Fatty acids essential, deficiency

An IV fat emulsion contains soybean or safflower oil and a mixture of natural triglycerides, predominately unsaturated fatty acids. It is used in the prevention and treatment of essential fatty acid deficiency. It also provides nonprotein calories for those receiving TPN when calorie requirements cannot be met by glucose. Examples of intravenous fat emulsion include Intralipid 10% and 20%, Liposyn II 10% and 20%, and Liposyn III 10% and 20%. Fat emulsion is used as a source of calories and essential fatty acids for... 

Small amounts of trans-unsamrated fatty acids are found in ruminant fat (eg, butter fat has 2-7%), where they arise from the action of microorganisms in the rumen, but the main source in the human diet is from partially hydrogenated vegetable oils (eg, margarine). Trans fatty acids compete with essential fatty acids and may exacerbate essential fatty acid deficiency. Moreover, they are strucmrally similar to samrated fatty acids (Chapter 14) and have comparable effects in the promotion of hypercholesterolemia and atherosclerosis (Chapter 26). 

The role of essential fatty acids in membrane formation is unrelated to prostaglandin formation. Prostaglandins do not reheve symptoms of essential fatty acid deficiency, and an essential fatty acid deficiency is not caused by inhibition of prostaglandin synthesis. 

Symptoms of Essential Fatty Acid Deficiency in Humans Include Skin Lesions Impairment of Lipid Transport... 

In adults subsisting on ordinary diets, no signs of essential fatty acid deficiencies have been reported. How-... 

Intravenous lipid emulsions are used as an energy source in PN and to prevent or treat essential fatty acid deficiency. 

The essential fatty acids in humans are linoleic acid (C-18 2 N-6) and a-linolenic acid (C18 3 N-3). Arachidonic acid (C20 4 N-6) is also essential but can be synthesized from linoleic acid. Administration of 2% to 4% of total daily calories as linoleic acid should be adequate to prevent essential fatty acid deficiency in adults (e.g., infusion of 500 mL of 20% intravenous lipid emulsion once weekly).7 Biochemical evidence of essential fatty acid deficiency can develop in about 2 to 4 weeks in adult patients receiving lipid-free PN, and clinical manifestations generally appear after an additional... 

Essential fatty acid deficiency Deficiency of linoleic acid, linolenic acid, and/or arachidonic acid, characterized by hair loss, thinning of skin, and skin desquamation. Long-chain fatty acids include trienes (containing three double-bonds [e.g., 5,8,11-eicosatrienoic acid, or Mead acid trienoic acids) and tetraenes (containing four doublebonds [e.g., arachidonic acid]). Biochemical evidence of essential fatty acid deficiency includes a trieneitetraene ratio greater than 0.4 and low linoleic or arachidonic acid plasma concentrations. 

FIGURE 3-7 Pathways for the interconversion of brain fatty acids. Palmitic acid (16 0) is the main end product of brain fatty acid synthesis. It may then be elongated, desaturated, and/or P-oxidized to form different long chain fatty acids. The monoenes (18 1 A7, 18 1 A9, 24 1 A15) are the main unsaturated fatty acids formed de novo by A9 desaturation and chain elongation. As shown, the very long chain fatty acids are a-oxidized to form a-hydroxy and odd numbered fatty acids. The polyunsaturated fatty acids are formed mainly from exogenous dietary fatty acids, such as linoleic (18 2, n-6) and a-linoleic (18 2, n-3) acids by chain elongation and desaturation at A5 and A6, as shown. A A4 desaturase has also been proposed, but its existence has been questioned. Instead, it has been shown that unsaturation at the A4 position is effected by retroconversion i.e. A6 unsaturation in the endoplasmic reticulum, followed by one cycle of P-oxidation (-C2) in peroxisomes [11], This is illustrated in the biosynthesis of DHA (22 6, n-3) above. In severe essential fatty acid deficiency, the abnormal polyenes, such as 20 3, n-9 are also synthesized de novo to substitute for the normal polyunsaturated acids. 

Physical examination should focus on assessment of lean body mass (LBM) and physical findings of vitamin, trace element, and essential fatty acid deficiencies. 

Biochemical assessment of trace element, vitamin, and essential fatty acid deficiencies should be based on the nutrient s function, but few practical... 

Essential fatty acid deficiency is rare but can occur with prolonged lipid-free parenteral nutrition, very low fat enteral formulas, severe fat malabsorption, or severe malnutrition. The body can synthesize all fatty acids except for linoleic and linolenic acid, which should constitute approximately 2% to 4% of total calorie intake. 

Essential fatty acid deficiency can be prevented by giving IVFE, 0.5 to 1 g/ kg/day for neonates and infants and 100 g/wk for adults. 

Aik Phos, alkaline phosphatase ALT, alanine aminotransferase (SCPT) AST, aspartate aminotransferase (SGOT) Bili, bilirubin EFAD, essential fatty acid deficiency IVFE, intravenous fat emulsion PN, parenteral nutrition. 

There are a number of signs and symptoms of essential fatty acid deficiency. They include scaly and thickened skin, alopecia, increased capillary fragility so that bruising readily occurs, poor wound healing, increased susceptibility to infection and growth retardation in infants and children. Some of these symptoms can be explained by deficiency of eicosanoid synthesis and/or failure to complete cell cycles in various tissues (Chapter 20). Consequently, it is important to detect a deficiency before symptoms develop. The principle underlying the method to do this is described ... 

