Abstract
The N3 and N6 long chain polyunsaturated fatty acids (LCPUFA) docosahexaenoic acid (DHA) and arachidonic acid (AA) are essential for proper neurodevelopment in early life. These fatty acids are passed from mother to infant via the placenta, accreting into fetal tissues such as brain and adipose tissue. Placental transfer of LCPUFA is highest in the final trimester, but this transfer is abruptly severed with premature birth. As such, efforts have been made to supplement the post-natal feed of premature infants with LCPUFA to improve neurodevelopmental outcomes. This narrative review analyzes the current body of evidence pertinent to neurodevelopmental outcomes after LCPUFA supplementation in prematurely born infants, which was identified via the reference lists of systematic and narrative reviews and PubMed search engine results. This review finds that, while the evidence is weakened by heterogeneity, it may be seen that feed comprising 0.3% DHA and 0.6% AA is associated with more positive neurodevelopmental outcomes than LCPUFA-deplete feed. While no new RCTs have been performed since the most recent Cochrane meta-analysis in 2016, this narrative review provides a wider commentary; the wider effects of LCPUFA supplementation in prematurely born infants, the physiology of LCPUFA accretion into preterm tissues, and the physiological effects of LCPUFA that affect neurodevelopment. We also discuss the roles of maternal LCPUFA status as a modifiable factor affecting the risk of preterm birth and infant neurodevelopmental outcomes. To better understand the role of LCPUFAs in infant neurodevelopment, future study designs must consider absolute and relative availabilities of all LCPUFA species and incorporate the LCPUFA status of both mother and infant in pre- and postnatal periods.
Highlights
Introduction iationsThe N3 and N6 long-chain polyunsaturated fatty acid (LCPUFA) families comprise fatty acids with double carbon bonds at the N3 or N6 positions, respectively
Kim et al estimated the N3 and N6 PUFA intakes of 960 mothers during pregnancy, and of their infants via breast milk and weaning feeds in the postnatal period, to assess the effects of N3 and N6 intakes upon neurodevelopment at 6 months as measured by BSID second edition (BSID-II); greater linoleic acid (LA):alpha-linolenic acid (ALA) and N6:N3 ratios were both associated with lower Motor Development Index (MDI) and Psychomotor Development Index (PDI) scores in infants, while multiple logistic regression analysis showed that infants of mothers with the highest LA:ALA ratios had >2 times the risk of neurodevelopmental delay of infants whose mothers had the lowest LA:ALA ratios [100]
Infants born before term do not receive this placental transfer of LCPUFA and can be severely LCPUFA-deficient in both brain and adipose tissue in comparison to term-born infants
Summary
DHA and AA together comprise a quarter of all brain fatty acids, contributing to myelination and being enriched in neuronal synapses and cellular membranes [12], where their structure lends fluidity that aids neuronal functions such as neurotransmission [13,14]. In rats, improving LCPUFA availability to the offspring by supplementing the maternal diet can reduce the neurological damage associated with neonatal hypoxic-ischaemic brain injury [17]. 2022, 23, 700 with positive MRI findings of brain microstructure development and with improved neurodevelopmental scores in infants born prematurely [24]. AA has multiple essential and wide-ranging roles in general infant development as well; dietary AA deficiency has been associated with growth impairment, which improves on return of dietary supply [25]. Infants born prematurely and/or at a low-birth weight, with reduced adipose stores of LCPUFA, are more likely to experience neurosensory impairment, achieve lower levels of educational attainment, and have lower IQ scores [27]
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