The potential role for arachidonic and docosahexaenoic acids in protection against some central nervous system injuries in preterm infants
Crawford M, Golfetto I, Ghebremeskel K, Min Y, Moodley T, Poston L, Phylactos A, Cunnane S, Schmidt W (2003) Lipids Apr;38(4):303-15 doi: 10.1007/s11745-003-1065-1.
Abstract:
The risk of central nervous, visual, and auditory damage increases from 2/1000 live births in the normal birthweight to > 200/1000 as birthweight falls below 1500 g. Such babies are most likely to be born preterm.Advances in infant care have led to increasing numbers of very-low-birthweight, preterm infants surviving to school age with moderate to severe brain damage. Steroids are one of the current treatments, but they cause significant, long-term problems.
The evidence reported here suggests an additional approach to protecting the very preterm infant by supporting neurovascular membrane integrity. The complications of preterm, very-low-birthweight babies include bronchopulmonary dysplasia, retinopathy of prematurity, intraventricular hemorrhage, periventricular leukomalacia, and necrotizing enterocolitis, all of which have a vascular component.
Arachidonic acid (AA) and DHA are essential, structural, and functional constituents of cell membranes. They are especially required for the growth and function of the brain and vascular systems, which are the primary biofocus of human fetal growth.
Molecular dynamics and experimental evidence suggest that DHA could be the ligand for the retinoid X receptor (RXR) in neural tissue. RXR activation is an obligatory step in signaling to the nucleus and in the regulation of gene expression.
Very preterm babies are born with minimal fat stores and suboptimal circulating levels of these nutrients. Postnatally, they lose the biomagnification of the proportions of AA and DHA by the placenta for the fetus. No current nutritional management repairs these deficits.
The placental biomagnification profile highlights AA rather than DHA. The resultant fetal FA profile closely resembles that of the vascular endothelium and not the brain. Without this nourishment, cell membrane abnormalities would be predicted.
We present a scientific rationale for a common pathogenic process in the complications of prematurity.
FAB RESEARCH COMMENT:
The proposal made in this paper is that many of the serious complications of prematurity may result from deficits in omega-6 arachidonic acid (AA) and omega-3 docosahexaenoic acid (DHA).These fatty acids are provided in high concentrations by the placenta - particularly in the last trimester - so premature infants miss out on receiving them, and the standard nutrition provided to premature infants does not make up for this loss. See:
Almost 20 years later, a clinical trial has reported 'groundbreaking' results in support of this proposal. Retinopathy of prematurity (usually leading to permanent vision loss) was reduced by 50% in premature infants supplemented with both AA and DHA.
For more details on these findings, see:
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