Ebook Neonatal fatty acid status and neurological development
LCPUFAs are abundantly present in the CNS of infants. Their accumulation in the brain occurs, especially during the last trimester of gestation and during early postnatal life, a process that is affected by nutrition. It is conceivable that dietary supplementation of LCPUFAs enhances incorporation of LCPUFAs into the membranes of the CNS and possibly improves the neurologic condition of the young child. At present, there is increasing evidence of a beneficial effect of LCPUFA supplementation on visual function and psychomotor development in preterm and term infants. No consistent evidence has been provided of a positive effect of LCPUFA supplementation on developmental outcome at 1 to 3 y, and no data are available on the effect of LCPUFA supplementation on neurobehavioral development beyond the age of 3 y. Less is known about the effect of the infant’s neonatal fatty acid status on neurodevelopmental outcome.
A recent study by our own group indicated that a lower neonatal status of docosahexaenoic acid [(DHA), a member of the n-3 fatty acid series], AA (a member of the n-6 fatty acids), EFA in the umbilical vein is associated with a less favorable neurologic condition on postnatal days 10 to 14. Helland et al. reported that supplementation with cod liver oil (rich in n-3 fatty acids) during pregnancy and lactation resulted in higher levels of n-3 fatty acids in blood plasma at birth, which were associated with more mature electroencephalography (EEG) scores on the second day of life.
Neonatal fatty acid status was not related to EEG maturity at 3 mo. Follow-up at 4 y indicated that neonatal DHA in plasma at birth was not related to intelligence. A negative correlation was found between neonatal Mead (20:3n-9) and Osbond (22:5n-6) acids, which represent lower EFA status and intelligence at 4 y. Malcolm et al., in a study in which pregnant women received supplementation with either fish oil capsules rich in DHA or placebo capsules, did not find a relationship between the infant’s DHA status in red blood cells and plasma at birth and latencies to visually evoked potentials recorded to flash stimuli shortly after birth and at the ages of 10 wk and 6 mo. However, they did find a relationship between neonatal DHA status and latencies to visually evoked potentials recorded to pattern-reversal stimuli at 10 wk and 6 mo.
Two other studies found no relationship between neonatal LCPUFA status and cognitive function at 4 and 7 y of age. Taken together, it is as yet unclear whether neonatal LCPUFA status affects neurodevelopmental outcome, and if so, which LCPUFA plays a prominent role. To detect the possible subtle effects of neonatal fatty acid status on neurologic condition, sensitive evaluation instruments are required. Previous studies by our group indicated that the assessment of the quality of GMs is a sensitive tool for evaluating the effect of nutritional status on neurologic condition. GMs are spontaneous movements involving all parts of the body.
They arise early in fetal life and persist until 3–4 mo after term age when goal-directed behavior emerges. Normal GMs are characterized by variation, complexity, and fluency. These characteristics disappear when movements become abnormal. The presence of definitely abnormal GMs at 2–4 mo predicts the development of cerebral palsy with a high accuracy. The presence of mildly abnormal GMs at 2–4 mo is associated with an increase in the risk of the development of minor neurologic dysfunction, attention problems, and aggressive behavior at school age. In previous studies, we evaluated the effect of LCPUFA supplementation of infant formula and that of the influence of duration of breastfeeding on the quality of GMs. None of the participating healthy term infants had definitely abnormal GMs. We found that LCPUFA supplementation was associated with a reduction of mildly abnormal GMs and that breastfed infants showed better movement quality when they had received human milk for more than 6 wk.
The present paper is based on the groups of infants who participated in the LCPUFA supplementation study. We addressed the question whether the fatty acid composition of the umbilical blood vessels at birth of infants who showed mildly abnormal GMs at 3 mo differed from that of infants with normal GMs. The problem was tackled with multivariate statistics to be able to take into account the role of type of postnatal feeding and other confounders.
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