blocked arteries. Some even have undergone angioplasties or failed bypasses.
For all the high tech involved, many medical critics don’t give high marks to these procedures and say that they are performed too often and are not as effective or urgent as patients are usually led to believe.
According to a 1990 report in Circulation, a leading medical journal, a ten-year follow-up of survival among heart attack patients showed that individuals with one, two or all three of their major coronary arteries blocked do quite well without surgery. A 1989 study in the American Journal of Cardiology said that patients who don’t have surgery live as long or longer than those who undergo operations.
One problem with vascular operations is that they often need to be repeated. Up to 40 percent of bypass grafts may reblock after only five years, and a third to a half of angioplastied arteries reblock again after four to six months. The original procedures are then performed at additional cost.
Looking Beyond Cholesterol, Surgery And Drugs
For years, we’ve all been told to lower our cholesterol and eat less fat. Yet many people who suffer heart attacks have normal or even low-normal cholesterol levels and people with enormously high cholesterol live long and healthy lives.
Why is it that despite the billions of dollars invested into pharmaceutical and surgical solutions for the cholesterol theory, vascular disease still ranks as the country’s leading killer?
And why is it that many people who avoid other important risk factors, who do not smoke, who are not overweight, overstressed or hypertensive, and who exercise routinely, or who have no history of heart disease in their families, still suffer from vascular disease?
These are agonizing paradoxes that have long confounded physicians.
Thanks to modern research, answers are the answers are steadily coming in and filling the gaps in our understanding about arterial disease. The research is leading us to a whole new generation of risk, survival and prevention factors.
When we go beyond merely considering cholesterol and fat, and drug and surgical treatments, we find ourselves able to actually reverse the disease process. For instance, Dean Ornish, M.D., has proven that lifestyle modification alone — a vegetarian diet, meditation, and exercise — can reverse arterial disease.
A large volume of exciting research in recent years has demonstrated how nutritional status and the levels of vitamins and minerals in your body are involved .
For instance, experts now regard the anti-oxidant vitamins, and particularly vitamin E, as important agents to prevent the oxidation of “bad cholesterol” on the artery walls. Interestingly, some cholesterol-lowering drugs have been found to significantly lower the levels of antioxidant nutrient protectors in the blood!
Among the most significant studies was a University of Cambridge trial in which vitamin E supplements reduced heart attacks by a dramatic 77 percent among 2,000 patients with heart disease.
In the past, vitamins and minerals were regarded narrowly by most physicians as simply necessary elements in food that would prevent nutritional deficiency states. The prevailing attitude was that we supposedly get all we need from our diet and there was no need to supplement our diet if we ate a “balanced diet.”
Now nutritional surveys tell us that a great many people eat poorly. Their diets are far from “balanced” and are alarmingly deficient in many nutrients important for health. Increasingly, in recent years, research is showing that nutrients used at doses higher than those usually present in the diet have a medically-significant preventive and therapeutic effect for serious diseases, including vascular disease.
For years, my approach to vascular disease has taken me way beyond cholesterol. I test for cholesterol, but I also carefully weigh diet, nutritional status, stress, lifestyle and other risk factors into the treatment equation. Then I use all the many options — integrating the best from both conventional and alternative approaches — into a comprehensive strategy for achieving optimum health.
And now we have the homocysteine option — an effective and refreshingly inexpensive method to greatly reduce human suffering, avoid unnecessary operations and drugs with multiple side effects, and, in the process, save big-time on medical bills.
The Homocysteine Story
The story of homocysteine is the story of the persistence of Kilmer McCully, M.D., a physician who trained and taught at Harvard University.
As a young pathologist at Massachusetts General Hospital in 1968, McCully encountered the case of a two-month-old boy who died of homocystinuria, a rare genetic disease associated with very high levels of homocysteine in the blood and urine. Autopsy revealed hardened and clogged arteries, comparable to the degeneration seen in aged individuals who die from arterial disease. The same pathology had been described among children in Ireland and in a case involving an eight-year-old boy at the same hospital more than 30 years before.
