Effects of preterm infant formula supplementation with a-linolenic acid with a linoleate/a-linolenate ratio of 6:1: a multicenter study.
Effects of preterm infant formula supplementation with a-linolenic acid with a linoleate/a-linolenate ratio of 6:1: a multicenter study.
Year: 1997
Authors: C Billeaud, D Bougle, P Sarda, N Combe, S Mazette, F Babin, B Entressangles, B Descomps,
Publication Name: Eur. J. Clin. Nutr.
Publication Details: Volume 520.
Abstract:
Although the essentiality of n-3 fatty acids has been well documented in humans, the dietary requirement for preterm infants still remains unknown. However, numerous studies suggest the needs are particularily high. In addition, a precise balance between C20 LCPUFAs (AA and EPA) of the n-6 and n-3 series is necessary for the normal synthesis of eicosanoids of the 1, 2, and 3 series. Currently, there are two ways of supplementing preterm infant formulas with n-3 fatty acids: in the form of LCPUFAs (EPA and DHA), or as n-3 series precursors (ALA). It has been postulated, however, that supplementation with ALA may result in insufficient endogenous LCPUFA synthesis due to potential inability of the preterm infant to desaturate and elongate ALA to EPA and DHA. In addition, the presence of high levels of LA may impair the synthesis of n-3 LCPUFAs making the n-6:n:3 ratio critical. Thus, the aim of this current study is to investigate the effects of a milk formula supplemented with ALA, with a ratio of n-6:n-3 near 6:1, on the plasma and red blood cells fatty acids in premature infants and compare these results with infants fed non supplemented formula. The study design was a multicenter study that included a reference group of preterm infants fed human milk. Infants with a gestational age of less that 34 weeks were enrolled in the study and were randomly assigned to either a high linolenic formula group (HLF, n=31, ALA=1.95% total FAs and 0.77% total energy), or a low linolenic formula group (LLF, n=32, ALA=0.55% total FAs and 0.22% total energy). The 18:2 n-6/18:3 n-3 ratio was 6:1 in the HLF group and 22:1 in the LLF group, and the source of ALA was low erucic rapeseed oil (LEAR) for both. Oral intake of both formulas was gradually increased to reach 140 kcal/kg/d for a duration of 37 weeks. Total plasma cholesterol, plasma triglycerides (TG), cholesterol ester (CE), phospholipids (PL), and RBC phosphatidylethanolamine (RBC-PE) were analysed at day 2, 15, and week 37. It should be noted that preterm infants in the control group were not randomized for ethical considerations and therefore no statistical analysis were performed between this group and the two formula groups. Results indicated that ALA levels in TG was significantly higher in the HLF versus the LLF group at D2, D15 and W37. A significant effect was also observed in the HLF group for the incorporation of ALA in CE at D2, D15, and W37 (3-fold, 5-fold, and 3-fold respectively) when compared to the LLF group. There was also a significant rise in EPA concentration of plasma PL at D15 and W37 in the HLF group; however, the EPA values were still considered low. In RBC, the PE-EPA levels remained within the confidence interval values of the human milk group; however, there was a significant difference in the PE-DHA levels between the two test groups. The PE-DHA decrease in the HLF group was significantly less important than the LLF group. In addition, the PE-DHA values in the HLF group remained stable throughout the study. In conclusion, these results provide indirect by indisputable evidence that the conversion of ALA to DHA is efficient in preterm infants. In addition, ALA supplementation in the HLF group resulted in the maintenance of PE-DHA values within the confidence interval values displayed by the human milk fed group. Also observed was a minimal effect of ALA supplementation on fatty acids of the n-6 series. Overall, ALA supplementation from LEAR at a n-6:n-3 ratio of 6:1 in premature infant formula appears to efficiently contribute to the maintenance of the n-3 status in preterm infants.
