To determine whether docosahexaenoic acid (DHA) supplementation of breast-feeding mothers increases the DHA contents of breast milk and infant plasma phospholipids (PPs), breast-feeding women were randomly assigned to 3 DHA-supplementation groups (170-260 mg/d) or a control group. Group 1 (n = 6) consumed an algae-produced high-DHA triacylglycerol; group 2 (n = 6) consumed high-DHA eggs; group 3 (n = 6) consumed a high-DHA, low-eicosapentaenoic acid marine oil; and group 4 (n = 6) received no supplementation. From before to after supplementation (2 and 8 wk postpartum), mean (+/-SD) maternal PP DHA increased in groups 1, 2, and 3 by 1.20 +/- 0.53, 0.63 +/- 0.82, and 0.76 +/- 0.35 mol% of fatty acids, respectively (23-41%), but decreased in group 4 by 0.44 +/- 0.34 mol% (15%). Breast-milk DHA of groups 1, 2, and 3 increased by 0.21 +/- 0.16, 0.07 +/- 0.11, and 0. 12 +/- 0.07 mol%, respectively (32-91%) but decreased in group 4 by 0.03 +/- 0.04 mol% (17%). Mean infant PP DHA in groups 1, 2, and 3 increased by 1.63 +/- 0.79, 0.40 +/- 1.0, and 0.98 +/- 0.61 mol%, respectively (11-42%), but only by 0.18 +/- 0.74 mol% (5%) in group 4. Correlations between the DHA contents of maternal plasma and breast milk and of milk and infant PPs were significant. Breast-milk and maternal and infant PP 22:5n-6 concentrations were lowest in group 2. DHA supplementation increases the plasma and breast-milk DHA concentrations of lactating women, resulting in higher PP DHA concentrations in infants.

This paper is number six of the series: Lipids of Ocular Tissues.1 Abbreviations used are: iV-RPE, Schiff base of retinal and phosphatidylethanolamine; ROS, rod outer segments.

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Some humans and animals with inherited retinal degenerations (RD) have lower blood levels of docosahexaenoic acid (22:6n-3) than controls. As a result of recent studies, clearly the low blood 22:6n-3 phenotype is found in multiple RD phenotypes and no mutation thus far identified in humans or animals is involved in lipid metabolism. Therefore, it seems reasonable to suggest that the primary defect is not in 22:6n-3 metabolism, but rather in some common convergent pathway that ultimately leads to the reduction of blood and tissue 22:6n-3 levels. One possibility is that the different mutations produce a metabolic stress that provokes structural and biochemical adaptive changes in photoreceptor cells and their rod outer segments. If the stress is oxidant, the retina could downregulate 22:6n-3 and upregulate antioxidant defenses. How such a stress could lead to changes in blood levels of 22:6n-3 is not obvious. However, the consistent finding of the 22:6n-3 phenotype in many different retinal degeneration genotypes suggests that some form of communication exists between the retina and other tissues that serves to reduce blood levels of 22:6n-3.

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