Cardiovascular Risk Factors and Dietary Plant Omega-3 Verus Omega-6 Fatty Acids

Abstract

LEARNING OUTCOME: To compare the effects on selected risk factors for coronary heart disease when α-linolenic acid is substituted for linoleic acid in an American Heart Association Step 1 type-diet.Increased intakes of the plant omega-3 fatty acid, a-linolenic acid (ALA) may protect against coronary heart disease (CHD). It has been demonstrated that feeding the marine omega-3 fatty acid, eicosapentenoic acid (EPA) can result in decreased triglycerides, fibrinogen and platelet aggregation which are considered beneficial for CHD. ALA can be converted to EPA in the body so that increased consumption of ALA should result in increased concentrations of EPA. The aim of the current study was to compare two low saturated fat diets, both similar to the American Heart Association Step I diet, with the only variable being the ratio of ALA to linoleic acid (ALA:LA). This was achieved by the substitution of flaxseed oil for safflower oil. After consuming a stabilisation diet with 37% energy (en) from fat (16 % en, saturated fat) for two weeks, healthy men aged 18 to 35 years (n=30) consumed the low saturated fat diet, 10% en saturated fat, 13% en monounsaturated fat and 7% en polyunsaturated fat. Half ate a diet with ALA:LA of 1.4:1 (ALA-rich) and the remainder ALA:LA of 1:34 (ALA-poor). Subjects maintained their weight throughout the study and all food was supplied. Blood was sampled at the beginning, middle and end of six weeks on the test diets to measure changes in CHD risk factors. This included analyses of plasma cholesterol, triglycerides, factor VIIc and fibrinogen. In addition, platelet aggregation induced by collagen was measured and platelet membrane fatty acids were determined It was expected the reduction of saturated fat from 16% to 10% en would result in decreased cholesterol and factor VIIc but while LDL cholesterol declined in both groups during the stabilisation diet, no further reductions occurred on either test diet and factor VIIc was unchanged. The percentage of platelet EPA tripled from 0.2 to 0.6% (P<0.0001) on the ALA-rich diet. Triglycerides, fibrinogen and platelet aggregation were unaltered by the test diets. Hence while an increase in platelet EPA was achieved no apparent benefit of the ALA-rich diet over the ALA-poor diet in modifying these risk factors resulted. These findings were in young men who entered the study with normal concentrations of analytes and may differ from older populations with already established pathologies.