Omega-3 Fatty Acids & Cardiovascular Disease

Good through December 2010

Omega 3s dramatically reduce deaths from heart attacks.
Omega 3s and not Olive oil may explain benefits of Mediterranean diet
Is Fish Brain Food?
References
Post Test

There are 2 major classes of polyunsaturated fatty acids (PUFA), omega-6 and omega-3. There are three principle omega-3 fatty acids. They are alpha-linolenic acid (ALA), eicosapentaenoic  acid (EPA) and docosahexaenoic acid (DHA). ALA is found in large amounts in flaxseed and its oil. It is also found in smaller amounts in soybean and canola oils and to a lesser extent in other terrestrial plants. Grains are high in omega-6 fatty acids and have relatively little omega 3s. EPA and DHA are found mainly in seafood and particularly fatty, cold-water fish like salmon, sardines, mackerel and herring. They are also found in varying amounts in algae and other water-based plants. About 90% of the PUFA in the US diet today is omega-6 and about 10% is omega-3.[1]

Both omega-6 and omega 3 fatty acids are now believed to be essential for human beings. They are important structural components of cell membranes and serve as substrate for the synthesis of a variety of potent hormones known collectively as prostaglandins. In some cases the function of prostaglandins synthesized from these 2 classes of essential fatty acids are very different. This has led some researchers to hypothesize that both the amount and ratio of these two groups of essential fatty acids (EFA) in the diet may have an important physiological impact on health. There is no consensus yet on what the ideal amount or ratio of these EFA should be in the human diet. However, it is clear that in modern societies the ratio of omega-6 to omega-3 (>10:1) is much higher than it is humans living as hunter-gatherers (<4:1). It is likely that human beings evolved on a diet with a much lower ratio of omega-6 to omega-3s than is found in modern diets.[2]

Although humans are capable of converting ALA into EPA and DHA, there is still scientific debate as to whether or not ALA intake alone will result in adequate tissue levels of EPA and DHA in most people. Indeed, the FDA official statement on Omega 3 fatty acids states "Although PUFA other than omega-3 may affect the risk of CHD .... most of the relevant research testing the hypothesis that omega-3 fatty acids reduce the risk of CHD have been conducted using fish or EPA and DHA because these fatty acids are known to have physiological effects." "For this reason omega-3 fatty acids are defined as EPA and DHA."[3] Diets high in omega-6 PUFA may impair the conversion of ALA to EPA and DHA.

There is also some evidence to suggest that a high ratio of omega-6 to omega-3 PUFA may contribute to the development of insulin resistance and Type-2 DM.[4] High intakes of trans-fatty acids also interfere with the conversion of ALA to EPA and DHA. Only about 9% of the PUFA in the average American diet comes from ALA with about 1-2% coming from EPA and DHA combined. The other 90% of the PUFA are omega-6 (mostly linoleic acid). The high intake of ALA and trans fatty acid in the Western diet could well be interfering with the production of EPA and DHA and altering normal cell lipid membrane function. This could be contributing to a host of diseases seen in industrialized countries.

Interest in the potential cardiovascular disease (CVD) protective effects of increasing omega-3s began with studies of the Inuit. These Greenland Eskimos were found to have a low risk of ischemic heart disease (IHD) despite a diet that was high in fat and cholesterol.[5] Since the 1970s, the beneficial physiological impact of dietary omega 3s has continued to expand.

Omega 3s, and particularly EPA and DHA, do appear to reduce the risk of dying from CVD. There are several possible ways that omega 3s may reduce the risk of CVD. They do appear to have a modest blood pressure lowering effect.[6] The blood pressure lowering effect of fish oils appears to be related to the DHA rather than the EPA.[7] Omega 3s appear to improve blood lipids. Omega 3s in the form of fish or fish oils almost always decrease serum TG and VLDL-C levels, often by 30% or more. Omega-3s lower fasting serum TG primarily by inhibiting both TG and apolipoprotein (apo) B synthesis in the liver.[8] This reduces the production of VLDL particles, which carry the bulk of serum TG during the fasting state. However, omega-3s are somewhat more likely to increase LDL-C than to lower it, although there is considerable individual variability in the response to the addition of fish oils to the diet.[9]

The impact of omega 3s on HDL-C and TC is usually modest and quite variable.[10] In general, omega 3s have a modest HDL-C raising impact, particularly in those with moderate to high TG levels (>200 mg/dl). In people with high TG levels, TC will also usually fall. However, in those with high TG, LDL-C is actually more likely to increase modestly than fall when omega 3s are increased in the diet.[11] Overall, the impact of omega 3s on blood lipids is in the direction of reduced IHD risk. However, the modest impact of omega 3s on blood pressure and blood lipids, while favorable, is not likely to explain the major impact on the risk of dying of a heart attack seen in intervention studies lasting only a few years.

The consumption of just 2 servings of fish per week was associated with about a 40% decrease in deaths from IHD in a large prospective study of 20,000 physicians.[12] Overall mortality was also lower in those consuming a little fish weekly compared to those who ate very little or no fish. However, in this study the consumption of more than 7 oz of fish per week did not provide additional cardiovascular disease protection. The consumption of fish, primarily because it contains both SFA and cholesterol, does tend to increase LDL-C (unless it displaces other foods in the diet with even more SFA and/or cholesterol like cheese and red meats).

