Placental delivery of arachidonic and docosahexaenoic acids: implications for the lipid nutrition of preterm infants.
Arachidonic (AA) and docosahexaenoic (DHA) acids are major components of cell membranes and are of special importance to the brain and blood vessels. In utero, the placenta selectively and substantially extracts AA and DHA from the mother and enriches the fetal circulation. Studies indicate that there is little placental conversion of the parent essential fatty acids to AA and DHA. Similarly, analyses of desaturation and reductase activity have shown the placenta to be less functional than the maternal or fetal livers. There appears to be a correlation with placental size and plasma AA and DHA proportions in cord blood; therefore, placental development may be an important variable in determining nutrient transfer to the fetus and, hence, fetal growth itself. In preterm infants, both parenteral and enteral feeding methods are modeled on term breast milk. Consequently, there is a rapid decline of the plasma proportions of AA and DHA to one quarter or one third of the intrauterine amounts that would have been delivered by the placenta. Simultaneously, the proportion of linoleic acid, the precursor for AA, rises in the plasma phosphoglycerides 3-fold. An inadequate supply of AA and DHA during the period of high demand from rapid vascular and brain growth could lead to fragility, leakage, and membrane breakdown. Such breakdown would predictably be followed by peroxidation of free AA, vasoconstriction, inflammation, and ischemia with its biological sequelae. In the brain, cell death would be an extreme consequence.