Omega-3 Supplements and Omega-3 Pills and Fish Oil

Learn about Omega-3 Fish Oil supplements and why fish oil (and other Omega-3 products) are good for you:

What are omega-3 fatty acids?

Omega-3 fatty acids are long-chain polyunsaturated fatty acids (18–22 carbon atoms in chain length) with the first of many double bonds beginning with the third carbon atom (when counting from the methyl end of the fatty acid molecule).

The fish-based and fish-oil–based omega-3 polyunsaturated fatty acids (also referred to as n-3 PUFA) consist of EPA (20 carbon atoms, 5 double bonds) and DHA (22 carbon atoms, 6 double bonds). Whereas plant foods and vegetable oils lack EPA and DHA, some do contain varying amounts of the n-3 PUFA alpha-linolenic acid (ALA), which has 18 carbon atoms and 3 double bonds.

Many vegetable oils are greatly enriched in omega-6 fatty acids (mainly as linoleic acid in corn, safflower, sunflower and soybean oils), but canola oil (nonhydrogenated), ground flaxseed and walnuts are rich sources of ALA. The typical North American diet provides about 1–3 g of ALA per day but only 0.10–0.15 g of EPA plus DHA per day. The very high intake of n-6 PUFA, mostly as linoleic acid (LA) in our diet (12–15 g/day) from common vegetable oils (corn, safflower, soybean) and other sources, yields an overall n-6:n-3 dietary ratio (total omega-6 fatty acids in the diet: total omega-3 fatty acids in the diet) of about 8:1. Health Canada has recommended that this ratio be as low as 4:1 to reduce the competitive influence of high LA intakes on ALA metabolism to its longer chain products (such as EPA and DHA).

Although high intakes of LA can provide some modest blood cholesterol lowering, experimental studies in animals have raised concerns regarding the enhancing effect of these high intakes on certain cancers. This association has not been established in human studies.

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Omega-3 EPA (Fish Oil and Krill Oil supplements) linked to heart disease protection

People with high cholesterol levels and taking statins reduced their frequency of major cardiac events by about 20 per cent when supplemented with the omega-3 of eicosapentaenoic acid (EPA), researchers have reported.

The research, published in this week's issue of The Lancet, followed 18 645 Japanese patients with high cholesterol levels (hypercholesterolaemia) taking statins, and randomly assigned half to receive a daily EPA supplement (1.8 g). After a following the subjects for about four and a half years, the researchers reported that EPA supplementation had additional significant effects on angina (24 per cent reduction) and non-fatal coronary events (19 per cent reduction). "Overall, this study shows that EPA, at a dose of 1800 mg per day, is a very promising regimen for prevention of major coronary events, especially since EPA seems to act through several biological mechanisms," wrote the researchers. Omega-3 fatty acids have been linked to a wide-range of health benefits, including cardiovascular disease (CVD), good development of a baby during pregnancy, joint health, behaviour and mood, and certain cancers.

But some much publicised studies, and in particular a recent meta-analysis (British Medical Journal, doi: bmj.38755.366331.2F), have claimed that there was no evidence linking omega-3 intake and improvements in heart health.

However, results from the Japan EPA Lipid Intervention Study (JELIS) suggest that regular supplementation with the omega-3 fatty acid may have significant benefits for cardiovascular, although the use of an exclusively Japanese subjects prevented the researchers generalising their results to other populations.

Subjects with total cholesterol levels of at least 6.5 mmol/L were recruited and randomly assigned to receive 1.8 g of EPA daily (Mochida Pharmaceuticals, Tokyo) with statin (10 mg of pravastatin or 5 mg of simvastatin) or statin only. After an average follow-up of 4.6 years, the researchers detected the primary endpoint (major coronary event, such as sudden cardiac death, fatal and non-fatal heart attack, and other non-fatal events such as unstable angina) in 262 patients in the EPA group and 324 in controls. This was equivalent to a 19 per cent reduction in major coronary events for the EPA group.

No differences between the groups were observed for LDL-cholesterol levels (both groups recorded 25 per cent reductions in levels), while no difference was observed for sudden cardiac death and coronary death.

The mechanism behind the apparent benefits could be linked to effects of the omega-3 polyunsaturated fatty acids on reduced platelet aggregation, and increased plaque-stabilisation.

How Omega-3 fish oils reduce inflammation:

Further support for the action of omega-3 fatty acids on inflammatory conditions comes from new research on lipids in humans that are triggered by aspirin, as well as fish oil.

Omega-3 fatty acids are known to benefit patients with cardiovascular disease and arthritis, although the mechanism for these actions is not yet fully understood. Discovery of mechanisms help support the use of nutritional ingredients for prevention of disease and could add to evidence of omega-3's benefit to joint health.

Foods containing omega-3s are allowed to make a qualified health claim in the US for their action on heart health. A similar claim is expected in coming weeks from the UK’s voluntary health claims body. However joint health claims have less support.

Makoto Arita from the Brigham and Women's Hospital and Harvard Medical School and US-based colleagues have recently identified a new class of aspirin-triggered bioactive lipids in humans, called resolvins, that could partly explain fish oils’ anti-inflammatory effects on joints and blood flow. Resolvins are made from the omega-3 fatty acids by cellular enzymes and can reduce inflammation in mice. The main bioactive component of this class of lipids, identified in mice, has been named resolvin E1.

The researchers have now identified this lipid in plasma taken from volunteers given omega-3 fatty acids and aspirin.

Writing in the 7 March issue of The Journal of Experimental Medicine (vol 201, no 5, 713-722), the authors said that human resolvin E1 inhibits both the migration of inflammatory cells to sites of inflammation and the turning on of other inflammatory cells.

This study also reveals a potential pitfall of COX-2 inhibitors, drugs designed to block inflammation but recently been shown to have negative side effects on the cardiovascular system.

COX-2 is involved in making resolvin E1 and the authors suggest that inhibition of vascular COX-2 by these drugs might block the synthesis of resolvin E1, which would eliminate an important anti-inflammatory pathway.