Essential fats: an inside look

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OH-MEGA! The skinny on omega fats

These days almost everyone has heard of omega-3 (n-3) and omega-6 (n-6) fats, which belong to a broader group of fats called polyunsaturated fatty acids (PUFAs). The human body can make most types of fats it needs from other fats. That isn’t the case when it comes to omega-3 and omega-6 fatty acids, which is why these are considered essential fatty acids (EFAs). They are essential because your body cannot produce them on its own so they must come from your diet. The primary EFAs are known as linoleic acid (LA; an omega-6), alpha-linolenic acid (ALA; an omega-3 that comes from plants), as well as the long-chain omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). (1)

The body cannot produce essential fatty acids (EFAs) such as omega-3s or omega-6s…As a result, EFAs need to be obtained through diet or supplementation.

What makes omega-3 and omega-6 fats special?

For one thing, they are an integral part of cell membranes throughout the body and affect its fluidity, flexibility, permeability, and the activity and function of membrane-bound receptors.(2) Additionally, they act as potent chemical messengers that play critical roles in immune and inflammatory responses, (3) regulation and availability of neurotransmitters, (4) and regulation of gene expression, including those involved with fatty acid metabolism and inflammation. (5, 6)

However, whereas increasing omega-3 fatty acid intake have a positive effect in the body, (7-9) what many people don’t realize is that omega-6 fats have nearly the opposite effect by promoting inflammation and contributing to modern chronic illnesses such as heart disease, obesity and diabetes. (10, 11)

Unfortunately, omega-6 fats are all too common in our modern diet. They’re found in nearly all processed, refined and restaurant-cooked foods, and recent statistics suggest they may constitute as much as 20% of calories in the average American’s diet. (12)

Fish vs. Plant! A fishy proposition. Or is it?

Not all omega-3s are created equal. There are 2 sources: (1) marine based, and (2) plant-based. Despite their sharing the same categorical name, they perform vastly different functions (explored in subsequent posts). Below, we provide a snapshot on what they are:

  • MARINE-BASED OMEGA-3 − Fish contain a variety of fatty acids, but the ones that are believed to confer the majority of the benefits are the long-chain omega-3 fats, found EXCLUSIVELY in fish and marine algae:
    1. Eicosapentanaenoic acid (EPA)
    2. Docosahexaenoic acid (DHA)
  • PLANT-BASED OMEGA-3 − The primary type of omega-3 fat found in plants such as flax seed, chia, hemp and a few other foods is alpha-linoleic acid (ALA).


Metabolism & Bioavailability

As you can see from Figure 1, humans are capable of synthesizing longer EFAs (e.g., EPA and DHA) from other sources of omega-3 such as ALA through a series of desaturation (addition of a double bond) and elongation (addition of two carbon atoms) reactions. (13, 14)

omega3 omega6 pathway

Fig. 1 - Omega-6 (n-6) and omega-3 (n-3) fatty acids comprise the two classes of essential fatty acids (EFA). The parent compounds within each class, linoleic acid (LA - an omega-6) and alpha-linolenic acid (ALA - an omega-3) give rise to longer chain derivatives inside the body.

As seen in the figure, Omega-6 and omega-3 fatty acids compete for the same enzymes. An increase in the diet of one decreases metabolism of the other. (15) Omega-6 fatty acid metabolites result in prostaglandins that are inflammatory; omega-3 fatty acids result in prostaglandins that are anti-inflammatory.

In plain English: The more omega-3 fat you eat, the less omega-6 will be available to the tissues to produce inflammation.

Several studies have shown that the biological availability and activity of n-6 fatty acids are inversely related to the concentration of of n-3 fatty acids in tissue. (16) Greater composition of EPA & DHA in cell membranes reduces the availability of Arachidonic Acid (AA; see Figure 1) for eicosanoid (a pro-inflammatory molecule) production. (16) In the U.S. the average person’s tissue concentration of highly unsaturated n-6 fat is 75%. Since we get close to 10% of our calories from n-6, our tissue contains about as much n-6 as it possibly could. This creates a very inflammatory environment in the body. (17)

Although it is possible for the body to convert ALA to EPA and DHA by elongase and desaturase enzymes, research suggests that only a small amount can be synthesized in the body through this process. (18) For example, one study showed that only ~2 to 10% of ALA is converted to EPA, with <0.01% to DHA. (19-21) This efficiency gets worse as we age.

