Long-chain polyunsaturated fatty acids (LCP) are considered conditionally essential nutrients for the infant born prematurely, and attempts are being made to match fatty acid profiles of formula and breast fed infants. In this double-blind, randomized study we investigated the effects of a formula enriched with both n-6 and n-3 LCP on plasma fatty acid profiles, antioxidant status and growth of premature infants. 29 infants received either a formula devoid of LCP or a LCP supplemented formula (0.5 g/100 g fat linoleic acid metabolites, 0.8 g/100 g fat alpha-linolenic acid metabolites). 17 breast fed infants served as a control group. At study entry as well as two and four weeks later, plasma and urine samples were collected, growth data obtained and food tolerance was documented. At the end of the four week study period, plasma docosahexaenoic acid (DHA) levels of supplemented infants were significantly higher than those of unsupplemented infants and similar to those of infants fed human milk. Plasma n-6 LCP concentrations including arachidonic acid (AA) were similar between groups. The plasma alpha-tocopherol levels of breast fed and supplemented infants were similar and tended to be lower than in infants fed the formula devoid of LCP. Urinary malondialdehyde (MDA) excretion of formula fed infants was significantly higher compared to infants fed human milk, but did not differ between the two formula groups. Parameters of growth and milk tolerance did not differ between groups. Our results demonstrate that plasma LCP levels similar to those of breast fed infants can be achieved with the LCP supplemented formula used in this trial, without evidence of adverse effects of the LCP enrichment.

Pulmonary damage in cystic br osis (CF) is associated with chronic inflammation mediated in part by proinflammatory 5-lipoxygenase products (5-LOP, leukotrienes and 5-hydroxyeicosatetraenoic acid) from polymorph neutrophil granulocytes (PMN). The authors studied 5-LOP formation of PMN from CF patients and in vitro effects of added eicosapentaenoic acid (EPA) and fish oil. Circulating PMN were isolated from 10 CF patients without acute infections and 10 control persons of the same age (4-20 years). Total 5-LOP liberation from PMN of CF patients was significantly increased over controls after incubation with the calcium ionophore A23 (1 mumol L-1) without arachidonic acid (AA) (380 +/- 24 vs. 294 +/- 28 pmol mL-1) and with 10 mumol L-1 AA (1303 +/- 104 vs. 1015 +/- 104 pmol mL-1), and there were nonsignificant trends to high values after incubation with 5 mumol L-1 platelet activating factor (PAF, 134% of controls) and 1 mumol L-1 formyl-methionylleucyl-phenylalanine (FMLP, 125%). The addition of 100 micrograms mL-1 fish oil to PMN of CF patients challenged with A23 completely suppressed synthesis of proinflammatory 5-LOP of the 4-series, while inactive 5-LOP metabolites of the 5-series were produced. Added EPA (10 mumol L-1) also suppressed 4-series 5-LOP and significantly reduced leukotriene B4 concentration by 48% from 39.9 +/- 3.2 to 20.6 +/- 11.4 pmol L-1, again with a concomittant increase of inactive 5-series metabolites. The authors conclude that the turnover of endogenous and exogenous AA is enhanced in CF, possibly due to stimulated phospholipase A2 activity. The relatively small effect of the receptor dependent stimuli PAF and FMLP may be caused by a down-regulation of PMN receptors in CF. Supplementation of long-chain omega-3-fatty acids may be beneficial for reducing excessive inflammation in CF patients and should be further evaluated.

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