Ohana Health - Prevention and Renewal

Omega-3 and the Heart

General Overview

Omega-3Significant intake of omega-3 fatty acids by eating fish or taking a dietary supplement may help reduce the risk of a myocardial infarction (heart attack) or cerebral stroke. Omega-3 fatty acids have also been shown to help prevent or reduce the severity of a second heart attack.

Research shows that omega-3 fatty acids reduce blood lipids, blood pressure and blood clotting, and help prevent atherosclerosis and cardiac arrhythmia. Omega-3 fatty acids are mainly found in fatty fish. These include sardines, mackerel, herring and salmon. To help prevent heart attack, increase your intake of omega-3 fatty acids by eating more fish or taking a high-quality omega-3 supplement. About 1 to 2 grams of omega-3 fatty acids per day is the dose that doctors recommend to prevent heart disease.

Traditional Inuit dietary habits

Populations that eat a lot of fish such as the coastal people of Alaska and Japan or the northern Inuit people, experience less myocardial infarction. Yet when Greenlanders move to Denmark, as many did in the 1960s, they adopted the local dietary habits and subsequently the same disease pattern as the Danes. A clinical study from Alaska showed that native Alaskans experienced little atherosclerosis while settlers from the US Mainland in their 40's and 50's whose habitual diet was rich in saturated fat and vegetable oils often had advanced atherosclerosis. (1) Atherosclerosis is responsible for myocardial infarction and stroke, the two main killers in the industrialized part of the world.

2-4 grams per day can balance the risk factors

If you have had a heart attack or you have risk factors such as hypertension, diabetes, elevated blood lipids (particularly triglycerides), or if you are a smoker, you will benefit from taking omega-3 fatty acid supplements, but the dose should be doubled to 2 to 4 grams per day. In an English study, half the heart attack patients were advised to increase the intake of fatty fish or take omega-3 supplements upon leaving the hospital, while the rest were given no such advice. The difference in mortality was significant after just three months and the positive effect of supplementation persisted in subsequent years. (2)


  1. Newman WP et al. The Lancet 1993;341:1056-1057
  2. Burr ML et al. The Lancet 1989;241:757-761
Atherosclerotic Diseases

Omega-3 fatty acids for the prevention and treatment
of atherosclerotic diseases

Circulatory insufficiency is the #1 cause of death in the industrialized world and has been since 1918. Recent statistics from the US indicate that life expectancy would rise by 7 years, from today’s 77 years, if all forms of major cardiovascular diseases (CVD) were eliminated. For comparison the gain would be only 3 years if all forms of cancer were abolished.(1)

The main cause of CVD is atherosclerosis; an inflammatory and degenerative disease of the arteries caused by aging, heritage, and well defined risk factors leading to restricted circulation of arterial blood. Risk factor intervention, dietary measures, certain drugs, and even surgical procedures may positively influence clinical features of atherosclerosis, mainly myocardial infarction and stroke. Atherosclerosis is a dynamic disease with a progressive pattern, and clinical data clearly indicate that proper measures may postpone the development of arterial narrowing and obliteration of blood flow.

Atherosclerosis has previously been described as a “plumbing problem”, with fat-laden debris gradually building up on the internal surface of artery walls. If a deposit of plaque grew large enough, it eventually closed off the affected “pipe”, preventing the blood from reaching its intended tissue. The plaques could be large or small, the large plaques easily spotted on an angiogram while the small ones often left undetected and usually considered harmless. The large plaques may change the blood flow pattern by a gradual increment of the arterial l lumen, but the small plaques are prone to burst suddenly and start a cascade of events leading to a thrombus, obliterating the coronary or cerebral artery flow and creating a myocardial infarction or stroke.(2)

The small, vulnerable plaques contain lipid pools and inflammatory cells covered by a thin inflamed fibrous cap.(3) Activated by cytokines, both inflammatory cells and smooth muscle cells produce matrix-degrading metalloproteinases that weaken the fibrous cap, increasing the risk of bursting.(4) The change of paradigm from a “plumbing problem” to a dynamic, inflammatory process which may be altered by immunosuppressive measures, is new, opening up new possibilities for prevention as well as treatment of CVD.