The case ignited McCully’s curiosity and he began investigating homocysteine. His research led him to hypothesize, in a 1969 article published in the American Journal of Pathology, that elevated homocysteine and nutrient deficiencies might be centrally involved in widespread arterial disease.
However, the idea that an amino acid, rather than cholesterol or fat, could cause arterial disease, did not fit into the cholesterol “paradigm.” McCully’s theory was ignored or criticized. Despite impressive credentials, McCully’s innovative thinking led to him to be sacked from his medical appointments. He eventually was employed as a pathologist at the Veterans Affairs Medical Center in Providence, and from that position has continued to this day to expand his understanding and research, and inspire many other investigators to look into homocysteine.
In the following years, confirmation began to appear in medical studies around the world. Major validation occurred in the early 1980s when researchers analyzed a group of 300 doctors in the Boston area and found their likelihood of a heart attack was more than three-fold among individuals with the highest homocysteine level. The conclusion: excess homocysteine was equivalent to smoking and high blood cholesterol as a risk factor.
In the following years, a veritable avalanche of research has confirmed McCully’s theory. In 1994, a study published in the Netherlands Journal of Medicine determined that individuals with abnormal homocysteine had 13 times the relative risk of vascular disease, including cerbrovascular and peripheral vascular disease, at a young age.
Other recent studies, conducted in the U.S. and Europe, conclude that as many as 30 percent of patients with premature vascular disease have moderately elevated homocysteine levels.
In 1997, a group of Norwegian experts reported in the New England Journal of Medicine that homocysteine was “the strongest modifiable predictor of overall mortality and mortality due to cardiovascular causes among patients with...coronary artery disease.” By modifiable, the researchers meant that it could be corrected and normalized.
The bottom line: more than 200 studies have firmly established elevated homocysteine as a major independent risk factor and predictor not just for heart attacks, but for strokes, blood clots in the legs and general systemic damage to the arteries.
Moreover, elevated homocysteine also causes major trouble elsewhere in the body. It has been implicated in spontaneous abortion, neural tube defects, low birth weight, kidney failure, rheumatoid arthritis, alcoholism, osteoporosis, neuropsychiatric disorders, non-insulin dependent diabetes and complications of diabetes. High homocysteine has also been found in patients with fibromyalgia and chronic fatigue.
How Homocysteine Builds Up in Your Body
You are going to hear a lot about homocysteine. Here are the basic facts about it:
Homocysteine is an amino acid that builds up into damaging, toxic levels in the blood vessels as a result of defective disposal by the body.
Protein is a basic constituent of all the food we eat. One of the components of protein is the amino acid methionine, an essential dietary ingredient for proper growth and maintenance of all the cells and tissues in the body.
Normally, the liver processes methionine. It breaks it down into homocysteine. Some of this homocysteine is then reconverted back into methionine again and used throughout the body. The homocysteine that is not used, is further broken down and excreted in the urine.
This smooth operation depends on an adequate supply in the body of three members of the B complex vitamin family — folic acid, vitamin B-6 and vitamin B-12. These vitamins are needed to make the enzymes that convert methionine and homocysteine.
Without adequate vitamins to fuel the enzymatic action, homocysteine starts building up. The excess homocysteine is carried throughout the body and enters into the tissue of the inner linings of arteries. There, according to scientific studies, it triggers a destructive sequence of chemical and oxidative reactions involving proteins, fatty proteins, platelets and hormones, as well as circulating blood components that promote the formation of blood clots. In this way, homocysteine starts the development of artery-blocking plaques and vascular disease.
The Homocysteine Theory And Cholesterol
Most people tend to think of the plaques clogging their arteries as greasy fat deposits. Not so, says Kilmer McCully, who, as a pathologist has examined countless arteries.
While they do have fatty content, most of them, even in advanced disease, “are tough, inelastic, thickened and heavily encrusted with calcium deposits, making them difficult to dissect with scalpel or scissors,” he explains.
Advanced plaques, he says, are “complex structures that include cholesterol crystals, fatty deposits, protein deposits, areas of degeneration or death of tissue, blood clots, the growth of small blood vessels into the artery wall and areas of bleeding that predispose to complete blockage by formation of blood clots.”
