Plant- and marine-derived n-3 polyunsaturated fatty acids have differential effects on fasting and postprandial blood lipid concentrations and on the susceptibility of LDL to oxidative modification in moderately hyperlipidemic subjects.
Plant- and marine-derived n-3 polyunsaturated fatty acids have differential effects on fasting and postprandial blood lipid concentrations and on the susceptibility of LDL to oxidative modification in moderately hyperlipidemic subjects.
Year: 2003
Authors: Finnegan, Y.E., Minihane, A.M., Leigh-Firbank, E.C., Kew, S., Meijer, G.W., Muggli, R., Calder, P.C., Williams, C.M.
Publication Name: Am. J. Clin. Nutr.
Publication Details: Volume 77, Pages 783-95.
Abstract:
Background: Dietary alpha-inolenic acid (ALA) can be converted to long-chain n 3 polyunsaturated fatty acids (PUFAs) in humans and may reproduce some of the beneficial effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on cardiovascular disease risk factors.
Objective: This study aimed to compare the effects of increased dietary intakes of ALA and EPA+DHA on a range of atherogenic risk factors.
Design: This was a placebo-controlled, parallel study involving 150 moderately hyperlipidemic subjects randomly assigned to 1 of 5 interventions: 0.8 or 1.7 g EPA+DHA/d, 4.5 or 9.5 g ALA/d, or an n-6 PUFA control for 6 mo. Fatty acids were incorporated into 25 g of fat spread and 3 capsules to be consumed daily.
Results: The change in fasting or postprandial lipid, glucose, or insulin concentrations or in blood pressure was not significantly different after any of the n-3 PUFA interventions compared with the n-6 PUFA control. The mean (± SEM) change in fasting triacylglycerols after the 1.7-g/d EPA+DHA intervention ( -7.7 ± 4.99%) was significantly (P < 0.05) different from the change after the 9.5-g/d ALA intervention (10.9 ± 4.5%). The ex vivo susceptibility of LDL to oxidation was higher after the 1.7-g/d
EPA+DHA intervention than after the control and ALA interventions (P < 0.05). There was no significant change in plasma alpha-tocopherol concentrations or in whole plasma antioxidant status in any of the groups.
Conclusion: At estimated biologically equivalent intakes, dietary ALA and EPA+DHA have different physiologic effects. Author's Abstract.
Objective: This study aimed to compare the effects of increased dietary intakes of ALA and EPA+DHA on a range of atherogenic risk factors.
Design: This was a placebo-controlled, parallel study involving 150 moderately hyperlipidemic subjects randomly assigned to 1 of 5 interventions: 0.8 or 1.7 g EPA+DHA/d, 4.5 or 9.5 g ALA/d, or an n-6 PUFA control for 6 mo. Fatty acids were incorporated into 25 g of fat spread and 3 capsules to be consumed daily.
Results: The change in fasting or postprandial lipid, glucose, or insulin concentrations or in blood pressure was not significantly different after any of the n-3 PUFA interventions compared with the n-6 PUFA control. The mean (± SEM) change in fasting triacylglycerols after the 1.7-g/d EPA+DHA intervention ( -7.7 ± 4.99%) was significantly (P < 0.05) different from the change after the 9.5-g/d ALA intervention (10.9 ± 4.5%). The ex vivo susceptibility of LDL to oxidation was higher after the 1.7-g/d
EPA+DHA intervention than after the control and ALA interventions (P < 0.05). There was no significant change in plasma alpha-tocopherol concentrations or in whole plasma antioxidant status in any of the groups.
Conclusion: At estimated biologically equivalent intakes, dietary ALA and EPA+DHA have different physiologic effects. Author's Abstract.
