Metabolism of polyunsaturated omega 6 linoleic and

omega 3 linolenic acid

A competitive interaction exists between the metabolism of fatty acids. The omega-6 fatty acids suppress the metabolism of the omega-3 fatty acids and vice versa, at the rate limiting step (cyclo-oxygenase) and they both suppress the metabolism of n-9 fatty acids.

The body cannot produce omega-6 or omega-3 fats and relies on food sources to obtain them. The effects of n-3 fats are widespread because they are incorporated into every cell, tissue and organ from the heart and blood vessels to joints, lungs, muscles, brain and reproductive organs.

The omega-3 fat, eicosapentaenoic acid or EPA is produced in the body from n-3 linolenic acid, but can be found in seafood and small amounts in lean meat (if animal is not grain fed there will be more n-3 fat). Docosahexaenoic acid or DHA is produced from EPA and is also found in in tuna and other fish oils and breast milk.

N-6 linoleic acid is also essential, whilst chemically similar to n-3 linolenic, the omega-6 fats tend to act in different and generally opposite ways. Arachidonic acid is also derived from linoleic acid, and is converted into substances that regulate inflammation and transmit messages between cells. Found in human milk, brain, eye and nerves.

Many of the properties attributed to n-3 fatty acids are believed to be due to them replacing arachidonic acid (derived from n-6 fats) in membrane phospholipids. Membrane arachidonic acid is the initial substrate for prostaglandin production and EPA competes with arachidonic acid for the cyclo-oxygenase and lipoxygenase enzymes involved in prostaglandin synthesis (Allman, Food Australia 1995; 47 (3):14-17).

N-6 linoleic is converted to arachidonic acid and the potent aggregatory prostaglandin thromboxane A2 (in platelet membranes) and leukotriene B₄ (in neutrophils) which is pro-inflammatory. N-3 linolenic is converted to EPA and thromboxane A3 (in platelet membranes) which is not aggregatory and prostaglandin I₃that is anti-aggregatory and leukotriene B₅(in neutrophils) is not inflammatory.

The amount of substitution of arachidonic acid with EPA in membrane phospholipids will depend upon linolenic competing with linoleic acid for the enzymes involved in desaturation and elongation. Therefore the ratio of n-6 to n-3 is important. Emken et al (1992) showed that when the diet contains 15g linoleic the conversion to EPA was 18.5%, but it dropped to 11% when it was doubled. The affinity of the acylation enzymes is greater for n-6 fats than that for the n-3 fats. Thus even when the intake of plant n-3 fats is greater than that of plant n-6 one will still find large amounts of arachidonic acid in the membranes (Emken et al. Nutr. 1992; 8: 213-4). Emken et al also showed that doubling the normal intake of the n-6 linoleic acid reduced the conversion of n-3 linolenic to n-3 EPA by about 40%. However, the rate of conversion of linolenic on average intakes of n-6 fats will be adequate for most of the population provided 2g/day of n-3 linolenic is eaten. Australians however consume on average <1g linolenic.

Linolenic is poorly incorporated into membrane phospholipids and adipose tissue and it appears unlikely that it competes directly with arachidonic acid. It may be that linolenic which is not converted to its longer chain fatty acids will undergo b-oxidation.

In summary

If your intake of n-6 fat is too high it can compete with the n-3 fats and stop them doing their good work. The n-6 and n-3 poly fats compete with each other metabolically for conversion to longer chain fats. Thus diets rich in corn, safflower, sunflower and peanut oils all of which are high in n-6 and low in n-3 can lead to n-3 fatty acid deficiency, and a high ratio of n-6 to n-3 accentuates this deficiency (Connor AJCN 1999; 69: 827-8).

Last Updated: March 27, 2001.