apoproteins in humans. Am J Clin Nutr 1983;37:355-60.
Burdge GC, Finnegan YE, Minihane AM, Williams CM, Wootton SA. Effect of altered dietary n-3 fatty acid intake upon plasma lipid fatty acid composition, conversion of [13C] a -linolenic acid to longer-chain fatty acids and partitioning towards beta-oxidation in older men. Br J Nutr 2003;90:311-21.
Burr ML, Fehily AM, Gilbert JF, Rogers S, Holliday RM, Sweetnam PM, Elwood PC, Deadman NM. Effects of change in fat, fish and fibre intakes on death and myocardial reinfarction: Diet and Reinfarction Trial (DART). Lancet 1989;2:757-61.
Crawford M, Galli C, Visioli F, Renaud S, Simopoulos AP, Spector AA. Role of plant-derived omega-3 fatty acids in human nutrition. Ann Nutr Metab 2000;44:263-5.
Dallongeville J, Yarnell J, Ducimetiere P, Arveiler D, Ferrieres J, Montaye M, Luc G, Evans A, Bingham A, Hass B, Ruidavets JB, Amouyel P. Fish consumption is associated with lower heart rates. Circulation 2003;108:820-5.
de Deckere EAM, Korver O, Verschuren PM, Katan MB. Health aspects of fish and n-3 polyunsaturated fatty acids from plant and marine origin. Eur J Clin Nutr 1998;52:749-53.
Department of Health and Human Services, US Food and Drug Administration. Substances affirmed as generally recognized as safe: menhaden oil. Federal Register. June 5, 1997. Vol. 62, No. 108: pp 30751-30757. 21 CFR Part 184 [Docket No. 86G-0289]
Djousse L, Pankow JS, Eckfeldt JH, Folsum AR, Hopkins PN, Province MA, Hong Y, Ellison RC. Relation between dietary linolenic acid and coronary artery disease in the National Heart, Lung, and Blood Institute Family Heart Study. Am J Clin Nutr 2001;74:612-9.
Dolecek TA, Graditis G. Dietary polyunsaturated fatty acids and mortality in the Multiple Risk Factor Intervention Trial (MRFIT). World Rev Nutr Diet 1991;66:205-16.
Dolecek TA. Epidemiological evidence of relationships between dietary polyunsaturated fatty acids and mortality in the multiple risk factor intervention trial. Proc Soc Exp Biol Med 1992;200:177-82.
Emken E. Alpha-Linolenic Acid Conversion to n-3 LC-PUFAs. PUFA Newsletter (Sept) 2003
ESPGAN, Committee on Nutrition: Aggett PJ, Haschke F, Heine W, Hernell O, Koletzko B, Launiala K, Rey J, Rubno A, Schoch G, Senterre J, Tormo R. Comment on the content and composition of lipids in infant formulas. Acta Paediatr Scand 1991;80:887-96.
Ezaki O, Takahashi M, Shigematsu T, Shimamura K, Kimura J, Ezaki H, Gotoh T. Long-term effects of dietary a-linolenic acid from perilla oil on serum fatty acids composition and on the risk factors of coronary heart disease in Japanese elderly subjects. J Nutr Sci Vitaminol 1999;45:759-72.
Fleming CR, Smith LM, Hodges RE. Essential fatty acid deficiency in adults receiving total parenteral nutrition. Am J Clin Nutr 1976;29:976-83.
Food and Nutrition Board: Institute of Medicine. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (Macronutrients). National Academy Press: Washington, DC, 2002.
GISSI-Prevenzione Investigators. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Lancet 1999;354:447-55.
Goodgame JT, Lowry SF, Brenan MF. Essential fatty acid deficiency in total parenteral nutrition: time course of development an suggestions for therapy. Surgery 1978;84:271-7.
Holman RT, Johnson SB, Hatch TF. A case of human linolenic acid deficiency involving neurological abnormalities. Am J Clin Nutr 1982;35:617-23.
Howe PRC, Meyer BJ, Record S, Baghurst K. Dietary intake of long chain omega-3 polyunsaturated fatty acids: contribution of meat sources. Nutrition 2005. In press.
Howe PRC, Meyer BJ, Record S, Baghurst K Contribution of red meat to very long chain omega3 fatty acid (LC ?3) intake. Report to Meat & Livestock Australia. Adelaide: University of South Australia, June 2003.
Hu FB, Stampfer MJ, Manson JE, Rimm EB, Wolk A, Colditz GA, Hennekens CH, Willett WC. Dietary intake of a-linolenic acid and risk of fatal ischemic heart disease among women. Am J Clin Nutr 1999;69:890-7.
