Heart Foods, Heart Frauds

For the past 60 years coronary artery disease has been like a plague on Western Nations taking its toll in the form of pain, disability and death. Literally half of all American deaths in that time are related to this disease. Such an epidemic of heart attacks has never-before occurred in all human history. To assuage our anxiety in the face of this mysterious disease that loomed especially large over the life of almost every male between age 40 and 70 and every female over age 60, our government has had to wage a crusade. And that requires an enemy. That public enemy has been identified as a molecule, a fatty alcohol, a normal part of every cell membrane in the human body and a source of the steroid hormones that regulate sex, stress, calcium and electrolytes—the major activities of mammalian biology. Yes, it is cholesterol that has taken the rap. Cholesterol and the surgeon general have been to the second half of the 20th Century what sex and Freud were to the first half—an obsession. And this obsession is supported by our health bureaucracy, who would have us join their crusade to accept a low fat, low cholesterol diet as our salvation. And if that should fail, we can sing ‘hallelujah’ as we submit to coronary angiography, angioplasty and coronary artery by-bass grafts.


The health establishment has allocated several billions of dollars to educate the American public in the virtues of a low fat, low cholesterol diet even without proof that this actually rewards us with a drop in over-all mortality. For the past 25 years anyone who dared challenge the cholesterol theory ran afoul of the establishment. One sad case involves a medical genius named Kilmer McCully. He originated the idea that high protein diets, particularly animal proteins, such as meat, fish, fowl, milk, cheese and eggs, could cause heart attacks because they contain methionine, an essential amino acid. That was way back in 1968 and it was so contrary to conventional thinking that it was rejected by practically every scientist of the day. How could an essential nutrient in food be lethal? That seemed to be a conundrum beyond anyone’s imagining. Somehow the herd couldn’t see the parallel to cholesterol, an essential food substance that was and is believed to be a major cause of “hardening of the arteries.”


McCully was very impressed by observing atherosclerosis and heart attacks in very young children with a then newly described genetic disease, homocystinuria. The chemistry involved deficiency of enzymes required to convert methionine into cystathionine. Homocysteine is produced as an intermediate, which normally transforms into cystathionine, which is used in the brain and as a source of the important antioxidants, cysteine and taurine. If the reaction is blocked then homocysteine can accumulate. Specific enzymes are needed to convert homocysteine into safe products, such as this transamination into cystathionine, a reaction that requires vitamin B6, or re-methylation, which recycles methionine, in a reaction that takes a carbon (methyl) from folic acid and transfers it to homocysteine, thus making methionine. This is nature’s way of conserving and re-using this essential amino acid.

Dr. McCully wondered if there might be a mild form of homocystinuria which would spare the child but eventually kill the adult and he wrote a landmark paper on this subject in 1969. The implications were obvious: the high protein intake of affluent America could be a death trap for some, especially if folic acid, B12, and B6 were deficient, these vitamins being co-factors of the sometimes weak enzymes. For being too far ahead of his time he was laughed off the stage and out of his job at Harvard University. The conventional medical mind of that time could not accept the possibility that megadoses of vitamins could be useful against disease. Megavitamins have been subject to repeated and unnecessary warnings by conventional authorities and especially mainstream medical journals. As a result, the public has been denied relief and their physicians have been scared off the track! That is also why my book, Meganutrition, drew a wall of silence from my colleagues.


In the past ten years there have been a series of research studies confirming McCully’s hypothesis, including the idea that larger doses of vitamins folic acid, B12, B6 and betaine can clear the homocysteine and prevent damage. The most recent publication presents a graph depicting blood levels of homocysteine compared to mortality rates in patients with coronary artery disease already diagnosed by angiography. This was a prospective study in which 587 patients were studied after diagnosis by coronary arteriogram. Of these 318 were treated with by-pass, 120 by angioplasty and 149 by medical drugs only. After 5 years (average 4.6 years) there were 64 deaths. Those with entry homocysteine below 9 uM/L had the lowest mortality. By comparison, those above 20 uM had a 4.5 times higher death rate! Hereditary homocystinuria causes collagen damage in the eye, joints and blood vessels in childhood and the blood levels are usually over 100 uM. Even a small increase, 10 to 20 uM in the blood can cause osteoporosis in menopausal women and death in patients with coronary artery disease.


I had been impressed 20 years ago that homocysteine is dangerous because it is very reactive molecule, believed to unravel the collagen in the arterial wall. In fact, it reacts with so many substances and is so easily oxidized that it is technically difficult isolate and measure pure homocysteine. Most laboratories test for mixed disulfides instead. I had also been discouraged by finding such low levels of homocysteine in my patients. Now that we know these low levels correlate reliably with extent of mortality we should have more confidence in using the test data. From now on homocysteine testing should be a routine procedure in all patients with suspected coronary artery disease. The level of homocysteine is predictive.


