And essential fatty acid deficiency

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... 

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)... 

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. 

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. 

Severe negative nitrogen balance may occasionally have to be corrected by hyperalimentation or total parenteral nutrition (TPN). Intravenous solutions used in TPN contain essential and nonessential amino acids, plus a source of calories in the form of fat and carbohydrate. They "spare" the administered amino acids and allow them to be used for tissue repair. The TPN fluid must also contain all other nutritional factors required for life, including essential fatty acids, vitamins, and minerals. Severe metal and essential fatty acid deficiencies have been observed in situations in which such inclusions had not been made. 

Biotin deficiency and the functional deficiency associated with lack of holo-carboxylase synthetase (Section 11.2.2.1), or biotinidase (Section 11.2.3.1), causes alopecia (hair loss) and a scaly erythematous dermatitis, especially around the body orifices. The dermatitis is similar to that seen in zinc and essential fatty acid deficiency and is commonly associated with Candida albicans infection. Histology of the skin shows an absence of sebaceous glands and atrophy of the hair follicles. The dermatitis is because of impaired metabolism of polyunsaturated fatty acids as a result of low activity of acetyl CoA carboxylase (Section 11.2.1.1). In biotin-deficient experimental animals, provision of supplements of long-chain 6 polyunsaturated fatty acids prevents the development of skin lesions (Mock et al., 1988a, 1988b Mock, 1991). 

Hou, S. Y. E., Mitra, A. K., White, S. H., Menon, G. K., Ghadialiy, R. and Elias, P. M. (1991). Membrane stmctures in normal and essential fatty acid deficient stratum comeum—Characterization by ruthenium tetroxide staining and x-ray diffraction. J. Invest. Derm. 96 215. 

The nutrition-focused physical examination consists of an assessment of lean body mass (LBM) and the physical findings of vitamin deficiency, trace element deficiency, and essential fatty acid deficiency. The assessment should characterize the presence and degree of muscle wasting, edema, loss of subcutaneous fat, dermatitis, glossitis, cheilosis, and/or jaundice (Table 135-2). 

A comprehensive nutrition assessment must include an evaluation of possible trace element, vitamin, and essential fatty acid deficiencies. Because of their key role in metabolic processes (as coenzymes and cofactors), a deficiency of any of these nutrients may result in altered metabolism and cell dysfunction, and may interfere with metabolic processes necessary for nutritional repletion. The evaluation of single-nutrient-deficiency states includes an accurate history to identify symptoms and risk factors that may indicate deficiency or predispose the patient to developing a deficiency state. A focused physical examination for signs of deficiencies and biochemical assessment to confirm a suspected diagnosis also should be done. Ideally, biochemical assessment would be based on the nutrient s function (e.g., metalloenzyme activity) rather than simply measuring the nutrient s serum concentration. Unfortunately, few practical methods to assess micronutrient function are available currently, and most assays measure serum concentrations of the individual nutrient. 

Dietary glucose and fructose inhibit the enzyme whereas protein diets and essential fatty acid deficient diets enhance the reaction independently of hormonal effects. 

Very soon after the discovery of essential fatty acid phenomena in rats, medical researchers at the University of Minnesota began investigations on humans. The first medical phenomenon related to essential fatty acids was a dermatitis associated with intractable eczema. Hansen and his co-workers chose cases which did not respond to the usual treatments for eczema and gave these patients supplements of lard which contains approximately 10% of linoleic acid and a few percent of arachidonic acid (Hansen, 1937). They found that in the cases of intractable eczema the serum iodine number was low, and that when the diets were supplemented with lard, the iodine value rose to normal and the skin cleared up in 75% of the cases. An example of this disease which responded to essential fatty acids is shown in Figure 4 (Azerad Crupper, 1949). A study of the histological features of normal and essential fatty acid deficient human skin shown in Figure 5 indicates that in the deficient condition... 

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. 

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... 

Hepatic steatosis usually is a result of excessive administration of carbohydrates and/or lipids, but deficiencies of carnitine, choline, and essential fatty acids also may contribute. Hepatic steatosis can be minimized or reversed by avoiding overfeeding, especially from dextrose and lipids.35,38 Carnitine is an important amine that transports long-chain triglycerides into the mitochondria for oxidation, but carnitine deficiency in adults is extremely rare and is mostly a problem in premature infants and patients receiving chronic dialysis. Choline is an essential amine required for synthesis of cell membrane components such as phospholipids. Although a true choline deficiency is rare, preliminary studies of choline supplementation to adult patients PN caused reversal of steatosis. 

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. 

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. 

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. 

The lower intake of food can result in a deficiency of micronutrients and essential fatty acids (especially vitamins Bi2 and folic acid - see below). 

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... 

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. 

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