McCully’s homocysteine theory puts the onus of disease on protein. The cholesterol theory emphasizes fat.
Here’s how McCully puts it:
“The homocysteine approach is radically different from the traditional view which relates arteriosclerosis to dietary consumption of excess fats and cholesterol. In the conventional view, the arteries are believed to be damaged by a build-up of cholesterol in the LDL component of plasma coupled with a related lowering of the HDL component (the so-called “good cholesterol” — ed). The view of the homocysteine theory is that arteries are damaged by the injurious effect of homocysteine on cells and tissues of arteries, setting in motion the many processes that lead to loss of elasticity, hardening and calcification, narrowing of the lumen and formation of blood clots within arteries. The homocysteine theory considers arteriosclerosis a disease of protein intoxication. The cholesterol/fat approach considers the disease to be caused by intoxication from fats.”
What is interesting in McCully’s comparison is that the body’s natural mechanisms to handle both cholesterol and homocysteine appear to go wrong because of poor nutrition. Both fail — and contribute to disease — because of inadequate levels of important nutrients.
The Vitamin Connection
Research indicates homocysteine levels rise in the body usually as the result of an insufficiency of certain vitamins. When one or more are deficient, the enzyme systems fail that are related to homocysteine processing. The amino acid then builds up over time.
In 1993, data collected on more than a thousand elderly participants in the famous Framingham Heart Study in Massachusetts, showed a strong link between elevated homocysteine and low levels of vitamins B-6, B-12 and folic acid in the blood. The report appeared in the Journal of the American Medical Association.
In 1997, the same journal, reported on a study involving more than 1,500 elderly men and women at 19 European clinical centers. The risk of vascular disease among them was directly related to homocysteine levels, which in turn were related to levels of folic acid, and vitamins B-6 and B-12 in red blood cells.
Many scientific studies have now linked high homocysteine to low levels of these vitamins.
At a 1995 meeting of the Federation of American Societies for Experimental Biology, one scientist after another commented on the significance of the vitamin—homocysteine connection. One of them, Irwin Rosenberg, M.D., of Tufts University, called it “the most exciting example of the relationship between vitamin metabolism and disease.”
In a moment I will describe how Cardiocysteine, a unique high-potency vitamin supplement, can help provide nutritional support for normal and healthy homocysteine levels.
Vitamin Deficiencies — How Do They Happen?
As a physician specializing in nutrition and preventive medicine for many years, it is not surprising to me that so many people with vascular disease are being consistently found to be deficient in important vitamins. Many Americans simply make poor food choices that fail to nourish them properly. That’s a major reason for so much chronic disease in the country.
Nutritional surveys conducted by the U.S. Department of Agriculture find vast numbers of Americans with low or suboptimal intakes of essential nutrients. The well-known Harvard nutritional researchers Meir Stampfer, M.D., and Walter Willett, M.D., say that research “strongly indicates that such low intakes are associated with serious health consequences.”
One such health consequence appears to be arterial damage caused by elevated homocysteine.
The B vitamins important for homocysteine conversion in the body must be obtained from food. However, the typical American diet of highly-processed food preserved for long shelf life eliminates much of the natural nutrient content, contributing to widespread marginal or even grossly deficient intakes.
For instance, much of the B-6 and folic acid content, along with other essential nutrients, are lost in the processing of whole grains to refined grains. When whole wheat is manufactured into refined white flour, the usual type of flour used for breads, cookies, cakes, pastries, and pasta, some 83 percent of B-6 and 75 percent of folic acid is lost.
There are other problems. We eat too much fat in our diet. That reduces our body’s ability to absorb vitamin B-6 and folic acid, thus creating a greater risk for deficiencies.
We also eat too much sugar. Virtually every processed food — including mayonnaise, ketchup, ice cream, soft drinks, luncheon meats, and even baby food — has added sugar. To metabolize sugar, your body requires many B complex vitamins, including B-6. Thus, the more sugary foods you eat, the bigger the risk of creating deficiencies, and the greater the risk of elevated homocysteine.