You might wonder if it will help to measure B6, B12 and folic acid. Surprisingly not! Homocysteine is dangerously high even in the presence of normal levels of these vitamins. It is not a vitamin deficiency problem only; rather it is usually a genetic weakness of the coenzyme. The vitamins are required in large doses to overcome the enzyme weakness. In order to lower the homocysteine level, therapeutic doses of vitamins B6, B12, betaine and folic acid are required. This is megadose therapy. That means folic acid dosages of at least 1 mg per day and up to 10 mg per day are required, as well as B12 1000 mcg, B6 100 mg or more and betaine 600 to 1200 mg per day.


Homocysteine is said to be directly reactive with collagen but it also reacts indirectly, by forming a bond with copper (the negatively charged carboxyl group of homocysteic acid attracts the positive charge on copper), thus removing this trace metal from the blood vessel wall. This interferes with a key enzyme, lysyl lyase, needed to catalyze lysine cross-linking. The cross linking of lysine is requires in order to strengthen collagen. The constant wear and tear on blood vessels, due to trauma, movement, viruses, pesticides, and immune reactions, requires ongoing repair. Copper deficiency interferes with the lyase enzyme needed for cross-linking of collagen, and thus causes defective repair of the blood vessel wall. Copper deficiency is common, affecting about 70 percent of Americans, because of lack of consistent intake of whole grains, seeds, nuts, mushrooms and shellfish.

Those who are subject to excess homocysteine are clearly at extra risk of death, due not only to atherosclerosis, defective repair of the wear and tear damage to the intimal lining of the blood vessels, which is not fatal, but due to thrombosis, which is caused by platelets that are attracted to the ragged collagen, accumulate, release clotting factors, and create a clot, which can block the lumen of the already narrowed vessel.


Anticoagulant activity can prevent the thrombosis and that is why fish oils, flax oil, and vitamin E are protective: each cuts heart attack deaths by about 50 percent, because they prevent platelet clumping, which otherwise can initiate blood coagulation and thrombosis. Even in the presence of homocysteine and copper deficiency, anti-coagulation prevents death. All of which highlights the fact that cholesterol is not the villain it has been made out to be. It just happens to accumulate in areas of repair, possibly a mishap of Mother Nature’s attempt at repair. At least it is not an insurmountable health hazard. And low fat, low cholesterol diets, which avoid seeds, nuts and shellfish, do not solve the more fundamental needs for vitamin E, trace minerals, and copper, which are unusually well supplied in these foods. In fact, they can make it worse in those who may be particularly sensitive to lack of these nutrients.


But even if that were not so, the case for invasive procedures, such as angioplasty and by-pass graft surgery is not strong enough to deserve the high status that they now have. In fact, one critic, Dr. Charles T. McGee, (M.D.) contends that there is inherent fraud in the present situation. He calls it “The Misapplication of high technology in heart disease,” because by-pass surgery is advertised and sold to millions of desperate patients at great cost but without proven benefit. His book, Heart Frauds, published in 1993 (MediPress, Coeur d’Alene, ID) presents scientific studies that prove that X-ray angiograms do NOT reliably diagnose coronary artery blockage; and that by-pass surgery does NOT extend life-span. On the other hand, he also documents orthomolecular therapies that have been proven to reverse coronary atherosclerosis. And he emphasizes that because these therapies are denied or ignored—many patients needlessly die.


I am impressed that by adjusting the balance of nutrients in diet and with the addition of supplements, true miracles of rejuvenation are possible—and at relatively low cost. It is macabre that the medical profession supports the use of Coronary Artery By-pass Graft (CABG), a $30,000 surgery that does not yield any survival advantage; but fails to teach the public that antioxidant therapies confer at least a 50 percent advantage, ie. decreased coronary death rate, in the first decade after starting on vitamin therapy. That’s what public health is all about: teaching people to take advantage of the facts! To fail at this is negligence, incompetence or fraud. Dr. McGee takes the latter view, therefore his title, “Heart Frauds.”

Beyond the by-pass fraud, he argues that our political and medical authorities persist in support of obsolete and harmful strategies, such as the promotion of margarines and hydrogenated oils, continuing the multi-billion dollar anti-cholesterol campaign, and then failing to educate the public about the proven benefits associated with the use of vitamin E and carotene. Dr. McGee considers this to be “incredible negligence.”


Heart Frauds is an expose; it tells it like it is. I expected as much from Dr. McGee because he was one of the charter members of the Orthomolecular Medical Society at its founding in 1976. I knew at the time that his formal medical training was in surgery and gynecology, but his first book, How to Survive Modern Technology, published in 1979, proved that he was not merely specialized in diseases of women but that he understood the impact of environmental pollution and food technology on human degenerative diseases. His first book deftly summarized the orthomolecular and environmental therapies, including megavitamin therapy, desensitization of allergies, and detoxification of pollutants.

His new book, Heart Frauds, is every bit as incisive as the first. Heart attacks still take almost half a million lives every year in the United States and one of them was Dr. McGee’s father, who died of a heart attack when McGee was in medical school over thirty years ago. This tragedy motivated Dr. McGee to follow the complicated and often contradictory research in cardiology, from Framingham to the Lipid Clinics studies, thus building his authority and his ability to see that Medicine has failed thus far to solve the riddle of coronary artery disease.

