Most still believe that a high cholesterol diet is the cause of heart disease. But new research is showing that this view is an oversimplification of a complex process that has more to do with modern food preparation. foods.
Hardening of the arteries and subsequent coronary artery disease is the biggest single threat to all our lives. Heart disease will kill 40 per cent of us, and those of us who don’t die from it may be affected by arteriosclerosis in the form of decreased mental capacity or decreased blood flow to vital organs. Small wonder that discovery of the cause of this condition rates even higher than discovery of the cause of cancer as the Holy Grail of medicine.
Until recently, medical scientists have been pursuing the trail of risk factors. Because it’s been noted that a high blood level of cholesterol, particularly if correlated with a high level of low density lipoprotein, is a risk factor for heart disease, doctors have made the erroneous assumption that a high cholesterol intake itself causes heart disease. However, one of the more important holes in the cholesterol/fat theory is the lack of an explanation for the rapid rise in the incidence of arteriosclerosis, heart disease and stroke during the early and mid parts of the 20th century and the sudden and rapid decline beginning in the mid 1960s.
Studies of the American diet have failed to find any correlation between the cholesterol and fat content of an individual’s diet and the changes produced by arteriosclerosis. The fat and cholesterol content of the US diet has changed very little in the last few decades, even though there has been a two to threefold decline in the incidence of patients with arterial disease. Studies also showed there were no significant changes in blood levels of cholesterol and low density lipoproteins.
While most medical scientists were busy continuing to follow down the path of cholesterol, one unlikely renegade, a pathologist at the Veterans Affairs Medical Center in Providence, Rhode Island named Dr Kilmer McCully, detoured away from fats and cholesterol and began looking at the role of homocysteine, an amino acid derived from the normal breakdown of proteins in the body.
The first clue that homocysteine levels might cause heart disease came from studying people who had died from homocysteinuria. In this rare genetic disease, the liver is unable to dispose of homocysteine normally because of a genetic error in the liver enzyme cystathione synthase. Many sufferers of homocysteinurea die in childhood from blood clots in the brain, heart and kidneys causing heart attacks, strokes or kidney failure. Interestingly, on post mortem examination, all the arteries of these patients are highly abnormal. Even eight year old children have hardening and loss of elasticity in the arterial walls conditions usually only present in the elderly. The urine of these patients always contains homocysteine.
The enzyme adenosyl methionine converts homocysteine to form methionine, an amino acid found in all proteins. This complicated process has been found to require the action of both vitamin B12 and folic acid. Other researchers have found that in some patients with homocysteinuria, the amount of homocysteine in the urine is dramatically decreased by moderately large doses of vitamin B6.
>From his studies, McCully saw that vitamins B6, folic acid and B12 are all important in the processes involved with homocysteinuria, and that in this rare genetic disease, homocysteine causes damage and hardening of the arteries by a direct effect on the cells and tissues lining the arteries.
This research tied in with earlier work done in in 1949, when Dr James Rinehart and his associates at the University of California published several papers showing that a partial deficiency of vitamin B6 in a synthetic diet fed to monkeys caused arteriosclerotic changes in the arteries if the exposure was carried out over a prolonged period of six to eighteen months (Am J Pathology, 1949; 25: 481-91).
A colleague of Dr Rinehart , cardiologist Dr Moses Suzman from South Africa learned of Dr Rinehart’s work, and he started to routinely give vitamin B6 and other vitamins to his cardiac patients. While on the regime, they no longer experienced symptoms of chest pain on exertion, and
were able to increase their exercise tolerance. Their electrocardiographs improved. Generally, their risk of heart attack was reduced.
McCully went on to theorise that arteriosclerosis is attributable, not to excess cholesterol and fats, but to abnormal processing of protein in the body because of deficiencies of B vitamins in the diet.
He postulated that populations are at risk from this disease because the methionine of dietary protein is not prevented from forming excess homocysteine. This means that there is a dietary imbalance between too much methionine from protein and deficiencies of vitamins B6, B12 and folic acid.
The implications of McCully’s theory are staggering. It means that arteriosclerosis is a disease of protein intoxification, rather than one of intoxification from fat, and the solution lies in a few vitamins, not an entire cholesterol lowering programme.
One of the major studies emphasising the importance of homocysteine in heart disease was the Framington Heart Study in America. This huge study, which has been ongoing for decades, provides much of the epidemiological evidence of what we know about risk factors in coronary artery disease. It showed that the higher the level of blood homocysteine, the greater the degree of narrowing of the carotid arteries (New Eng J Med, 1996; 332: 286-91). A later study found that the risk of early heart disease and strokes correlated with blood homocysteine levels of greater than 14 micromoles per litre.
The single most valuable study of risk factors relating to homocysteine levels was the Horderland study from Norway (JAMA, 1995; 274: 1526-33), which studied more than 16,000 healthy men and women aged 40 to 67. It showed that the risk of arteriosclerotic disease is linked with even minor changes in blood homocysteine from what is regarded as the normal range of 6-10 micromoles.
Many studies have now shown that making certain dietary changes and supplementing with vitamins B6, B12 and folic acid can lower blood levels of homocysteine. One study in South Africa showed that patients taking these supplements could decrease elevated blood homocysteine levels by more than 50 per cent. Once the patients stopped taking these supplements for four months, blood homocysteine levels again rose. When the patients went back on the vitamin supplements, their homocysteine levels again fell within six weeks (Clinical Investigator 1993; 71: 993-8). In the Hordeland Norwegian study, taking B vitamin supplements had a more consistent and stronger effect in lowering blood homocysteine than did fruits and vegetables.