Omega 3s dramatically reduce deaths from heart attacks

Omega 3s alter the production of prostaglandins in the body. Omega-3s inhibit the production of thromboxane A2 (Tx A2) and inflammatory cytokines. Both of these changes tend to reduce the tendency of blood to clot, which should the risk of a fatal heart attack.[13] However, it is unlikely that a reduction in the tendency of blood to clot is the only mechanism by which omega-3s protect against fatal heart attacks. This is because the decrease in death rate from heart attacks with a higher intake of omega-3s was similar in people who were taking aspirin as in those who were not. Since aspirin works to reduce IHD primarily by blocking the formation of Tx A2 and inflammation, one would expect that the use of aspirin would have attenuated the protective effect of omega-3s. Since the protection was just as great in those taking aspirin as those not on aspirin, the omega-3s appear to be reducing the risk of fatal heart attacks by some other mechanism.

Another likely mechanism whereby omega 3s could protect against a fatal heart attack is by reducing the risk of cardiac arrhythmias, particularly after an ischemic event. Ventricular fibrillation in patients with advanced coronary heart disease (CAD) can often result from an ischemic event and is usually fatal if not short-circuited by an electric shock to the chest. Omega 3s have been shown to have an antiarrhythmic effect in animal studies.[14] In humans, an increase in heart rate variability (HRV) following an MI is associated with a decreased risk of fatal arrhythmias.[15] Recently it was shown that supplementation of omega 3s (and particularly DHA) can increase HRV in healthy men but only in those who initially had low HRV.[16]

A 10-year follow-up of the Nurses' Health Study showed a protective effect of omega-3s against a fatal heart attack. The women who consumed the most omega-3s were found to have only about half as many fatal heart attacks compared to those who consumed the least. However, the women consuming more omega-3s were no less likely to have a nonfatal heart attack.[17] This is consistent with a secondary prevention trial in which the subjects who were advised to consume 2 or more servings of fish a week were found to have a 29% reduction in fatal MI compared to those who did not increase fish intake. As with the Nurses' Health Study, there was no decrease in the number of MI in those subjects advised to eat more fish[18].

The impact of omega 3s in stabilizing heart muscle cell membranes and perhaps in reducing clot formation appear to be the primary mechanisms by which they reduce CVD. There is growing evidence that omega-3s help to stabilize the heart muscle cell membranes during an ischemic event. This reduces the risk of a fatal arrhythmia (ie, ventricular fibrillation) developing.[19] Because omega 3s do not appear to reduce the risk of having a heart attack (only a fatal one), it appears they may have only a modest impact on the progression of atherosclerosis.

Omega 3s and not Olive oil may explain benefits of Mediterranean diet

The protective effect of a Mediterranean-style diet may be due more to increased omega 3s than to an increase in monounsaturated fat.[20] A 46-month follow-up of the Lyon Diet Heart Study showed a significant reduction in both CVD and all cause mortality. There were 24 deaths/100 patients in the control and this reduced to 14 deaths/100 patients in the experimental group.[21] Since these trials showed relatively modest effects on blood lipids or blood pressure, it seems likely that most of the protective effects of a Mediterranean-style diet may be due more to stabilization of myocardial cell membranes and/or a reduced tendency of blood to clot and/or improved endothelial function rather than to decreased atherosclerosis. This makes it unlikely that consuming more olive oil is a likely explanation for reduced death rate from CVD seen in Mediterranean countries.

A secondary prevention trial of people who already had had a heart attack lends support to the importance of omega-3s in preventing IHD mortality. In this study, a supplement of 1 g of omega 3s daily in the form of fish oils significantly reduced both CVD and overall mortality compared to a placebo.[22] Research in animals has demonstrated that omega-3s help to stabilize heart muscle cell membranes and alter electrophysiological events by modulating sodium and calcium channels, which may be how they prevent fatal cardiac arrhythmias. If so, making sure Americans consume at least 1% of their total calories as omega-3s may help to dramatically reduce the 250,000 or so sudden cardiac deaths each year caused by fatal arrhythmias.[23]

Is Fish Brain Food?

Omega-3s appear to improve the conduction of electrolytes through cellular membranes. A diet low in omega-3s could impair the growth and functioning of neurons.[24] The retina of the eye matures rapidly in the first 6 months after birth. A small study that compared the visual acuity of infants fed breast milk (which has DHA) or formula (without DHA) found visual acuity was impaired in those fed the DHA-free formula.[25] Another study that examined problem-solving ability at 10 months of age in infants fed a standard formula or one supplemented with DHA and arachidonic acid (ARA - an omega-6 PUFA). Even though the PUFA supplemented formulas were fed for just the first 4 months of infancy, at 10 months of those infants given the DHA and ARA supplemented formula exhibited significantly greater problem solving ability than those fed the standard formulas. This suggests that infants who do not receive enough DHA and ARA in early infancy may end up with lower IQs.[26]

Omega-3s may not only be essential for the normal development of neurons in babies but may also be needed in adults to help maintain normal brain function. A prospective study of about 5,000 people (55y +) in a suburb of Rotterdam, found that dementia with a vascular component was most strongly associated with a diet high in fat and saturated fat. The consumption of fish was inversely associated to the incidence of dementia, and in particular to Alzheimer's disease. The results of this study suggest that eating a diet high in total fat, saturated fat and cholesterol may increase the risk of senility whereas the consumption of fish may reduce the risk of senility, as we grow older.[27] Perhaps grandma was right after all when she said, "fish is brain food!"

Fish Oil Supplements Versus Fish

Very high intakes of fish oil decreases blood clotting which could be a problem if one has internal bleeding in a car crash or a hemorrhagic stroke. Indeed, Eskimos have been known to die from nose bleeds on their very high omega-3 diet.

Fish has more nutrients than fish oil supplements and so are generally preferable. Also, adding fish to the diet will reduce the consumption of other meat and poultry products which are generally higher in SFAs. Fish is a fairly high satiety food but fish oil supplements have little satiety value so would tend to add calories to ones ad libitum energy intake.

References:

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