This review addresses the effect of prenatal long-chain polyunsaturated fatty acid (LCPUFA) status on neurodevelopmental outcome. It focuses on the major LPCUFA doxosahexaenoic acid (DHA; 22:6ω3) and arachidonic acid (AA; 20:4ω6). Due to enzymatic competition high DHA intake results in lower tissue levels of AA.
LCPUFA accumulation in the brain starts early and increases during the third trimester. Initially brain AA-accretion exceeds DHA-accretion; after term age DHA-accretion surpasses AA-accretion.
Animal studies indicated that early ω3-depletion results in poorer developmental outcome. They also showed that early ω3-supplementation had no effect on cognitive outcome, promotes visual development and impairs auditory and motor development. Only limited human data are available. Correlational studies suggest that neonatal AA status shows a positive relation with early neurodevelopmental outcome and that neonatal DHA status also might be correlated with improved outcome beyond infancy. Results of human intervention studies are equivocal: most studies were unable to demonstrate a positive effect of prenatal ω3-supplementation.
It is concluded that only limited evidence exists to support the notion that prenatal ω3-supplementation favours developmental outcome. Caution is warranted for an unbalanced high DHA intake during the first two trimesters of pregnancy, i.e., DHA without additional AA supplementation.