Prevention of CVD is based on risk factor reduction and certain pharmaceuticals, such as aspirin and cholesterol lowering drugs. But even the inflammatory process should be addressed. Nature’s own way of suppressing the immunological response to activation are the omega-3 fatty acids, that are the starting material for production of local acting hormones that suppress immunological actions. Omega-3 fatty acids are therefore frequently used for treatment of autoimmune diseases such as rheumatic disease. People with a high intake of omega-3 fatty acids through fish and sea mammals do not develop atherosclerosis to the same extent and at the same age as people who do not. The immunosuppressive effects of omega-3 fatty acids may explain this.

Newman and colleagues examined two groups of inhabitants from Alaska who had died from non-CVD causes for the presence of atherosclerosis: First Nations peoples and non-native immigrants, mainly Caucasians, Asian and Hispanic.(5) Fat tissue, abdominal aorta and coronary arteries were sent to New Orleans and analysed without knowledge from which group the specimen had come from. The fat tissue concentrations of omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were much higher in the First Nations group, indicating a high intake of fatty seafood. Surface involvement with atherosclerosis was very different between the groups: Aorta as well as the coronary arteries from the First Nations group had significantly less atherosclerosis compared to the other groups.

Surface involvement of the aorta related to age groups demonstrates that there was about a 10 year delay in the First Nations group, with high EPA and DHA in their fat tissue, for equal development of atherosclerosis compared to the other groups. It seems that the formation of atherosclerosis was prevented as a function of high intake of omega-3 fatty acids.

The study by Newman and colleagues is interesting but there were many confounding factors not accounted for in this epidemiologic study. Therefore, the therapeutic principle was tested in a controlled clinical study in patients with atherosclerotic plaques of the neck arteries.(6) The patients on a waiting list for operation were randomly allocated to treatment with EPA/DHA omega-3 fatty acids, sunflower oil, or placebo. After an average treatment time of 42 days, the atherosclerotic plaques were removed and analysed with respect to the content of EPA/DHA, plaque morphology, and immunological activation. The plaques from the omega-3 treated group had significantly higher content of EPA/DHA and the plaques were more often organised and not so often of the soft type prone to rupture. In the other two groups plaques were more often of the vulnerable type with thin, fibrous caps and significant signs of inflammation.

Interestingly, the degree of vulnerability could be significantly altered after on-average 6 weeks of treatment, underlining the dynamic pattern of atherosclerotic plaques and the potent actions of omega-3 fatty acids to stabilise plaques. The anti-inflammatory effects of EPA/DHA seems to offer a very potent and effective means of preventing and treating atherosclerotic diseases as an ideal combination to a standard risk reduction regimen.


  1. Heart disease and stroke statistics. American Heart Association, 2003:1-42
  2. van Belle E. et al. Coronary angioscopic findings in the infarct-related vessel within 1 month of acute myocardial infarction Circulation 1998; 97:26-33
  3. Libby P. et al. Macrophages and atherosclerotic plaque stability Current Opinion in Lipidology 1996; 7:330-335
  4. Ganz P et al. Pathogenetic mechanisms of atherosclerosis: effect of lipid lowering on the biology of atherosclerosis Am J Med 1996; 101(suppl 4A): 10S-16S
  5. Newman WP, Middaugh JP, Pedersen HS, et al. Atherosclerosis in arctic populations: autopsy studies. Prevention and treatment in vascular disease. Springer Verlag 1995:77-84
  6. Thies F, Garry JM, Yacoob P, et al. Association of n-3 polyunsaturated fatty acids with stability of atherosclerotic plaques: a randomized controlled trial. Lancet 2003; 361:477-485
Cardiovascular Disease

Omega-3 fatty acids in the prevention and treatment of cardiovascular disease

Epidemiological studies have correlated a high intake of omega-3 fatty acids (FA) with a low incidence of coronary artery disease (CAD). This has been documented in the Inuit population of Greenland (1,2) as well as in the coastal population of Japan (3). Furthermore, observations have been made regarding the effect of increasing the intake of fish on the risk of developing CAD.(4) It has also been demonstrated that dietary intake of omega-3 FA reduces the risk of cardiac arrest.(5) Controlled intervention trials using omega-3 supplements have shown both a primary and a secondary preventive effect in patients with CAD.(6,7)

Atherosclerosis is the arterial disease responsible for the development of cardiovascular disease, and the pathophysiological events leading to this disease are very complex. Indeed, omega-3 FA have been shown to interfere in several of these events in a positive way.

Elevated serum lipids are an important risk factor for CAD, but the therapeutic concept of cholesterol lowering alone has been extended to encompass lowering LDL cholesterol and triglycerides, while increasing the HDL cholesterol that attacks the so-called lipid triad.

