Common PUFA oil products with linoleic acid increase all cause mortality, and mortality from cardiovascular and coronary heart disease.

A recent report in the British Medical Journal signals the danger of substituting Omega-6 polyunsaturated fats, linoleic acid for saturated fats in diet. 

Advice to substitute linoleic acid for saturated fat is one component of dietary guidelines to reduce the risk of coronary heart disease; however, clinical benefits specific to linoleic acid have not been established. Linoleic acid is one of the commonest polyunsaturated fats in the diet and is present in many consumer products such as safflower oil and safflower polyunsaturated margarine and Corn oil.

A comprehensive analysis of the effects of linoleic acid on death from coronary heart disease and cardiovascular disease was previously not possible, owing to missing outcome data from the Sydney Diet Heart Study, a randomized controlled clinical trial. This is the first prospective randomized control study showing the potential harmful effects of linoleic acid.

In this cohort, substituting omega 6 linoleic acid for saturated fat did not provide the intended benefits, but increased all cause mortality, cardiovascular death, and death from coronary heart disease

An updated meta-analysis incorporating these missing data showed no evidence of benefit, and suggested a possible increased risk of cardiovascular disease from replacing saturated fat with omega-6 linoleic acid.

The proposed mechanism of underlying damage is via the oxidized LA metabolites. Omega-6 LA is the most abundant fatty acid in native low density lipoprotein particles. Oxidized LA metabolites (OXLAMs) are the most abundant oxidized fatty acids in oxidized low density lipoprotein, which is potentially more atherogenic than unmodified low density lipoprotein. A potential mechanism contributing to higher cardiovascular mortality in the LA intervention group is a diet induced increase in the production of bioactive OXLAMs, including 9- and 13-hydroperoxy-octadecadienoic acid, and 9- and 13-hydroxy-octadecadienoic acid. These OXLAMs are enriched in the lipid laden, macrophage foam cells; vascular endothelial cells; and migrating vascular smooth muscle cells of atherosclerotic lesions. OXLAMs, particularly the isomers and enantiomers produced by free radical mediated oxidation, have been mechanistically linked to cardiovascular disease pathogenesis. Mechanisms include inducing the formation of macrophage foam cells; endothelial cell activation;migration, proliferation, and foam cell formation of vascular smooth muscle cells; and inhibition of lysosomal hydrolysis of low density lipoprotein cholesteryl esters.

These findings could have important implications for worldwide dietary advice to substitute omega-6 linoleic acid (or polyunsaturated fatty acids in general) for saturated fatty acids. The key is the use of Omega-3 acid, which has EPA and DHA ; in PUFA that has a good content of Omega 3 FA does not increase the death from coronary heart disease.

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