Fatty acid profiles, antioxidant status, and growth of preterm infants fed diets without or with long-chain.

January 1, 2003 Human Health and Nutrition Data 0 Comments

Fatty acid profiles, antioxidant status, and growth of preterm infants fed diets without or with long-chain.

Year: 2003
Authors: B Koletzko, U Sauerwald, U Keicher, H. Saule, S. Wawatschek, H Bohles, K Bervoets, M Fleith,
Publication Name: Eur. J. Nutr.
Publication Details: Volume 42; Number 5; 243-253.


Preterm infants are at a disadvantage with regard to EFA status at birth as a portion of intrauterine accretion of long-chain polyunsaturated fatty acids (LCPUFA) during the last trimester of pregnancy, may not occur. This is particularly true for docosahexaenoic acid (DHA) and arachidonic acid (AA). Furthermore, utilization of LCPUFA may exceed an infant’s capacity to synthesize n6 and n3 LCPUFA from the precursors linoleic acid (LA) and alpha-linolenic acid (ALA). As a result, rapid depletion of AA and DHA in plasma phospholipids and erythrocytes occurs in preterm infants fed a diet devoid of LCPUFA. Low levels of AA and DHA have been correlated with poorer intra- and extrauterine growth, and lower test scores on visual and cognitive development, respectively. As such, supplementation of infant formula with both AA and DHA has been the subject of numerous studies. However, adverse effects of supplementing preterm infants with LCPUFA have been reported and therefore must be considered. First, supplementation with n3 LCPUFA alone may result in a reduction in AA levels; second, the amount of n6 and n3 LCPUFA supplementation may effect the rate of endogenous LCPUFA synthesis; and lastly, LCPUFA are oxidatively unstable , which may subject the infant to damage via reactive oxygen species. Current research is focusing on matching the fatty acid profile of preterm infant formula with that of breast milk. The aim of this study was to investigate whether feeding preterm infants formula containing n3 and n6 LCPUFA, with a lower ratio of n6:n3 than typically found in human milk, would result in an equivalent fatty acid status to preterm infants fed human milk. Forty-six premature infants participated in this double-blind randomized study. Twenty-nine infants were randomly assigned to receive either a formula devoid of LCPUFA (Group F, n=14), or formula supplemented with LCPUFA (Group LCP-F, n=15). Formula LCP-F contained 0.5g LA metabolites/100g fat (n6) and 0.8g/100g fat derived from egg lipid extracts, black currant seed oil, and low EPA fish oil. Both formulas contained 2.9g protein, 11.8g carbohydrates, and 5.2g fat, and 0.68mg vitamin E per 100ml. In addition, 17 breast fed infants acted as controls (Group HM), receiving at least 90% of their energy intake as human milk during the study period. Formula fed infants received their assigned study formula for 28 d following study entry. Measurement of growth parameters for all infants were well documented at birth, upon study entry (day 0), and at day 14 and 28. Blood samples were collected on the day 0, 14, and 28 for analysis of plasma phospholipid fatty acid and vitamin E concentrations. Throughout the study, all infants showed good feeding tolerances with no significant differences in frequencies of gastric residuals, vomiting or stools per day. In addition, average weight, length, and head circumference did not differ between dietary groups on study days 0, 14, or 28. ALA increased significantly over time in groups HM and LCP-F, while increases in group F did not reach statistical significance. The higher EPA content of formula LCP-F compared to formula F resulted in significantly higher EPA phospholipid concentrations in the LCP-F group, which were also similar to those observed in breast fed infants. At the end of the 28d study period, plasma DHA levels in the LCP-F group were significantly higher in comparison to group F, and similar to infants fed human milk. Plasma n6 LCPUFA concentrations, including AA, were similar between groups. Plasma alpha-tocopherol levels in the HM and LCP-F group were similar, both being lower than infants in the LCP-F group. This data indicates that plasma LCPOFA levels similar to those of breast fed infants can be achieved with formula supplemented with LCPUFAs, as in this study. Furthermore, the authors found no evidence of adverse effects of LCPUFA enrichment. The results are very significant with regard to the development of formulas to ensure sufficient LCPUFA intake and status in preterm infants.

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