LDL cholesterol is comprised of the transport particles carrying cholesterol and triglycerides (TG) to their destinations in the human body. If their load of triglycerides is high, the particles become small and dense. These particles are poorly handled by the LDL receptor mechanism, which keeps them in circulation for a long time, then eventually makes them end up in the subendothelial space of the arteries. There, they become oxidized. This phenomenon initiates the vascular inflammation process, which is very closely related not only to the build-up of atherosclerotic plaques, but also to the rupture of these pathological structures.

Omega-3 FA lower TG very effectively. Since TG themselves constitute a risk factor, and a reduction of the TG load to small, dense LDL particles could change their physical properties and re-establish a better affinity to the LDL receptor, this therapeutic regimen could create a more comprehensive means of reducing the effects of lipid risk factors. At the same time, omega-3 FA have been shown to increase HDL cholesterol.

The inflammatory process in the arterial wall caused by oxidised LDL may be alleviated by omega-3 FA. This is mainly due to two defined effects of omega-3 FA on the immunological mechanisms of the cell-mediated system:

  • A reduction of pro-inflammatory eicosanoids, and the prevention of white cell recruitment by down-regulating the presentation of cell-adhesion molecules. The first effect is mediated by a mechanism where if EPA is used as a substrate for the production of these eicosanoids, the products will have a lower biological potency than the substrate had been derived from the omega-6 series. The net effect on inflammatory parameters will be to prohibit the release of Interleukin-1 and Tumour necrosis factor, two cytokines active in the local inflammatory process. These may be important mechanisms for the long-term prevention of atherosclerosis, meaning that a diet rich in omega-3 FA may have positive effects on the incidence of CAD.

  • Meanwhile, it is well documented that a regular intake of omega-3 FA reduces thrombocyte adhesion, and thus also aggregation, preventing the build up of red thrombi. This is, in turn, explained by the use of EPA as a substrate for eicosanoids, in this case thromboxane, which is less active than when omega-6 is used. Another effect is the reduction of vascular tone, which is often elevated locally in patients with overt atherosclerosis. Furthermore omega-3 FA also have a moderate effect on elevated blood pressure, another risk factor for CAD.

Last but not least, omega-3 FA have anti-arrhythmic effects that are probably mediated by the effect of changes in the cell-membrane on ion channels. This may possibly explain the beneficial and rapidly occurring effect of omega-3 FA in the DART study.(6) Another related effect is the normalization of the so-called heart-rate variability (HRV), which is seen in patients treated with omega-3 FA.(8,9) Decreased HRV is associated with increased mortality in postmyocardial infarction patients.

In conclusion, the intake of omega-3 FA, preferably as fatty fish or as a dietary supplement, may offer broad-scale protection against the development of atherosclerosis. Based on a dietary principle, this prophylaxis has been shown to postpone or prevent what is usually perceived as normal aging of the arteries.(10)


  1. Dyerberg J et al. Eicosapentaenoic acid and prevention of thrombosis and atherosclerosis. Lancet 1978;2(8081):117-119
  2. Kromann N and Green A. Epidemiological studies in the Upernavik districts, Greenland. Acta Med Scand 1980;208:401-406
  3. Hirai A et al. Eicosapentaenoic acid and adult diseases in Japan: epidemiological and clinical aspects. J Intern Med Suppl 1989,225 (731):69-75
  4. Kromhout D, Bosschieter EB and de Lezenne Coulander C. The inverse relation between fish consumption and 20-year mortality from coronary heart disease. N Engl J Med 1985;312:1205-1209
  5. Siscovick DS et al. Dietary intake and cell membrane levels of long-chain n-3 polyunsaturated fatty acids and the risk of primary cardiac arrest. J Amer Med Assoc 1995;274:1363-1367
  6. Burr ML et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet 1989;2:757-761
  7. Singh RB et al. Randomized, double-blind, placebo-controlled trial of fish oil and mustard oil in patients with suspected acute myocardial infarction: the Indian experiment of infarct survival. Cardiovasc Drugs and Ther 1997;11:485-491
  8. Christensen JH et al. Effect of fish oil on heart rate variability in survivors of myocardial infarction: a double blind randomised controlled trial. Br Med J 1996;312:677-678
  9. Christensen JH et al. Heart rate variability and n-3 fatty acids in patients with chronic renal failure - a pilot study. Clin Nephrol 1998;49:102-106
  10. Newman WP et al. Atherosclerosis in Alaska natives and non-natives. Lancet 1993;341:1056-1057



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