Studies on polyunsaturated fatty acid content and lipid peroxidation in preterm infant nutrition from non-maternal sources.

Abstract

Long-chain polyunsaturated fatty acids (LCPUFAs) are essential for infants’ health and development. Preterm infants have particularly high requirements for LCPUFAs, due to premature interruption of the maternal-foetal transfer. Research suggests that current feeding practices are insufficient to meet preterm infants’ LCPUFA requirements. Furthermore, LCPUFAs are highly susceptible to lipid peroxidation, giving rise to potentially harmful lipid peroxidation products (LPPs), which are related to major preterm morbidities. Donor human milk (DHM) and preterm formula milk (FM) are used when maternal breast milk is not available, sufficient, or suitable. Therefore, the first objective of this research was to quantify the LCPUFA intake of preterm infants from DHM and preterm FM and to explore how to increase these levels. The main focus of this thesis lies on LCPUFAs, however, other fatty acids, such as linoleic acid, were also considered. The second objective was to investigate the extent and nature of LPP formation in these non-maternal sources. LCPUFA levels available to preterm infants from the non-maternal sources DHM and FM were measured, for the first time in the U.K., since this data is scarce in the U.K and Europe. DHM provided LCPUFAs below European Society for Paediatric Gastroenterology, Hepatology and Nutrition recommendations. Although, with fortification, recommended levels of docosahexaenoic acid (DHA 22:6n-3; 11.5 ± 2.3 vs. 8 mg/100 mL) but not arachidonic acid (ARA 20:4n-6; 8.3 ± 2.9 vs. 12 mg/100 mL) could be reached. Preterm FM provided LCPUFA levels in agreement with these recommendations. Results further suggest that preterm FM and DHM provided ARA and DHA levels of less than 27 and 67% of estimated in utero accretion rates, respectively. Current hospital storage conditions of preterm FM did not influence LCPUFA levels. Both DHM and preterm FM were found to be sources of LPPs (malondialdehyde, 4-hydroxy-2-nonenal HNE, hexanal), with the highest levels seen in DHM (23.5 ± 6.3 µM TBARS; 60.0 ± 75.1 µg/mL HNE). No detrimental effects of LPPs at levels expected in FM were detected in a preliminary in vitro model. However, as DHM and preterm FM may be the only nutritional source for an extended period, this may lead to a chronic intake of LPPs, which might contribute to the development of necrotising enterocolitis, bronchopulmonary dysplasia or retinopathy of prematurity. Human milk banking practices that might alter LCPUFA and LPP content of DHM were identified through a nationwide survey of human milk banks; and recommendations for human milk banking, to improve quality and quantity of LCPUFAs in DHM, were provided. Some of the suggested improvements only require small changes in practice and could be implemented immediately. Recommendations should be translated into (inter)national guidance, which generally need to be more specific to protect DHM nutritional quality. Overall, LCPUFA quality and quantity in non-maternal nutritional sources in the U.K. can be improved. Especially exclusive, unfortified DHM feeding might not be suitable long-term and might contribute to the development of major preterm neonatal morbidities. Further research is needed to facilitate improvements in LCPUFA levels and the nutritional quality of DHM. Every effort should be made to promote and enable breast feeding.