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Circulation. 2009;119:902-907
Published online before print January 26, 2009, doi: 10.1161/CIRCULATIONAHA.108.191627
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(Circulation. 2009;119:902-907.)
© 2009 American Heart Association, Inc.


AHA Science Advisory

Omega-6 Fatty Acids and Risk for Cardiovascular Disease

A Science Advisory From the American Heart Association Nutrition Subcommittee of the Council on Nutrition, Physical Activity, and Metabolism; Council on Cardiovascular Nursing; and Council on Epidemiology and Prevention

William S. Harris, PhD, FAHA, Chair; Dariush Mozaffarian, MD, DrPH, FAHA; Eric Rimm, ScD, FAHA; Penny Kris-Etherton, PhD, FAHA; Lawrence L. Rudel, PhD, FAHA; Lawrence J. Appel, MD, MPH, FAHA; Marguerite M. Engler, PhD, FAHA; Mary B. Engler, PhD, FAHA; Frank Sacks, MD, FAHA


Key Words: AHA Scientific Statements • diet • fatty acids • nutrition


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    Introduction
 
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
 
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 {approx}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 {gamma}-linolenic and dihomo-{gamma}-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 . . . [Full Text of this Article]




Related Internet Resources:

Supporting Materials From the American Heart Association
Correspondence on AHA Statements and Guidelines

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