Omega-6 fatty acid

history

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 which have in common a final carbon–carbon double bond in the n−6 position; that is, the sixth bond from the end of the fatty acid.

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.)

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.

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.

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.

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.

Chronic excessive production of n−6 eicosanoids is associated with heart attacks, thrombotic stroke, arrhythmia, arthritis, osteoporosis, inflammation, mood disorders and cancer. Many of the medications used to treat and manage these conditions work by blocking the effects of the potent n−6 fat, arachidonic acid. 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. 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. (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. Many of the anti-mania medications used to treat bipolar disorder work by targeting the arachidonic acid cascade in the brain.

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. Similar effect was observed on prostate cancer. Other analysis suggested an inverse association between total polyunsaturated fatty acids and breast cancer risk, but individual polyunsaturated fatty acids behaved differently »each other. »...'' a 20:2 derivative of linoleic acid »... was inversely associated with the risk of breast cancer''.

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. 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.

Dietary sources

, 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 Dietary sources of n−6 fatty acids

,include:

poultry
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

List of n−6 fatty acids

{| class="wikitable" ! Common name ! Lipid name ! Chemical name |- | Linoleic acid | 18:2 (n−6) | 9,12-octadecadienoic acid |- | Gamma-linolenic acid | 18:3 (n−6) | 6,9,12-octadecatrienoic acid |- | Eicosadienoic acid | 20:2 (n−6) | 11,14-eicosadienoic acid |- | Dihomo-gamma-linolenic acid | 20:3 (n−6) | 8,11,14-eicosatrienoic acid |- | Arachidonic acid | 20:4 (n−6) | 5,8,11,14-eicosatetraenoic acid |- | Docosadienoic acid | 22:2 (n−6) | 13,16-docosadienoic acid |- | Adrenic acid | 22:4 (n−6) | 7,10,13,16-docosatetraenoic acid |- | Docosapentaenoic acid | 22:5 (n−6) | 4,7,10,13,16-docosapentaenoic acid |- | Calendic acid | 18:3 (n−6) | 8E,10E,12Z-octadecatrienoic acid |}

Omega-6 fatty acid

Key n−6 fatty acids

Negative health effects

Dietary Linoleic Acid Requirement

Dietary sources

List of n−6 fatty acids

See also

References

Additional sources

Further reading