【摘要】  Background: Maternal essential fatty acid status declines during pregnancy, and as a result, neonatal concentrations of docosahexaenoic acid (DHA, 22:6n-3) and arachidonic acid (AA, 20:4n-6) may not be optimal.

Objective: Our objective was to improve maternal and neonatal fatty acid status by supplementing pregnant women with a combination of -linolenic acid (ALA, 18:3n-3) and linoleic acid (LA, 18:2n-6), the ultimate dietary precursors of DHA and AA, respectively.

Design: From week 14 of gestation until delivery, pregnant women consumed daily 25 g margarine supplying either 2.8 g ALA + 9.0 g LA ( n = 29) or 10.9 g LA ( n = 29). Venous blood was collected for plasma phospholipid fatty acid analyses at weeks 14, 26, and 36 of pregnancy, at delivery, and at 32 wk postpartum. Umbilical cord blood and vascular tissue samples were collected to study neonatal fatty acid status also. Pregnancy outcome variables were assessed.

Results: ALA+LA supplementation did not prevent decreases in maternal DHA and AA concentrations during pregnancy and, compared with LA supplementation, did not increase maternal and neonatal DHA concentrations but significantly increased eicosapentaenoic acid (20:5n-3) and docosapentaenoic acid (22:5n-3) concentrations. In addition, ALA+LA supplementation lowered neonatal AA status. No significant differences in pregnancy outcome variables were found.

Conclusions: Maternal ALA+LA supplementation did not promote neonatal DHA+AA status. The lower concentrations of Osbond acid (22:5n-6) in maternal plasma phospholipids and umbilical arterial wall phospholipids with ALA+LA supplementation than with LA supplementation suggest only that functional DHA status improves with ALA+LA supplementation.

【关键词】  Docosahexaenoic acid arachidonic acid linolenic acid linoleic acid Osbond acid pregnancy neonatal outcome essential fatty acids pregnant women fatty acid intakes birth weight gestational age

INTRODUCTION

It is well known that the essential fatty acid (EFA) status and long-chain polyene (LCP) status of pregnant women decrease during pregnancy ( 1 ). This particularly applies to arachidonic acid (AA, 20:4n-6) and docosahexaenoic acid (DHA, 22:6n-3), the major LCPs derived from linoleic acid (LA, 18:2n-6) and -linolenic acid (ALA, 18:3n-3), respectively. Because the developing fetus depends on its mother for LCP accretion ( 2, 3 ), neonatal LCP status may not be optimal under present dietary conditions ( 1, 4 ).

AA and DHA are important building blocks in all cell membranes and are present in high concentrations in neural and retinal tissues ( 5 - 7 ). Infants born preterm often experience neurodevelopmental problems ( 8, 9 ), and although a causal relation with their low LCP status at birth has not been ascertained, such an association is suggested by the results of postnatal intervention studies, which generally show that early LCP supplementation improves neuro-mental development, at least temporarily ( 10 - 12