You’ve probably seen recent headlines claiming that fish oil supplements may not help to protect your heart. However, when you dig into the research you’ll see...


You’ve probably seen recent headlines claiming that fish oil supplements may not help to protect your heart. However, when you dig into the research you’ll see that doctors and scientists still believe that omega-3-rich supplements keep the hearts of otherwise healthy men in good shape.

“We know that omega-3s, such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) found in fish oil, lower triglycerides, reduce inflammation, stabilize heart rhythms, and, at higher intakes, help prevent blood clotting”, says JoAnn Manson, an epidemiology professor at the Harvard School of Public Health. “Aside from heart-health benefits, fish oil may also sharpen brain function, boost mood, and reduce depression. In addition, because of its anti-inflammatory effects, Omega 3s may help ease muscle and joint aches and make skin look younger.” she adds.

If you’re not eating fatty fish like salmon and mackerel two or three times a week, it’s safe to assume you’re deficient in omega-3s. How much you need to take to supply this deficiency will depend on your diet, health and level of physical activity. Aim to consume one to three grams of Omega 3 DHA + EPA per day, or as suggested by a health care professional and not consume over the recommended dose.

The two key omega-3 fatty acids (EPA and DHA) have different mechanisms of action at the physiological level, and, as a result, the benefits of EPA and DHA are often very different. That’s the reason why you need them both.

Benefits of EPA:

One of the main goals of using omega-3 fatty acids is the reduction of cellular inflammation, mediated principally by eicosanoids. Eicosanoids are part of signaling molecules implicated in inflammation, allergies and immune responses and are derived from arachidonic acid (AA), an omega-6 fatty acid. EPA plays a very important role in regulating AA synthesis and liberation and reducing cellular inflammation by at least two different ways:

EPA inhibits the enzyme delta-5-desaturase (D5D), responsible for AA synthesis (1). This way the more EPA you have in the diet, the less AA you will produce. Essentially, EPA “chokes off” the supply of AA necessary for the production of pro-inflammatory eicosanoids.

Additionally, EPA can also decrease the ability of other enzyme, phospholipase A2 (PLA2) to liberate AA from the membrane where it is stored. In fact, the inhibition of this PLA2 is precisely the mechanism of action used by corticosteroids. So, by taking adequate levels of EPA to compete with AA, you can obtain many of the anti-inflammatory benefits of corticosteroids without suffering their side effects.

Finally, it is often assumed that, since there are not high levels of EPA in the brain, it is not important for neurological function. This is due to the fact that EPA it is rapidly oxidized enters into the brain (2-5), but its action is essential for reducing neuro-inflammation by competing against AA for access to the same enzymes needed to produce inflammatory eicosanoids in the nervous system. The only way to control cellular inflammation in the brain is to maintain high levels of EPA in the blood, playing an important role on preventing depression, ADHD, brain trauma, etc. (6-8).

Benefits of DHA:

DHA does not have the same anti-inflammatory features as EPA. Because of its increased spatial dimensions, DHA is not a good competitor of either D5D or PLA2 (the key inflammatory enzymes) and makes DHA having little effect on cellular inflammation. However, DHA can contribute in ways that EPA can’t do.

Probably the key benefit of DHA lies in its unique molecular structural characteristics. The bigger molecular dimensions and flexibility makes DHA to occupy significantly more space in the cell membrane, as compared with EPA. This makes cell membranes remarkably more flexible. The increase in membrane fluidity is particularly critical in the brain and the retina, as it allows neurotransmitters receptors enough flexibility to rotate more effectively, modulating the signal transmission from the surface of the membrane to the interior of the nerve cells and the liberation of synaptic vesicles and making DHA a critical component of these highly fluid portions of the nerves (10) .

The greater spatial characteristics of DHA also increase the size of LDL particles to a greater extent compared to EPA. As a result, DHA helps reduce the entry and deposit of these enlarged LDL particles into the muscle cells that line the artery, reducing the likelihood of developing atherosclerotic lesions (13). Thus, even though it presents less benefits than EPA in competing with AA for key enzymes important in the development of cellular inflammation, the increased spatial territory swept out by DHA is good news for making certain areas of membranes more fluid or lipoprotein particles larger and prevents possible potentially deleterious vascular problems.

Common Benefits from both EPA & DHA

There are some areas in which both EPA and DHA appear to be equally beneficial. As an example, both are equally effective in reducing triglyceride levels (10). There is also apparently equal activation of the anti-inflammatory gene transcription factor PPAR-gamma (12)(11) . Both fatty acids also seem to be equally effective in making powerful anti-inflammatory eicosanoids known as resolvins (14) . Finally, although both have no effect on total cholesterol levels, DHA can increase the size of LDL particle to a greater extent than can EPA (13) .


EPA and DHA do different things, so you need them both, especially for the brain. If your goal is reducing cellular inflammation, then you probably need more EPA than DHA. How much more? Probably twice the levels you are ingesting today, nonetheless you always cover your bets with omega-3 fatty acids by using both EPA and DHA at the same time.

1. Sears B (1995) The Zone. Regan Books.
2. Ouellet M, et al. (2009) Diffusion of docosahexaenoic and eicosapentaenoic acids through the blood-brain barrier: An in situ cerebral perfusion study. Neurochemistry International 55(7):476-482.
3. Chen CT, Liu Z, & Bazinet RP (2011) Rapid de-esterification and loss of eicosapentaenoic acid from rat brain phospholipids: an intracerebroventricular study. J Neurochem 116(3):363-373.
4. Chen CT, Liu Z, Ouellet M, Calon F, & Bazinet RP (2009) Rapid beta-oxidation of eicosapentaenoic acid in mouse brain: an in situ study. Prostaglandins Leukot Essent Fatty Acids 80(2-3):157-163.
5. Umhau JC, et al. (2009) Imaging incorporation of circulating docosahexaenoic acid into the human brain using positron emission tomography. J Lipid Res 50(7):1259-1268.
6. Martins JG (2009) EPA but not DHA appears to be responsible for the efficacy of omega-3 long chain polyunsaturated fatty acid supplementation in depression: evidence from a meta-analysis of randomized controlled trials. J Am Coll Nutr 28(5):525-542.
7. Gustafsson PA, et al. (2010) EPA supplementation improves teacher-rated behaviour and oppositional symptoms in children with ADHD. Acta Paediatr 99(10):1540-1549.
8. Ueda M, Inaba T, Nito C, Kamiya N, & Katayama Y (2013) Therapeutic impact of eicosapentaenoic acid on ischemic brain damage following transient focal cerebral ischemia in rats. Brain Res 1519:95-104.
10. Stillwell W & Wassall SR (2003) Docosahexaenoic acid: membrane properties of a unique fatty acid. Chem Phys Lipids 126(1):1-27.
11. Chapkin RS, et al. (2008) Bioactive dietary long-chain fatty acids: emerging mechanisms of action. Br J Nutr 100(6):1152-1157.
12. Li H, et al. (2005) EPA and DHA reduce LPS-induced inflammation responses in HK-2 cells: evidence for a PPAR-gamma-dependent mechanism. Kidney Int 67(3):867-874.
13. Mori TA, et al. (2000) Purified eicosapentaenoic and docosahexaenoic acids have differential effects on serum lipids and lipoproteins, LDL particle size, glucose, and insulin in mildly hyperlipidemic men. Am J Clin Nutr 71(5):1085-1094.
14. Serhan CN, et al. (2002) Resolvins: a family of bioactive products of omega-3 fatty acid transformation circuits initiated by aspirin treatment that counter proinflammation signals. J Exp Med 196(8):1025-1037.


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