Essential fatty acid consideration at birth in the premature neonate and the specific requirement for preformed prostaglandin precursors in the infant.
The essentiality of certain PUFA is probably related to their capability to be incorporated into lipids and to act as precursor in the formation of ecosanoids. Esterified to phospholipids, the EFA influence the physico-chemical characteristics of biomembranes. Normal growth of infants is dependent upon an adequate supply of EFA. The human fetus, like the adult, is unable to synthesize the EFA, which must therefore be derived from the maternal circulation and pass through the placenta. Increased concentration of the polyenoic fatty acids with advanced gestational age may result from increased synthetic activity of these fatty acids by the fetus or the placenta or by preferential transfer of these fatty acids across the placenta. Several clinical manifestations have been ascribed in the human infant to prolonged EFA deficiency; however, none of these findings were noted in a group of sick newborn infants with very rapid onset of deficiency. Platelet dysfunction, decreased prostaglandin biosynthesis and turnover and altered pulmonary surfactant are among the effects of EFA deficiency on infants. Supplementation of the diet with EFA, parenterally or by the inunction of oil rich in linoleic acid, were reported to alleviate the symptoms of EPA deficiency. The minimal estimated requirement of linoleic acid is 1% of calories and 4% is an optimal intake. Most diets, including human breast milk, infant formulas and parenteral fat emulsions, far exceed the optimal intake of linoleic acid. Relatively little is known about the possible effects of high levels of linoleate in the diet.