Omega-6 and omega-3 fatty acids are distinct families of polyunsaturated fatty acids (PUFAs) that are essential for human growth and development and for good health. Their basic or parent form is an 18-carbon fatty acid with double bonds at various locations in the chain. In the case of omega-6s, the first double bond occurs 6 carbons away from the non-acid or omega end of the molecule (Figure 1). Omega-3s have their first double bond 3 carbons from the omega end.


Humans cannot make linoleic acid on their own or convert other families of PUFAs to the omega-6 type, so it must be obtained preformed in foods. For this reason, and because insufficient intake leads to deficiency symptoms, linoleic acid is considered essential. However, people consuming western diets are in no danger of deficiency. Quite the opposite! On average, people in the U.S. consume about 14 to 18 grams/day-some 5 to 15 times more than they need-according to the most recent National Health and Nutrition Examination, 2003-2004. Actual need for linoleic acid is as little as 3 to 4 grams. Most dietary linoleic acid comes from vegetable oils where it predominates in corn, sunflower, safflower, soybean and canola oils. Most comes from soybean oil.

A key function of linoleic acid is to maintain the integrity of the skin-its ability to block harmful substances from crossing, while permitting water to escape. In conditions where skin integrity is compromised, as in atopic dermatitis (eczema) and psoriasis, water loss is increased and PUFA metabolism is altered. Early research on omega-6 and omega-3 fatty acids demonstrated that omega-3 fatty acids could not reverse the skin disorder that develops in linoleic acid deficiency, but linoleic acid and its derivative, gamma (√£)-linolenic acid (GLA), could. GLA is discussed below.

Linoleic acid is also important as the parent or precursor fatty acid of arachidonic acid, a long-chain omega-6 PUFA found in every cell membrane. This conversion process entails several steps, but as with the omega-3, alpha-linolenic acid, the amount of linoleic acid converted to arachidonic acid is very low, less than 0.1%. In spite of the low conversion, western diets supply plenty of arachidonic acid, so shortage is not a concern.

Linoleic acid has other fates. It is rapidly oxidized or “burned” to provide energy and conversely can be stored in adipose tissue, especially when amounts greatly exceed the body’s need. Further, some of the carbons from linoleic acid later turn up in molecules of cholesterol and other fatty acids, showing that it is converted to other lipids.


20-carbon PUFA is a key long-chain product of the conversion of linoleic acid to its long-chain derivatives. It is considered essential and is one of the body’s most critical PUFAs, in part because of its high concentration in cell membranes, particularly in the brain and blood vessels. However, brain arachidonic acid content is not sensitive to dietary intake, whereas brain docosahexaenoic acid (DHA, a long-chain omega-3 PUFA) can be increased by dietary intake. Further, the arachidonic acid content in brain varies less widely than DHA and appears to be tightly regulated.

When released from the membrane, arachidonic acid may act within the cell to trigger cellular events or may be converted to a variety of highly active substances involved in immune reactions, blood clotting, hormone responses, the transmission of nerve signals, and communication within and between cells. Another option is transport out of the cell and interaction with neighboring cells, particularly neurons. It may also be re-incorporated into the cell membrane. In some ways, arachidonic acid can be imagined as a central command molecule whose release from the membrane triggers a series of cascading events with rapid, potent and diverse effects.

The myriad effects of arachidonic acid release are directly linked to familiar diseases, including inflammation, allergies and immune-based diseases such as rheumatoid arthritis, cardiovascular disease and stroke, gastro-intestinal conditions, Alzheimer disease, brain injury and trauma, mood disorders, periodontitis and everything with an inflammatory component. The actions of common medications, such as aspirin, ibuprofen, anti-histamines and COX (cyclooxygenase) inhibitors are targeted to combating the effects of arachidonic acid derivatives. The association of arachidonic acid with the unpleasant side effects of many health conditions, plus its established involvement in immune and inflammatory responses and blood clot formation in major arteries has given this PUFA a bad reputation.

However, the situation is more complex than it seems. Ingestion of large amounts of the fatty acid enhance the platelet aggregation, but have no appreciable adverse effects on immune responses in healthy men. Consumption of arachidonic acid up to 1.5 grams/day-usual intakes in western diets are a third of this or less-by healthy people appears to be without harmful effects. Moreover, some derivatives of arachidonic acid are clearly anti-inflammatory. The undesirable increase in platelet aggregation may be related to the amount of arachidonic consumed or the low intake of long-chain omega-3 PUFAs characteristic of the participants. When fish or long-chain omega-3 intake is high, platelet aggregation is substantially reduced, an effect that contributes to the heart-health benefits associated with consumption of these PUFAs.

It is also important to note that arachidonic acid is essential for fetal and infant development, is found in breast milk, and is now added to most infant formula. The diet provides ample arachidonic acid from eggs, meats, poultry and fish. The bottom line on arachidonic acid is that this omega-6 PUFA is crucial in human health, in spite of its involvement in several health conditions.


This omega-6 PUFA is produced in the body from the addition of a third double bond to linoleic acid. GLA is most abundant in borage (10% to 25%) and evening primrose (7% to 10%) oils. It can be further metabolized to arachidonic acid, but it has health effects different from either linoleic or arachidonic acids. For example, it is considered anti-inflammatory and oils rich in it have been used to treat eczema. In conjunction with the omega-3 PUFA, EPA, GLA consumption was reported to reduce the use of an inhaler in asthmatic adults. Other studies have examined whether GLA is related to the development or treatment of cancer. However, the encouraging findings from studies in cultured cancer cells and in some clinical treatments have been offset by contrasting observations in human populations, where GLA was associated with greater risk of prostate and breast cancers. Observational studies such as these do not demonstrate that the relationship is causal, but they suggest caution. Self-treatment of serious health conditions should be undertaken only with a physician’s recommendation, lest the condition become worse or the treatment interfere with other medications.


In the past several decades, linoleic acid consumption has soared, while omega-3 fatty acid intakes-never high to begin with-declined further. Most omega-3s consumed in western diets come from plant sources and the intake of the long-chain omega-3s is less than 100 mg/day in many western countries. Some experts believe this striking imbalance in the consumption of these two families of PUFAs contributes to the increase in several chronic conditions, namely heart disease, dementia, unfavorable changes in the lens of the eye, and homicide. Others maintain that decreasing the consumption of omega-6 PUFAs would likely increase the rates of heart disease and diabetes. It is now recognized that exaggerated immune responses underlie many chronic diseases and contribute to mortality. Generally speaking, omega-6 PUFAs enhance certain immune functions, while omega-3s decrease them. However, things are not quite so simple, as these fatty acids have both pro- and anti-inflammatory effects. What is not known is whether simply increasing the consumption of long-chain omega-3s without reducing omega-6 intakes would reduce chronic disease risk in healthy people, as it appears to do in those with heart disease and certain other conditions. Because the metabolism of these two fatty acids is interconnected, it has been estimated that lowering the intake of omega-6s would reduce the amount of long-chain omega-3s needed to obtain their health benefits without risking those of omega-6s.

What should consumers do? Plenty of evidence supports the recommendations of many authoritative groups to consume unsaturated fatty acids in preference to saturated ones. To lower omega-6 fatty intakes and obtain the health benefits of omega-3s, individuals need to boost their consumption of long-chain omega-3s (these are the most potent forms) and choose oils rich in monounsaturates, such as olive and canola oils and the recently developed high-oleic acid vegetable oils. Use omega-6 rich oils sparingly, if at all.

A fully referenced version of this article is available from the editor.

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