A multi centre European study comparing 750 vascular cases with 800 controls showed that consuming vitamins B6, B12 and folic acid reduced the risk of vascular disease by approximately two thirds (Irish J Med Science, 1995; 164 Suppl 15: 51A). In another study, where vitamin B6 was given to 3000 patients to treat carpal tunnel syndrome, the vitamin was also found to reduce the risk of acute heart attack and angina by 75 per cent over the five year period of the study (Research Comms Molecular Path and Pharm, 1995; 89: 208-20)
Although these and other studies are highly persuasive about the role of homocysteine in heart disease and the protective effect of B vitamins, the theory hasn’t yet been put to the definitive test with a randomised prospective trial. But even if such a study is finally conducted, in my view, homocysteine won’t be found to be the only cause of arteriosclerosis.
There are two large exceptions to the homocysteine theory. First, homocysteine levels do not rise in early diabetes a situation which would be expected if homocysteine were the only cause of arteriosclerosis. Second, oddly enough, there is no correlation between high blood pressure and homocysteine levels, even though hypertension is an obvious risk factor for arterial heart disease.
These two exceptions suggest that development of coronary arterial disease is complicated, and not simply a matter of a single vitamin deficiency. For instance, a great deal of evidence shows that a deficiency of the mineral chromium plays a major role in the development of diabetes and and also hardened arteries.
Other evidence links magnesium deficiency with hypertension. These two factors may be every bit as important as homocysteine and B vitamins in developing heart disease.
The importance of chromium
Over many years, Biolab Medical Unit in London conducted a computer analysis of more than 40,000 patients, which showed that chromium levels fall markedly as we age. Chromium levels are lower in men than women from age 20 onward, and then fall dramatically between 40 and 65, the ages when coronary artery disease is known to increase. Patients with type 2 diabetes have lower levels of chromium in the blood than non diabetics. Giving diabetics supplements of chromium has been shown to improve glucose tolerance, decrease blood cholesterol and triglycerides and increase high density lipoprotein cholesterol the “good” cholesterol (Clin Chemistry, 1988; 34: 1525-6).
One Israeli study found that the aorta, or main coronary artery, of patients dying of coronary artery disease contained very little chromium, compared to a group of controls (Amer Heart J, 1980; 99: 604-6).
Supplementing with chromium has also been shown to increase glucose control in Type 2 diabetes mellitus (Diabetes, 1997; 46: 1786-91). Natural sugars and grains do contain adequate concentrations of chromium to help along the metabolism of these high carbohydrate foods. However, almost all chromium is removed during the refining process of most of the sugars sucrose or glucose which we eat. There’s plenty of evidence showing that diets high in processed carbohydrates are deficient in chromium.
There’s also evidence that societies which increase their intake of refined sugar intake have a very high incidence of coronary artery disease. Low chromium levels have been shown to be a major factor in the formation of high blood cholesterol levels in numerous laboratory studies.
Although animal studies cannot be applied to humans, and so should be viewed with suspicion, we have seen that giving chromium supplements will lower high blood cholesterol and highly processed foods low in chromium will result in high cholesterol levels. This suggests that high blood cholesterol does not itself cause coronary artery disease, but is simply a marker that something else like inadequate chromium intake 1 is awry.
The role of magnesium
A good deal of research has linked magnesium deficiency the most common trace mineral deficiency in the Western world with heart disease. In the 1950s, this association became apparent both in farm animals and then in humans (MS Seelig, Magnesium Deficiency in the Pathogenesis of Disease, Plenum Medical Books, 1980). More than 30 years ago, scientists discovered that magnesium deficiency predisposes one to high cholesterol levels and to an increased ratio of low density lipoprotein to high density lipoprotein These risk factors for heart disease decrease once you begin taking magnesium supplements (Magnesium Bulletin, 1981; 3: 165-77).
Much has been written about the supposed Type A hard driving, achievement oriented personality, who has a greater risk of heart disease than the more laid back Type B. However, what’s been discovered is that Type As also have lower red blood cell magnesium levels, suggesting that magnesium may be the main factor behind their increased risk (J Amer Coll Nutr, 1985; 4: 165-72).
Magnesium deficiency also predisposes you to increased clotting tendency in the blood, the most important risk factor in the formation of coronary thrombosis ((Revue Francais Endocrinol Clinique, 1970; 11: 45-54). Besides B vitamins, a deficiency of magnesium is responsible for the build up of homocysteine levels.
Magnesium deficiency is associated with angina (Magnesium, 1984; 3: 46-9), which improves when you take supplements of magnesium.
As with chromium, in industrialised societies the intake of magnesium is low as a result of the refining and processing of foods (J Amer Col Nutr, 1985; 4:195-206).
In the early part of the 20th century there was virtually no coronary artery disease. By the middle of the century it had become the number one killer in the West. But heart disease rose in tandem with the development of the processed food industry and the establishment of intensive farming techniques. As processing became the norm, sugar consumption rose astronomically from 4lbs per person per year to 140 lbs per person per year, an increase of several thousand percent. Refined sugar which contains no added nutrients, requires huge amounts of chromium to process it. The addition of this in our diet must take the blame for the drastic reduction of chromium in the diet.
Water soluble B vitamins are easily destroyed or depleted by food processing and do not occur in refined sugars. In milling wheat into white flour, for example, 50-90 per cent of vitamin B6 is destroyed. Up to half of the content of vitamin B6 is lost in canning meats and fish and up to three quarters of the vitamin is lost in canning vegetables. Anytime a food is refined, prcessed or preserved, one to three quarters of the vitamin B6 content is destroyed.
Increasingly the evidence shows that heart disease is a disease of the industrialised food industry.