The capacity to generate DHA from ALA is higher in women than men. Studies of ALA metabolism in healthy young men indicate that approximately 8% of dietary ALA is converted to EPA and 0-4% is converted to DHA. (22) In healthy young women, approximately 21% of dietary ALA is converted to EPA and 9% is converted to DHA. (23) The better conversion efficiency of young women compared to men appears to be related to the effects of estrogen. (24, 25) Although ALA is considered the essential omega-3 fatty acid (remember: we humans cannot synthesize it), evidence that human conversion of EPA and, particularly, DHA is relatively inefficient suggests that EPA and DHA are conditionally essential nutrients.

A common misconception, especially among vegetarians and vegans, is that the need for EPA and DHA can be met by consuming flax oil and other plant sources of omega-3. ALA supplements (like flax oil) cannot raise plasma DHA levels in vegans. This, as I mentioned above, is due to the inefficient conversion of ALA to EPA and DHA. So unless they are supplementing with a marine-derived source of DHA, it is likely that most vegetarians and vegans will be deficient.


BALANCE ON THE BRINK − Over the course of human evolution there has been a dramatic change in the ratio of omega-6 and omega-3 fats consumed in the diet. (26, 27) The Paleolithic (400,000 – 45,000 yrs ago) diet contained approximately the same quantities of n−6 and n−3 fatty acids (i.e., the ratio is thought to have been 1:1). Sources of n−6 and n−3 fatty acids were wild plants, animals, and fish. (28)The ratio of omega-6 to omega-3 was about 1.5:1 as recently as 200 years ago. (29) Today, estimates of the ratio range from an average of 10:1 to 20:1, with a ratio as high as 25:1 in some individuals. (30) This change, perhaps more than any other dietary factor, has contributed to the epidemic of modern disease.

A diet with a lot of omega-6 and not much omega-3 will increase inflammation. A diet consisting of a lot of omega-3 and not much omega-6 will reduce inflammation.


What happened to the n-6 to n-3 ratio?

Dietary intake of omega-3 fatty acids has decreased, and dietary intake of omega-6 fatty acids has substantially increased during the last 100 years due to greater use of vegetable oils high in omega-6 fatty acids. (29, 31) At the onset of the industrial revolution (~150 years ago), there was a drastic shift in the ratio of n-6 to n-3 fatty acids in the diet. Consumption of n-6 fats increased at the expense of n-3 fats. This change was due to both the advent of the modern vegetable oil industry and the increased use of cereal grains as feed for domestic livestock, which in turn altered the fatty acid profile of meat that humans consumed.

Big Pharma is well aware of the effect of n-6 on inflammation. In fact, the way over-the-counter and prescription NSAIDs (i.e., ibuprofen, aspirin, Celebrex, etc.) work is by reducing the formation of inflammatory compounds derived from n-6 fatty acids. The same effect could be achieved by simply limiting dietary intake of n-6…but of course, the drug companies don’t want you to know that.

Sources of n-3 and n-6 fats

The following table lists the omega-6 and omega-3 content of various vegetable oils and foods:

Omega content of food

Table 1 - Omega-3 and omega-6 content of various oils and foods.

In subsequent posts, we will explore the the question of how much omega-3 to eat and how this factor depends in large part on how much omega-6 we eat.