ISSFAL (International Society for the Study of Fatty Acids and Lipids) Recommendations for the essential fatty acid requirement for infant formulas (online) 1994.
Jensen CL, Prager TC, Franley JK, Chen H, Anderson RE, Heird WC. Effect of dietary linoleic/a -linolenic acid ratio on growth and visual function of term infants. J Pediatr 1997;131:200-9.
Jeppersen PB, Hoy C-E, Mortensen PB. Essential fatty acid deficiency in patients receiving home parenteral nutrition. Am J Clin Nutr 1998;68:126-33.
Jeppersen PVB, Hoy CE, Mortensen PB. Deficiencies of essential fatty acids, vitamin A and E and changes in plasma lipoproteins in patients with reduced fat absorption or intestinal failure. Eur J Clin Nutr 2000;54:632-42.
Kromhout D, Bosschieter EB, de Lezenne Coulander C. The inverse relation between fish consumption and 20-year mortality from coronary heart disease. N Engl J Med 1985;312:1205-9.
Lands WEM, Hamazaki T, Yamazaki K, Okuyama H, Sakai K, Goto Y, Hubbard VS. Changing dietary patterns. Am J Clin Nutr 1990;51:991-3.
Lands WEM, Libelt B, Morris AS, Kramer NC, Prewitt TE, Bowen P, Schmeisser D, Davidson MH, Burns JH. Maintenance of lower proportions of (n-6) eicosanoid precursors in phospholipids of human plasma in response to added dietary (n-3) fatty acids. Biochim Biophys Acta 1992;1180:147-62.
LSRO (Life Sciences Research Office). Fat. In: Raiten DJ, Talbot JM, Waters JH eds. Assessment of nutrient requirements for infant formulas. Bethesda, MD: LSRO, 1998. Pp19-46.
Mascioli EA, Lopes SDM, Champagne C, Driscoll DF. Essential fatty acid deficiency and home total parenteral nutrition patients. Nutrition 1996;12:245-9.
Mori TA, Bao DQ, Burke V, Puddey IB, Beilin LJ. Docosahexaenoic acid but not eicosapentaenoic acid lowers ambulatory blood pressure and heart rate in humans. Hypertension 1999;34:253-60.
Nelson GJ, Schmidt PC, Corash L. The effect of a salmon diet on blood clotting, platelet aggregation and fatty acids in normal adult men. Lipids 1991;26:87-96.
O'Neill JA, Caldwell MD, Meng HC. Essential fatty acid deficiency in surgical patients. Ann Surg 1977;185:535-42.
Ou J, Tu H, Shan B, Luk A, DeBose-Boyd RA, Bashmakov Y, Goldstein JL, Brown MS. Unsaturated fatty acids inhibit transcription of the sterol regulatory element-binding protein-1c (SREBP-1c) gene by antagonizing ligand-dependent activation of the LXR. Proc Natl Acad Sci USA 2001;98:6027-32.
Pawlosky RJ, Hibbeln JR, Novotny JA, Salem N Jr. Physiological compartmental analysis of a-linolenic acid metabolism in adult humans. J Lipid Res 2001;42:1257-65.
Pischon T, Hankinson SE, Hotamisligil GS, Rifai N, Willett WC, Rimm EB. Habitual dietary intake of n-3 and n-6 fatty acids in relation to inflammatory markers among US men and women. Circulation 2003;108:155-60.
Report of a Joint FAO:WHO Consultation. Fats and Oils in Human Nutrition, FAO Nutrition Paper No. 57. Rome: FAO,1994.
Riella MC, Broviac JW, Wells M, Scribner BH. Essential fatty acid deficiency in human adults during total parenteral nutrition. Ann Intern Med 1975;83:786-9.
Shekelle RB, Missell L, Paul O, Shyrock AM, Stamler J. Fish consumption and mortality from coronary heart disease. N Engl J Med 1985;313:820.
Simopoulos AP. Omega-3 fatty acids in health and disease and in growth and development. Am J Clin Nutr 1991;54:438-63.
Sonnenberg LM, Quatromoni PA, Gagnon DR, Cupples IA, Franz MM, Ordovas JM, Wilson PWF, Schaefer EJ, Millen BE. Diet and plasma lipids in women. II. Macronutrients and plasma triglycerides, high-density lipoprotein and the ratio of total to high-density lipoprotein cholesterol in women: The Framingham Nutrition Studies. J Clin Epidemiol 1996;49:665-72.
World Health Organization. Diet, Nutrition and the Prevention of Chronic Diseases. Technical report series 916, Geneva: WHO, 2003.