Cutting Atherosclerosis and Heart Attacks with Supplements and Diet?


In discussing options for lowering cardiovascular disease risk without aggressive statin drug dosing, I have already stressed the critical importance of proper diet in my page The McCully Heart Protection Diet and the thoroughly documented values of such supplements as Coenzyme Q10 (see my page Statins and Ubiquinone Deficiency ). Now the time has come to review the value of other supplements: Omega 3, aspirin and vitamins B6, B12 and Folic Acid.

Omega 3
There are two types of omega fat, omega-3 and omega-6. Both are essential for human health. However, the typical American consumes far too many omega-6 fats in their diet while consuming very low levels of omega-3. The ideal ratio of omega-6 to omega-3 fats is 1:1. Our ancestors evolved over millions of years on this ratio, today our ratio of omega-6 to omega-3 averages from 20:1 to 50:1.

It has been conjectured that the diet of Paleolithic man may have been rich in seafood, nuts and other sources of omega-3 giving a very high level of protection against cardiovascular disease. Even the diet of our more immediate ancestors, fifty years ago was thought to have a favorable level of omega 3 to omega 6 but the introduction of processed foods with very low levels of omega-3 in the last fifty years has dramatically altered this ratio and is probably at least partially responsible for the fact that heart disease is the number one killer in the United States today.

No longer is there any doubt of the benefits of omega-3 fatty acids on cardiovascular disease. Evidence from randomized, controlled clinical trials consistently document how omega-3 fatty acids affect heart function. Such benefits include anti-arrhythmic effects, improvement in cardiac pumping action and enhancement of arterial endothelial stability. Omega 3 has been documented to decrease triglyceride levels and decrease growth rate of atherosclerotic plaque. Other trials have shown that omega-3 fatty acid supplements can reduce both fatal and non-fatal heart attacks and strokes.

The best sources of omega 3 are liberal intakes of fatty fish such as mackerel, lake trout, herring, sardines, albacore tuna and salmon. These are particularly high in both kinds of omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Omega 3 also is found in flaxseed and walnut oil. Another excellent source of omega 3 are the various omega 3 (and fish oil) supplements now available.

The best guidance regarding amounts is the word, "liberal". Our usual Western diet is very substantially depleted and toxicity from excess is virtually unknown. In its 2002 guidelines for omega 3 fatty acid intake, the Institute of Medicine of the National Academy of Sciences declined to establish a Tolerable Upper Intake Level (UL) for omega 3s.

Aspirin
You would think by now the aspirin issue long ago has long been put to rest. Yet the debate still continues with the primary care physician right in the center, trying to decide which tune to follow. In the late 1980's, a report circulated in the medical community that astonished many who saw it for the first time. The study involved 22,000 male physicians, all in good health, who were divided into two groups: half of them took a buffered aspirin every other day, and the others were given a placebo.

The findings made headline news around the country: for the doctors taking aspirin, the risk of a coronary was cut by almost half. Among those taking the aspirin, 104 heart attacks (with five deaths) occurred compared to 189 heart attacks -- 18 of them fatal -- among those taking the placebo. The statistics were too dramatic to ignore and -- to be fair -- the doctors monitoring the study recommended that the volunteers taking the placebo be advised of the results so that they, too, could take aspirin if they wished.

Another more recent report found that heart attack patients who took aspirin when their symptoms began, and then daily for one month, significantly lowered their risk of dying and of having another heart attack or stroke over the people in the study who were given the placebo. Now, just about all researchers agree that patients should be given aspirin during the first hour -- during pre-hospital transport or in the Emergency Room -- if a heart attack is suspected.

Aspirin can realistically be called a wonder drug because of the many remedial effects it can have on the human body. Basically, it interferes with the production of a series of chemicals in the body -- called prostaglandins -- that regulate many of the body's vital functions. By blocking certain prostaglandins, aspirin lowers body temperature, relieves minor aches and pains, relieves inflammation and interferes with the role of blood platelets in forming clots. It is this last effect that appears to impact on risk for heart disease.

And now we find that the results of longitudinal studies of large numbers of people are not nearly as supportive of aspirin as once thought. Much has changed, first of all the buffer coating on aspirin has proven to be critical for its vital magnesium content. Secondly, after critical appraisal of side effects and all cause death rates, the use of low dose aspirin in primary prevention can no longer be supported. Secondary prevention is quite another matter with very favorable outcomes for limited periods of times after the thrombotic event.

Thankfully, this still fits with the knowledge of relevant pathophysiology - the inhibition of platelet stickiness by aspirin. In secondary prevention you are dealing with an endothelial wound and aspirin during the healing period seems reasonable. In primary prevention there is no wound - this is a different kind of problem.

The challenge for rational aspirin use seems to be one of identifying those people at risk, those with open endothelial lesions or those very likely to have them. Since the vital role of inflammation in atherosclerosis is better understood, there is a need for better markers of inflammation to guide the identification of those at risk. CRP is a step in that direction but a much better marker is necessary.

Vitamins B6, B12 and Folic Acid
Dr. Kilmer McCully's persistent, even tenacious, adherence to his almost 'Eureka' concept of homocysteine toxicity causation of arteriosclerosis has gained wide acceptance from researchers in the field. From his first lonely review of arteriosclerotic changes in children who died from genetically pre-ordained homocystinuria, he now seems to have proven his point: cholesterol is not the cause of arteriosclerosis, homocysteine elevation secondary to vitamin deficiency appears to be one of the major players.

Homocysteine, the new villain, becomes predictably elevated in the body only when one or more of the B complex vitamins--folic acid, B6 or B12--are deficient. Arteriosclerosis, it would seem, is a deficiency disease, which makes it potentially treatable by dietary supplementation.

McCully also reports in The Heart Revolution that some 10-40 percent of patients with vascular disease in clinics and hospitals worldwide are shown to have high levels of homocysteine. The well-known Framingham Heart Study has determined that up to two-thirds of the elderly are deficient in B6, B12 or folic acid.

About 12 percent of the population worldwide carries a genetic defect for an enzyme, which affects their normal ability to metabolize homocysteine. People born with an abnormality of this enzyme need to consume more folic acid than usual to keep their homocysteine levels in check and thereby reduce the greater associated risk of developing arteriosclerosis and heart disease.

There is little doubt as to the validity of McCully's position and whether someone has a genetically preordained homocysteine elevation or the surprisingly prevalent acquired inability to take in sufficient daily amounts of these vital substances.

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor

 

 

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