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.