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What Doctors Don't Tell You © (Volume 10, Issue 8)

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)

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