Omega-3 Fatty Acids and Heart Disease


dr_duane_graveline_m.d._134By Duane Graveline, M.D., M.P.H.

There is no longer any doubt as to the vital role of omega-3 fatty acids in reducing cardiovascular disease risk. Not only have omega-3s been firmly documented to stabilize the myocardium electrically, resulting in reduced ventricular arrhythmias and sudden death, but they have also been found to have potent anti-inflammatory effects quite comparable to those of statin drugs.

Omega-3s ( also known as n-3 ) are essential unsaturated fatty acids that our bodies derive from food. Studies have found that omega-3 fatty acids have an anti-inflammatory effect due to their ability to convert into anti-inflammatory prostaglandins. In addition, omega-3 fatty acids can decrease the production of inflammatory prostaglandins by omega-6, resulting in a greater decrease in inflammation.

The inflammation suppression potential of omega-3s has played a sufficiently appealing role in arterial inflammation that Lee and his group at the Thrombosis and Vascular Biology Unit of Birmingham's City Hospital in the U.K., concluded that "The use of omega-3 fatty acids should be considered as part of a comprehensive secondary prevention strategy post-myocardial infarction." (Ref 1.)

Omega-3s are essential fatty acids ( EFAs ), vital for human health. There are two families of essential fatty acids: omega-3 and omega-6. They are termed "essential" because they cannot be produced by the body and must therefore be obtained from the diet.

The typical Western diet has evolved to be high in omega-6 and relatively low in omega-3 fatty acids. While omega-6 fatty acids are not necessarily bad and are actually quite necessary, a skewed ratio in favor of too much omega-6 can be detrimental to one's health by allowing the production of excess inflammatory prostaglandins. A balance of omega-6 and omega-3 fatty acids is essential for good health.

Research is still underway to define the precise mechanism by which omega-3s exert their beneficial effect on reduction of cardiovascular disease risk. The most important established truth is that the ratio of omega-3 to omega-6 in the Western diet has been falling for decades, closely paralleling the rise in heart disease during the same time period.

It seems that in the Paleolithic era, human dietary intake of omega-6 to omega-3 was about even at 1:1. Since that time, however, there has been a gradual trend for omega-6 intake to increase relative to omega-3; at first, simply because of the changing character of the human diet in agricultural societies.

In the past 100 years or so, other factors such as food preservation and processing measures have gradually curtailed omega-3 because its unsaturated state makes it far more sensitive to oxidative change. The ratio now is estimated by various authorities to be 10, 20, even 30:1, compared to the 1:1 of the hunter-gatherer era.

Even more recently, in the past 30 years or so, chickens and cattle are mostly no longer free-ranging with ready access to leafy greens of all kinds. It now is almost impossible to make an accurate estimate of the omega-6:3 ratio since both omegas-6 and 3 are nutritionally threatened by pen-raising and corn feeding. The eggs from penned chickens and the meat of pen-raised animals are radically different in omega-3 & 6 content compared to a few generations ago. 

Polyunsaturated fatty acids ( PUFAs - that include omega-3 and omega-6 ) are sleepers in the sense that only now are we beginning to appreciate just how powerful the effects are on our bodies from deficiencies or imbalance of these essential fatty acids. One can blame PUFAs in part for the heart disease and stroke epidemic back during my medical school days. Cholesterol was handy to blame but had nothing to do with it.

In 2007, the work of McMillin JB and others at the University of Texas Health Science Center, Houston ( Ref 2.) provided some of the first work helping to understand the more precise role of dietary omega-3 EFAs. In contrast to earlier studies using marine oil as the sole source of dietary lipid, the substitution of menhaden oil ( an oily fish ) in research dogs' diet resulted in substantial changes in the constituents of their mitochondria. To understand this one must recall that n-3 has differing biologic effects depending upon its origin - what side of the family it is from, so to speak.

After 60 weeks on this menhaden diet the mitochondria isolated from these dogs' hearts showed their n-3 phospholipid arachidonic acid (  a polyunsaturated omega-6 fatty acid ) to have been replaced by the n-3 fatty acids, eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids. Additionally the mitochondrial membrane phospholipid from the menhaden oil fed dogs demonstrated increased cardiolipin ( an important component of the inner mitochondrial membrane.)  

Mitochondrial levels of linoleic and linolenic acids, the original omega-6 EFAs, were not altered. Normal levels of the essential fatty acids in the n-3 enriched mitochondrial membrane phospholipids appeared to eliminate the mitochondrial dysfunction observed in essential fatty acid deficient membranes.

Several studies published in 2007 have been very supportive of the role of EFA supplementation. In the March 2007 edition of the journal Atherosclerosis, 81 Japanese men with unhealthy blood sugar levels were randomly assigned to receive 1800 mg daily of eicosapentaenoic acid (EPA - an n-3 essential fatty acid from fish oil) with the other half being a control group.

The thickness of the carotid arteries and certain measures of blood flow were measured before and after supplementation. This went on for approximately two years. A total of 60 patients (30 in the EPA group and 30 in the control group) completed the study. Those given the EPA had a statistically significant decrease in the thickness of the carotid arteries along with improvement in blood flow.

There was another study published on the benefits of EPA in The Lancet in March 2007 ( Ref 3.) This study involved over 18,000 patients with "unhealthy" cholesterol levels. The patients were randomly assigned to receive either 1,800 mg a day of EPA with a statin drug or a statin drug alone. The trial went on for a total of five years.

It was found at the end of the study those patients in the EPA group had superior cardiovascular function. Non-fatal coronary events were also significantly reduced in the EPA group. The conclusion was that EPA could be a promising treatment for prevention of major coronary events, especially non-fatal coronary events.

Fish oils that are rich in omega-3 fatty acids also reduce serum triglyceride levels. The mechanism of this well established effect - reduction of triglycerides in humans using supplemental omega-3 rich fish oils - is not definitively understood at this time. One review ( Ref 4.) identified the decrease of lipogenesis ( the conversion of simple sugars to fatty acids ) as the most consistent of several effects observed in rats with omega-3 fatty acids added to their diets.

We are constantly reminded in work of this kind that omega 6 is not the problem. Both omega-3 and omega-6 fatty acids are essential to health, one just as much as the other. The problem is the proper balance of omega-6 to omega-3 in meeting the needs of the body for essential fatty acids.

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor
 
Ref 1. http://www.ncbi.nlm.nih.gov/pubmed/12881589
Ref 2. http://ajpheart.physiology.org/content/263/5/H1479.abstract
Ref 3. http://www.ncbi.nlm.nih.gov/pubmed/17398308
Ref 4. http://www.ncbi.nlm.nih.gov/pubmed/16832161

Updated July 2011
 

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