Are deficits of arachidonic and docosahexaenoic acids responsible for the neural and vascular complications of preterm babies?

Abstract

We review evidence suggesting that pre- or postnatal deficits of arachidonic acid (AA) and docosahexaenoic acid (DHA) together with underdeveloped antioxidant protection contribute to neurovisual developmental disorders and other complications of premature birth. These two synergistic deficits occur at a time when 70% of energy is focused on brain development and when the brain and blood vessels are growing at high speed. The types of essential fatty acids fed to preterm babies bear no relation to what the infant would have received had it remained a fetus. This failure to meet essential fatty acid requirements exacerbates the AA and DHA deficits seen at birth; furthermore, the immature superoxide defenses remain depressed until the expected date of delivery. Deficits of these systems, which are required for cell membranes, the endothelium, and neural tissue, could provide the biochemical prerequisite for the membrane disorders to which these babies are at high risk: intraventricular hemorrhage, periventricular leucomalacia, retinopathy of prematurity, and bronchopulmonary dysplasia. Although poor vascular development during fetal and neonatal life may be repaired, the structural and antioxidant deficits identified in preterm babies may impair blood vessel development with long-term consequences. The conclusion drawn from this review is that present parenteral and enteral lipid nutrition for preterm babies is flawed and could be pathogenic. Fullterm milk composition is the basis for the design of preterm infant foods, but full-term milk is different from the placental product that is rich in AA and DHA. Preterm lipid nutrition should be revised to be more in line with placental lipid transfer to the fetus.