No less mysterious is the fact that heart attacks have declined by almost 50 percent in the past 20 years. Cholesterol is clearly not the answer because dietary cholesterol intake has been unchanged throughout the years. Nevertheless the experts seem to be convinced that angina (chest pain) and infarction (heart attacks) occur because cholesterol invades the walls of our arteries and forms plaque that gradually blocks the flow of blood. Since that has been regarded as irreversible, Coronary Artery By-pass Graft (CABG) surgery has become an accepted treatment. The development of heart-lung machines and safe anesthetic techniques, has made it possible to provide about 400,000 such surgeries each year in this country and about 300,000 balloon angioplasties are also performed, in which a catheter is threaded into the artery and inflated so as to enlarge the channel. Worldwide there are now about 800,000 by pass surgeries performed each year!

I agree that the technology is awesome; but the point that Dr. McGee makes in his book is that most of the time these procedures are unnecessary. In the past first place, there is abundant evidence that the usual method of diagnosis of coronary artery blockage, the angiogram, is unreliable unless it is done by the method of quantitative imaging. Even more startling: the injection of dye can cause the coronary vessels to go into spasm, thus producing X-ray pictures that look like blockage—but are not! Can a 2 dimensional X ray picture really provide a diagnosis in a 3 dimensional patient, who lives in the fourth dimension, time?

If the result of by-pass surgery were a guaranteed increase in longevity, one could make a case for CABG; but in fact no evidence of increased longevity exists, especially not for those with only minimal damage to the left ventricle of the heart, the main pumping chamber. By means of a non-invasive procedure, echocardiogram, the ejection fraction can be measured. If this is normal, the left ventricle is functional and surgery offers no extra years of survival. This turns out to be the case for over half of the patients who are considered for CABG because of chest pain or abnormal electrocardiogram tests. About all that can be expected is a significant degree of relief of angina, chest pain, after the surgery.


How does that stand up in the face of the demonstration by Dr. Dean Ornish that 85 percent of patients with coronary heart disease can reverse their artery blockage by means of a vegetarian diet, exercise and anti-stress training, such as meditation. This means that 5 out of 6 heart patients can open their blocked arteries without surgery. They can heal themselves! We also know that in many cases the heart can gradually develop new blood vessels that by-pass the blocked vessel. In many cases the angina resolves this way and the individual gets a new lease on life that may hold for many years, even decades, even without treatment. I have seen this in my own patients treated with antioxidants, vitamins, trace minerals and omega-3 fatty acids, and without exercise, meditation or a low fat, low cholesterol, vegetarian diet. In fact one of my patients survived twenty years on my treatment regimen before he accepted a by-pass surgery. Why did he suddenly need surgery? He had continued to smoke cigarettes all that time but in the last year or more he had stopped taking his vitamin supplements. Human nature? Lack of follow-up reinforcement after so many years?

Does the proven success of the Ornish Diet mean that all other medical therapies are obsolete? Strictly speaking, yes. But not everyone is motivated or well enough organized to adopt such a regimen. Some react adversely to low fat diet, which can induce digestive disturbances, hypoglycemia, nervous irritability and depression. Some of us just do not like vegetables. And besides, other medical approaches are still entrenched: diuretics, anti-hypertensive, beta blockers, calcium channel blockers, vasodilators, and cholesterol-lowering drugs all have their advocates. And the surgical treatments are pretty hard to refuse when you think your life is on the line. But there are a few statistics that are equally compelling.


For example, the expected death rate from coronary artery disease is about 2 percent per year. But the death rate from coronary artery by-pass surgery can run higher than that—up to 4% at some hospitals and higher in less competent hands. Granted, as experience and techniques have improved, operative mortality has declined; but there is another side to the story that deserves to be appreciated: 10 year survival after by-pass surgery in patients with intact heart function is about the same after surgery (86 %) as with drugs and diet (82%). In the 780 patients of the Coronary Artery Surgery Study (CASS), only those patients with impaired function of the left heart ventricle had a survival advantage from by-pass surgery: 80% compared to 59% in the medical group.


Because of the variability from one study to the next, it has been difficult to arrive at an over-all estimate of benefits and risk. Brain damage after by-pass surgery is not rare. In fact it is a big problem, much greater than operative mortality. A recent study of over 2000 patients in 24 hospitals in 1991-1993 surveyed neurological injury associated with by-pass surgery, and found that over 6 percent of the patients had neurological complications, about evenly divided between strokes and senile degeneration. Over-all, the operation carried 2 percent mortality, almost identical to the mortality in coronary patients who do not elect to have the by-pass surgery. In case of paralytic stroke, the in-hospital death rate increased to 21 percent; double the rate seen in senile type confusion or seizures.

[1] McCully KS. Vascular pathology of homocysteinemia: implications for the pathogenesis of arteriosclerosis. Am J Pathol 1969; 56:111-28.

[2] Alderman et al. Circulation 1990;82:1629-1646.

[3] Roach GW, Kanchuger M, Mangano CM et al. Adverse cerebral outcomes after coronary bypass surgery. New Engl J Med 1996; 335:1857-1863.

©2007 Richard A. Kunin, M.D.