Americans don’t eat enough fruits and vegetables — both excellent sources of vitamin B-6 and folic acid. More than 50 percent of adults fail to eat the recommended three servings of vegetables daily and 75 percent don’t eat the suggested two servings of fruit.
Vitamin B-12 is less a problem because it is supplied in meat, fish, poultry and dairy. However, it commonly becomes deficient among an aging population wherethe stomach becomes less efficient in its absorption.
Meat-Eaters, Vegetarians And The Homocysteine Theory
Protein from animal sources, such as meat, eggs or milk, are rich in methionine. That’s the amino acid that is broken down by the body into homocysteine. Thus, people who eat a lot of these foods need more vitamins B-6 and folic acid to keep blood levels of homocysteine in a safe range.
Dietary protein is also present in plant foods. However, proteins from plant food such as grains, legumes and vegetables, contain only a third or a half of the methionine in animal-based foods.
“The homocysteine theory explains why vegetarians and populations consuming a predominantly vegetarian diet are relatively protected against arteriosclerosis compared with populations that consume abundant meat and dairy products,” says McCully. The body simply has less homocysteine conversion work to do.
Animal studies have shown that elevated homocysteine can increase the formation of low-density lipoproteins in the body. Remember, that’s the LDL, or so-called “bad cholesterol,” that is the most vulnerable to damaging oxidation, an important risk factor for vascular disease.
Thus, adds McCully, diets that emphasize less intake of methionine by consuming proteins of primarily plant origin, and greater intake of vitamins B-6 and folic acid from minimally processed or raw foods, help to deter the formation of this most damage-susceptible type of cholesterol.
More Facts On Homocysteine You Should Know
Most cases of elevated homocysteine involve nutrient deficiencies that sabotage normal metabolic processing. Let’s look at some of the variations on this nutrient theme:
Genetics A serious genetic defect in homocysteine metabolism affects about one person in 160,000. A milder defect involves many more people, one out of 70. Genetic factors can cause premature heart disease, stroke or peripheral vascular disease.
In general, McCully says, these cases “cause greater susceptibility by increasing the quantities of dietary folic acid, vitamin B-6 or B-12 needed to prevent a buildup of homocysteine in the blood.”
Ensuring you get enough of these vitamins “can help overcome the deleterious effects of heredity on the risk of arteriosclerosis,” he adds.
Aging For reasons only partially understood, the aging process hinders the body’s ability to process excess homocysteine, and homocysteine levels start rising in the seventh decade of life. Meanwhile, the level of B-6 declines significantly with age, and to a lesser degree folic acid and B-12. Among the elderly, studies have linked low levels of these vitamins to high homocysteine.
Experts think that the absorption and retention of these vitamins may be affected by age-associated changes in the body.
Although aging is a risk factor for elevated homocysteine that cannot be changed, “beneficial dietary and lifestyle improvements can significantly lengthen life and improve health until the onset of senescence,” says McCully.
Hormones Gender is another permanent risk factor for homocysteine. Among pre-menopausal women, the production of natural estrogen and other ovarian hormones appears to protect against homocysteine build-up. After menopause, the level among women generally rises to that of men.
The use of synthetic estrogens and progesterones in contraceptive hormones interferes with vitamin B-6 in the body and leads to elevated homocysteine levels. Young women taking such preparations increase their risk of developing blood clots and arterial plaques.
Smoking Smokers have higher levels of homocysteine. The cessation of smoking, according to McCully, is “the most important controllable lifestyle factor, besides an optimal diet.” The carbon monoxide of cigarette smoke is believed to impair vitamin B-6 function in the body, including its ability to breakdown homocysteine.
Coffee If you’re a serious coffee drinker, beware. Your habit may elevate homocysteine. Researchers have found a dose-response relationship: eight or more cups a day significantly drives homocysteine upwards. Smoking and coffee is even worse.
Alcohol Chronic alcohol consumption increases homocysteine.
Medication Certain drugs, such as chemotherapeutic agents used in cancer treatment and anti-hypertensive medications, elevate homocysteine by interfering with folic acid and B-6 functions in the body.