  1. Whitney, E., and Rolfes, S.R. (2008). Understanding Nutrition (11th ed.) California: Thomson Wadsworth. p. 154
  2. Stillwell, W., Wassall, S.R. (2003). Docosahexaenoic acid: membrane properties of a unique fatty acid Chem. Phys. Lipids. 126(1): 1-27.
  3. AOCS The AOCS Lipid Library.
  4. Chalon, S., Vancassel, S., et al. (2001). Polyunsaturated fatty acids and cerebral function: focus on monoaminergic neurotransmission. Lipids. 36(9): 937-944.
  5. Price, P.T., Nelson, C.M., et al. (2000). Omega-3 polyunsaturated fatty acid regulation of gene expression. Curr. Opin. Lipidol. 11(1): 3-7.
  6. Calder, P.C., (2002). Dietary modification of inflammation with lipids. Proc. Nutr. Soc. 61(3): 345-358.
  7. Calder, P.C., (2013). n-3 fatty acids, inflammation and immunity: new mechanisms to explain old actions. Proc. Nutr. Soc. 72(3): 326-336.
  8. Calder, P.C., (2009). Polyunsaturated fatty acids and inflammatory processes: New twists in an old tale. Biochimie. 91(6): 791-795.
  9. Harris, W.S., Sands, S.A., et al. (2004). Omega-3 fatty acids in cardiac biopsies from heart transplantation patients: correlation with erythrocytes and response to supplementation. Circulation. 110(12): 1645-1649.
  10. Simopoulos, A.P. (2008). The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases. Exper. biol. med. 233(6): 674-688.
  11. Simopoulos, A.P. (2016). An increase in the omega-6/omega-3 fatty acid ratio increases the risk for obesity. Nutrients. 8(3): 128.
  12. Hiza, H.A.B., and Bente, L. (2007). Nutrient content of the US food supply, 1909–2004 a summary report. United States Department of Agriculture, Washington, DC
  13. Nakamura, M.T., Nara, T.Y. (2004). Structure, function, and dietary regulation of delta6, delta5, and delta9 desaturases. Annu. Rev. Nutr. 24: 345-376.
  14. Jump, D.B., Depner, C.M., et al. (2012). Omega-3 fatty acid supplementation and cardiovascular disease. J. Lipid. Res. 53(12): 525-545.
  15. Hibbeln, J.R., Nieminen, R.G.L et al. (2006). Healthy intakes of n−3 and n−6 fatty acids: estimations considering worldwide diversity. Am. J. Clin. Nutr. 83(6 Suppl): 1483S-1493S.
  16. Lands, W.E. (1992). Biochemistry and physiology of n-3 fatty acids. FASEB J. 6(8): 2530-2536.
  17. De Gomez Dumm, I.N., Brenner, R.R. (1975). Oxidative desaturation of alpha-linoleic, linoleic, and stearic acids by human liver microsomes. J. Lipid. Res. 10(6): 315-317.
  18. Neff, L.M., Culiner, J., et al. (2011). Algal docosahexaenoic acid affects plasma lipoprotein particle size distribution in overweight and obese adults. J. Nutr. 141: 207-213.
  19. Chiu, C.C., Su, K.P., et al. (2008). The effects of omega-3 fatty acids monotherapy in Alzheimer’s disease and mild cognitive impairment: a preliminary randomized double-blind placebo-controlled study. Prog. Neuropsychopharmacol. Biol. Psychiatry. 32: 1538–1544.
  20. Goyens, P.L., Spilker, M.E., et al. (2005). Compartmental modeling to quantify alpha-linolenic acid conversion after longer term intake of multiple tracer boluses. J. Lipid Res. 46: 1474–1483.
  21. Hussein, N., Ah-Sing, E., et al. (2005). Long-chain conversion of [13C]linoleic acid and alpha-linolenic acid in response to marked changes in their dietary intake in men. J. Lipid Res. 46: 269–280.
  22. Burdge, G.C., Jones, A.E., et al. (2002). Eicosapentaenoic and docosapentaenoic acids are the principal products of α-linolenic acid metabolism in young men*. Br. J. Nutr. 88(4): 355-364.
  23. Burdge, G.C., Wootton, S.A. (2002). Conversion of α-linolenic acid to eicosapentaenoic, docosapentaenoic and docosahexaenoic acids in young women Br. J. Nutr. 88(4): 411-420.
  24. Burdge G.C. (2004). α-linolenic acid metabolism in men and women: nutritional and biological implications. Curr. Opin. Clin. Nutr. Metab. Care. 7(2): 137-144.
  25. Giltay EJ, Gooren LJ, et al. (2004). Docosahexaenoic acid concentrations are higher in women than in men because of estrogenic effects. Am. J. Clin. Nutr. 80(5): 1167-1174.
  26. Simopolous, A.P., Leaf, A., et al. (1999). Essentiality of and recommended dietary intakes for omega-6 and omega-3 fatty acids. Ann. Nutr. Metab. 43: 127-130.
  27. Eaton, S.B., Konner, M. (1985). Paleolithic nutrition: a consideration of its nature and current implications. New Engl. J. Med. 312: 283-289.
  28. Simopolous, A.P. (1988). n−3 Fatty acids in growth and development and in health and disease. Part 1: the role of n−3 fatty acids in growth and development. Nutr. Today. 23: 10-19.
  29. Simopolous, A.P. (2002). The importance of the ratio of omega-6/omega-3 essential fatty acids. Nutr. Today. 56(8): 365-379.
  30. Russo, G.L. (2009). Dietary n-6 and n-3 polyunsaturated fatty acids: from biochemistry to clinical implications in cardiovascular prevention. Biochem. Pharmacol. 77(6): 937-946.
  31. Simopolous, A.P. (2000). Human requirement for N-3 polyunsaturated fatty acids. Poult. Sci. 79(7): 961–970.
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