Omega-6 Fatty Acids and Risk for Cardiovascular Disease

Abstract

A large body of literature suggests that higher intakes of omega-6 (or n-6) polyunsaturated fatty acids (PUFAs) reduce risk for coronary heart disease (CHD). However, for the reasons outlined below, some individuals and groups have recommended substantial reductions in omega-6 PUFA intake.1–4 The purpose of this advisory is to review evidence on the relationship between omega-6 PUFAs and the risk of CHD and cardiovascular disease. Omega-6 PUFAs are characterized by the presence of at least 2 carbon-carbon double bonds, with the first bond at the sixth carbon from the methyl terminus. Linoleic acid (LA), an 18-carbon fatty acid with 2 double bonds (18:2 omega-6), is the primary dietary omega-6 PUFA. LA cannot be synthesized by humans, and although firm minimum requirements have not been established for healthy adults, estimates derived from studies in infants and hospitalized patients receiving total parenteral nutrition suggest that an LA intake of ≈0.5% to 2% of energy is likely to suffice. After consumption, LA can be desaturated and elongated to form other omega-6 PUFAs such as γ-linolenic and dihomo-γ-linolenic acids. The latter is converted to the metabolically important omega-6 PUFA arachidonic acid (AA; 20:4 omega-6), the substrate for a wide array of reactive oxygenated metabolites. Because LA accounts for 85% to 90% of the dietary omega-6 PUFA, this advisory focuses primarily on this fatty acid, recognizing that dietary AA, which can affect tissue AA levels,5 may have physiological sequelae.6–8 LA comes primarily from vegetable oils (eg, corn, sunflower, safflower, soy). The average US intake of LA, according to National Health and Nutrition Examination Survey 2001 to 2002 data for adults ≥19 years of age, is 14.8 g/d.9 On the basis of an average intake of 2000 kcal/d, LA intake is 6.7% of energy. AA (≈0.15 g/d) is consumed preformed in meat, …