Keeping Homocysteine At Bay
First and foremost, we need to make sure our diet contains enough of the important vitamins related to homocysteine. That means eating as much wholesome, fresh and unprocessed food as possible.
“By consuming an optimal diet containing an abundance of these vitamins...an individual at risk can achieve a lifelong measure of protection against development of arteriosclerosis,” says McCully.
Studies conducted around the world clearly shown that a good intake of B complex vitamins — as part of the diet and as supplements — keeps homocysteine levels low. Some experiments have demonstrated the effectiveness of vitamin supplements in rapidly bringing down and normalizing high levels.
In one South African study reported in the American Journal of Clinical Nutrition, researchers gave a group of men with high homocysteine a daily vitamin supplement and found that within six weeks the concentrations had normalized. “Appropriate vitamin therapy may be both efficient and cost-effective to control elevated plasma homocysteine concentrations,” concluded Johan Ubbink and colleagues from the University of Pretoria.
In the multicenter European study on homocysteine I mentioned earlier, 28 international experts concluded that people taking supplements “appeared to have a substantially lower risk of vascular disease, a proportion of which was attributable to lower plasma homocysteine levels.”
Nutritional supplements have always played a major role in my prevention and treatment programs. To counteract homocysteine I wanted to offer my patients a combination of high potency B-6, B-12 and folic acid, along with certain co-factors or supporting nutrients that would enhance their absorption and utilization in the body. Many multiple vitamin formulas I checked out failed to meet my specific criteria.
Vitamin B-6 (25 milligrams)
B-6 is commonly deficient in our typical diet of processed food. It is used in the conversion of excess homocysteine to cystathione, a breakdown substance that becomes excreted in the urine. Human and animal studies both have shown that high protein intake without adequate vitamin B-6 causes a rise in homocysteine.
Pyridoxyl-5 Phosphate (5 milligrams)
Inside the body, vitamin B-6 is converted to pyridoxyl-5 phosphate, or P5P for short. This, actually, is the active form of the vitamin used by the body. This is what does the job.
Some individuals have trouble converting B-6 into P5P. Sufferers of carpal tunnel syndrome, a painful condition of the wrists and hands, often benefit from vitamin B-6. However, studies have shown that some patients don’t respond to it. Their problem may be an inability to convert B-6 into the active form of P5P. This is one reason why I want P5P in my supplementation program.
Trimethylglycine (250 milligrams)
Trimethylglycine, or TMG, is a quasi-vitamin that helps to normalize defective amino acid metabolism, and particularly in patients who have high homocysteine unresponsive to vitamin B-6 therapy. It helps to “remethylate” homocysteine, meaning that it reconverts homocysteine to methionine for use in the body. TMG is also a powerful antioxidant. Humans are able to synthesize it from choline, another B complex vitamin, but not in large enough quantity.
Vitamin B-12 (500 micrograms)
People usually get enough B-12 in their diets, however many older individuals suffer from inefficient absorption of nutrients which can cause a marginal deficiency.
Folic acid (800 micrograms)
Folic acid is typically deficient in the Western diet. Both folic acid and B-12 are important in the enzymatic conversion of homocysteine back into methionine. High homocysteine levels have been implicated in osteoarthritis and both folic acid and B-12 have been shown to benefit this condition, probably through the homocysteine mechanism
Final thoughts
Kilmer McCully is a true pioneer and I salute his breakthrough work. His research represents a major step forward in understanding and treating vascular disease.
The test for homocysteine is now readily available and easily performed right in a physician’s office. I encourage you to have it done, particularly if you are entering the high-risk years: over 40 for men and over 50 for women.
The good news, as I have described in this health report, is that high levels of homocysteine can be brought down by vitamins. From all the research I have read and from the striking benefits I see among my patients, I am convinced we now have a powerful and simple weapon at hand with which to make a strong stand against a deadly disease and many other common health problems as well.
For The Full Story On Homocysteine
Kilmer McCully, M.D., has written an important book, “The Homocysteine Revolution” (Keats Publishing, 1997), in which he details the evolution of his theory. I highly recommend it to anyone interested in their cardiovascular health.
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