There is some evidence that, in these patients, the interconversion between the polyunsaturated fatty acids is disturbed, which restricts the formation of eicosapentaenoic and docosahexaenoic acids. Such children are less likely to have been breastfed (breast milk contains these omega-3 fatty acids) they are more likely to suffer from allergies associated with essential fatty acid deficiency and also dry skin and hair and the membranes of the erythrocytes contain less omega-3 fatty acids compared with normal children. So far, the results of supplementation of the diet of these children with this disorder have not been conclusive. 

Alam, S. Q., and Y. Y. Shi. The effect of essential fatty acid deficiency on the fatty acid composition of different salivary glands and saliva in rats. Arch Oral Biol 1997 42(10-11) 727-734. Kumar, P. D. The role of coconut and coconut oil in coronary heart disease in Kerala, south India. Trop Doct... 

Intralipid For patients with essential fatty acid deficiencies... 

When trans-fatty acids are fed to rats with adequate amounts of essential fatty acids, they have little effect on growth, longevity, or reproduction, but when fed as the sole source of lipids they exaggerate the symptoms of essential fatty acid deficiency (111). An effect on the metabolism of long chain polyunsaturated fatty acids was noted however. 

Prout, R. E. S., Odutuga, A. A. In vivo incorporation of [l-14C]-]jnoleic acid into the lipids of enamel and dentin of normal and essential fatty acid deficient rats. Arch, oral Biol. 19, 1167 (1974)... 

Holman, R. T, 1973. Essential fatty acid deficiency in humans. In Dietary Lipids and Postnatal Development. C. Galli, G, Jacini, and A. Pecile (Editors). Raven Press, New York, p. 127. 

Jeppesen PB, Hoy CE, Mortensen PB. Essential fatty acid deficiency in patients receiving home parenteral nutrition. Am J Clin Nutr 1998 68(l) 126-33. 

Duerksen DR, Nehra V, Palombo JD, Ahmad A, Bistrian BR. Essential fatty acid deficiencies in patients with chronic liver disease are not reversed by short-term intravenous lipid supplementation. Dig Dis Sci 1999 44(7) 1342-8. 

Hou, S.Y., et al. 1991. Membrane structures in normal and essential fatty acid-deficient stratum corneum Characterization by ruthenium tetroxide staining and x-ray diffraction. J Invest Dermatol 96 215. 

G12. Gutteridge, J. M., Quinlan, G. J., and Yamamoto, Y., Hypothesis Are fatty acid patterns characteristic of essential fatty acid deficiency indicative of oxidative stress Free Radic. Res. 28, 109-114(1998). 

Another possible dietary factor concerns the essential fatty acid content of human and artificial milk. It has been postulated by Sinclair that many modern dietaries are deficient in the essential polyethenoid fatty acids (EFA) and that in consequence there is a rise in unesterified (and more active) vitamin D and in unesterified cholesterol. He has suggested that a part of the etiology of infantile idiopathic hypercalcemia may be attributed to EFA deficiency (S5). He has pointed to the lower content of certain unsaturated fatty acids in cow s milk as compared with human milk as a factor in the development of idiopathic hypercalcemia in artificially fed infants. He considers that dried milk has an even lower content of essential fatty acids than liquid cow s milk and that the longer it is stored the lower does the essential fatty acid content become. On the basis of some observations on rats, he suggests that a dietary deficiency of the essential fatty acids increases susceptibility to the possible toxic effects of vitamin D. The age of the rats, the duration of the essential fatty acid deficient diet, or the dosage of vitamin D is not mentioned, and there would appear to be no other experimental data to support these views. 

James etal. (Jl) investigated the possible role of deficiency of essential fatty acids in idiopathic hypercalcemia. They found no evidence that an essential fatty acid deficiency is a cause of, or is present in, infants with idiopathic hypercalcemia. Much further investigation is still required to determine the role of essential fatty acids in hypercalcemia. Existing knowledge on the general aspects of the subject has been surveyed at the 4th International Conference on Biochemical Problems of Lipids (II). 

Diets. Three basic diets were utilized (Table I), a 2% low fat diet (2% linoleic acid methyl esters), a 20% polyunsaturated fat diet containing 20% stripped corn oil, and a high saturated fat diet containing 18% coconut oil and 2% linoleic acid methyl esters to prevent an essential fatty acid deficiency (6 ). All diets were prepared to our specifications by ICN Life Sciences (Cleveland, OH) and analyzed both by ICN and our laboratory for fatty acids, antioxidants and some trace minerals. They are routinely stored in sealed plastic containers at 4°. Antioxidants when added (see Figure 2) were supplemented just prior to feeding and at 0.2% or 0.3% of the diet by weight as specified in each experiment. 

Holman, R.T., Essential fatty acid deficiency, Prog. Chem. Fats Other Lipids, 9, 275, 1968. 

Hartop, P.J., C.F. Allenby, and C. Prottey, Comparison of barrier function and lipids in psoriasis and essential fatty acid-deficient rats. Clin, Exp. Dermatol., 1978, 3 259-67. 

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