The chemical structure of linoleic acid, a common n−6 fatty acid found in many vegetable oils.

n−6 fatty acids (popularly referred to as ω−6 fatty acids or omega-6 fatty acids) are a family of unsaturated fatty acids that have in common a final carbon–carbon double bond in the n−6 position, that is, the sixth bond, counting from the end opposite the carboxyl group.

The biological effects of the n−6 fatty acids are largely mediated by their conversion to n-6 eicosanoids that bind to diverse receptors found in every tissue of the body. The conversion of tissue arachidonic acid (20:4n-6) to n-6 prostaglandin and n-6 leukotriene hormones provides many targets for pharmaceutical drug development and treatment to diminish excessive n-6 actions in atherosclerosis, asthma, arthritis, vascular disease, thrombosis, immune-inflammatory processes, and tumor proliferation. Competitive interactions with the n−3 fatty acids affect the relative storage, mobilization, conversion and action of the n-3 and n-6 eicosanoid precursors. (See Essential fatty acid interactions for more information.)

[edit] Key n−6 fatty acids

Linoleic acid (18:2, n−6), the shortest-chained n−6 fatty acid, is an essential fatty acid. Arachidonic acid (20:4) is a physiologically significant n−6 fatty acid and is the precursor for prostaglandins and other physiologically active molecules.

[edit] Negative health effects

Some medical research suggests that excessive levels of n−6 fatty acids, relative to n−3 fatty acids, may increase the probability of a number of diseases and depression.^[1][2][3]

Modern Western diets typically have ratios of n−6 to n−3 in excess of 10 to 1, some as high as 30 to 1. The optimal ratio is thought to be 4 to 1 or lower.^[4][5]

Excess n−6 fats interfere with the health benefits of n−3 fats, in part because they compete for the same rate-limiting enzymes. A high proportion of n−6 to n−3 fat in the diet shifts the physiological state in the tissues toward the pathogenesis of many diseases: prothrombotic, proinflammatory and proconstrictive.^[6]

Chronic excessive production of n−6 eicosanoids is associated with heart attacks, thrombotic stroke, arrhythmia, arthritis, osteoporosis, inflammation, mood disorders, obesity, and cancer.^[7] Many of the medications used to treat and manage these conditions work by blocking the effects of the potent n−6 fat, arachidonic acid.^[8] Many steps in formation and action of n-6 hormones from n-6 arachidonic acid proceed more vigorously than the corresponding competitive steps in formation and action of n-3 hormones from n-3 eicosapentaenoic acid.^[9] The COX-1 and COX-2 inhibitor medications, used to treat inflammation and pain, work by preventing the COX enzymes from turning arachidonic acid into inflammatory compounds.^[10] (See Cyclooxygenase for more information.) The LOX inhibitor medications often used to treat asthma, work by preventing the LOX enzyme from converting arachidonic acid into the leukotrienes.^[11][12] Many of the anti-mania medications used to treat bipolar disorder work by targeting the arachidonic acid cascade in the brain.^[13]

A high consumption of omega-6 polyunsaturated fatty acids (PUFAs), which are found in most types of vegetable oil, may increase the likelihood that postmenopausal women will develop breast cancer^[14]. Similar effect was observed on prostate cancer^[15]. Other analysis suggested an inverse association between total polyunsaturated fatty acids and breast cancer risk, but individual polyunsaturated fatty acids behaved differently [from each other]. [...] a 20:2 derivative of linoleic acid [...] was inversely associated with the risk of breast cancer^[16].

[edit] Dietary linoleic acid requirement

Adding more controversy to the n−6 fat issue is that the dietary requirement for linoleic acid (the key n−6 fatty acid), has been seriously questioned, because of a significant methodology error discovered by University of Toronto scientist Stephen Cunnane.^[17] Cunnane discovered that the seminal research used to determine the dietary requirement for linoleic acid was based on feeding animals linoleic acid-deficient diets, which were simultaneously deficient in n−3 fats. The n−3 deficiency was not taken into account. The n−6 oils added back systematically to correct the deficiency also contained trace amounts of n−3 fats. Therefore the researchers were inadvertently correcting the n−3 deficiency as well. Ultimately, it took more oil to correct both deficiencies. According to Cunnane, this error overestimates LA requirements by 5 to 15 times.

[edit] Dietary sources

The evening primrose flower (O. biennis) produces an oil containing a high content of γ-linolenic acid, a type of n−6 fatty acid.

Four major food oils (palm, soybean, rapeseed, and sunflower) provide more than 100 million metric tons annually, providing more than 32 million metric tons of n-6 linoleic acid and 4 million metric tons of n-3 alpha-linolenic acid ^[18]

• poultry
• avocado
• eggs
• cereals
• whole-grain breads
• baked goods
• nuts
• most vegetable oils
• evening primrose oil
• borage oil
• blackcurrant seed oil
• flax/linseed oil
• hemp oil
• soybean oil
• cottonseed oil
• sunflower seed oil
• corn oil
• safflower oil
• pumpkin seeds
• acai berry

[edit] List of n−6 fatty acids

[edit] See also

• Essential fatty acid interactions
• Essential nutrients
• n−3 fatty acid
• n−9 fatty acid

[edit] References

[edit] Additional sources

[edit] Further reading

• Erasmus, Udo. Fats That Heal, Fats That Kill. 3rd ed. Burnaby (BC): Alive Books; 1993.