Historical Introduction

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In 1918, Aron first proposed that fat may be essential for normal growth and development of animals. Butter, apart from its caloric value, was deemed to have an important nutritional value because of the presence of certain lipid molecules. Evans and Burr (1927) subsequently demonstrated that a deficiency of fat severely affected both growth and reproduction of experimental animals, despite addition of the fat-soluble vitamins A, D, and E to the diet. These authors suggested that fat contained a new essential substance termed vitamin F. The work of Burr and Burr in 1929 first showed the nutritional importance of specific lipids in fat. Weanling rats fed a fat-free diet showed impaired growth, scaly skin, tail necrosis, and increased mortality, conditions that were reversed by feeding linoleic acid (C18:2n-6). In further work, the same authors described impaired fertility and augmented water consumption as additional symptoms of a deficiency of either C18:2n-6 or a-linolenic acid (C18:3n-3). The term essential fatty acids (EFA) was coined by Burr and Burr for those fatty acids (FA) not synthesized in mammals and for which deficiencies could be reversed by dietary addition.

Arachidonic acid (C20:4n-6) was determined to be an EFA in 1938. It was found to be approximately three times as effective as C18:2n-6 in relieving essential fatty acid deficiency (EFAD) symptoms. C18:2n-6 was subsequently found to undergo biotransformation to C20:4n-6; thus, C18:2n-6 was judged to be the primary unsaturated FA required in the diet by animals. Although various researchers were able to generate EFAD in different species by feeding EFA-deficient diets, EFAD was first described in the human in 1958. Infants fed a milk-based formula diet lacking EFA showed severe skin symptoms that were alleviated by addition of C18:2n-6.

In human adults, EFAD was subsequently described as a consequence of parenteral nutrition in which fat-free solutions containing only glucose, amino acids, electrolytes, and micronutrients were continuously infused. The resulting rashes and low plasma concentrations of polyunsaturated fatty acids (PUFA) were reversed by infusion of intravenous emulsions containing C18:2n-6. Holman et al. (1982) reported the first example of deficiency symptoms attributed to C18:3n-3 deficiency in a 6-year-old girl maintained parenterally for 5 months on a safflower-oil-based emulsion rich in C18:2n-6. Deficiency symptoms, including neuropathy and low serum concentrations of C18:3n-3, were corrected by changing the parenteral nutrition recipe to include soybean oil emulsion rich in n-3 FA ( 1). Neuringer et al. (2) in 1984 demonstrated C18:3n-3 deficiency in the offspring of rhesus monkeys showing a loss in visual activity. C18:3n-3 deficiency was also described in nine patients who had received 0.02 to 0.09% of calories as n-3 FA via gastric tube feeding over a period of 2.5 to 12 years ( 3). The scaly dermatitis and depressed concentrations of n-3 FA in plasma and erythrocytes of the patients were reversed by supplementation with C18:3n-3.

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