The intake of omega-6 vegetable oils, particularly soybean oil, began to increase in the USA starting in the early 1900s at a time when the consumption of butter and lard was on the decline.1 This caused a more than two-fold increase in the intake of linoleic acid, the main omega-6 polyunsaturated fat found in vegetable oils, which now makes up around 8% to 10% of total energy intake in the Western world. The omega-6 fat linoleic acid should not be confused with conjugated linoleic acid found in pastured animal foods.
A systematic review of studies measuring the changes in linoleic acid concentration in subcutaneous adipose tissue in the USA revealed an approximate 2.5-fold increase in linoleic acid increasing from 9.1% to 21.5% from 1959 to 2008.2 Importantly, the concentration of linoleic acid in adipose tissue is a reliable marker of intake as the half-life of linoleic acid is approximately 2 years in adipose tissue. The authors of the study also noted that the increase in adipose tissue linoleic paralleled the increase in the prevalence of diabetes, obesity and asthma.2
The amount of linoleic acid in adipose tissue, but also in platelets, is additionally positively associated with coronary artery disease (CAD), whereas long-chain omega-3 (eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) levels in platelets are inversely related to CAD.3 This provides rather compelling evidence that omega-3s protect whereas omega-6 linoleic acid promotes heart disease. Importantly, the increased consumption of omega-6 polyunsaturated fat linoleic acid can reduce omega-3 in the body as it competes with the alpha-linolenic acid for metabolism to longer chain polyunsaturated fats. It has been known for decades that linoleic acid, as a percentage of total fatty acids in lipids, is reduced in patients with CAD, and this has been used as an argument to suggest that low intakes of linoleic acid may cause heart disease.4 However, total fatty acid concentrations, as opposed to percentages, are independent of changes in other fatty acids and hence are more reliable markers of linoleic acid intake (although likely less reliable compared with adipose tissue). Importantly, linoleic acid concentrations in both serum cholesteryl esters and phospholipid fatty acids are in fact higher in patients with CAD compared with those without CADcoronary artery disease.4 Again, since linoleic acid cannot be synthesised in the body, this suggests that patients who have heart disease consume more omega-6 linoleic acid than those without heart disease. Indeed, the authors of the study concluded, “(…) cholesteryl linoleate is widely believed to decrease in patients with CAD. Such decreases, however, represent decreases only in relative terms. We have shown in this study that linoleate actually is present in a higher concentration in individuals with CAD than in those without CAD”.4