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Homocysteine: the saga of a medical breakthrough
About the author: 

What causes heart disease? We've asked the question a few times in recent bulletins, and we've had several responses back

What causes heart disease? We've asked the question a few times in recent bulletins, and we've had several responses back. Answers have ranged from 'loads of things' to 'dunno', to 'trans fatty acids'.

Homocysteine has been mentioned in these articles, and as new research has thrown further light on the subject, it seems a good time to get a better understanding of its role in heart disease.

Homocysteine is an amino acid that accumulates in the blood. When levels become abnormally high it is known as homocystinuria, and it was first linked to heart disease in Irish research published in 1962.

But it was Kilmer McCully, then a resident pathologist at Massachusetts General Hospital, who recognized that homocysteine could cause cardiovascular diseases such as atherosclerosis at far lower levels than the Irish researchers thought. He published his findings in 1969, and he was rewarded for his efforts by being banished from Harvard University and he lost his job at the Massachusetts hospital.

His views certainly seemed heretical. Cholesterol and clogged arteries were not the cause of heart disease, but were merely the symptoms of an underlying cause - raised homocysteine levels. A diet rich in vitamin B6, B12 and folic acid could reduce homocysteine to levels that were not life-threatening, he postulated.

Although medicine has finally accepted the theory, it has done so begrudgingly and has never fully taken on board the full implication of McCully's discovery. To this day, many specialists still work with the old paradigm that cholesterol is the problem.

Their view seems to be supported by a new piece of research among 3,680 adult Americans who had suffered a heart attack. Half were given high-dose vitamin B, made up of 25 mg pyridoxine, 0.4 mg cobalamin and 2.5 mg folic acid, while the rest were given the same in low doses.

Although homocysteine levels were reduced more in the high-dose group, not surprisingly, there wasn't a significant difference between the two groups in terms of stroke and further heart attacks.

So is there a flaw in McCully's theory? Not necessarily, as the research team from Wake Forest University School of Medicine in North Carolina, admits. In the first place, the study period, at two years, could have been too short. It's equally as possible that the participants' homocysteine levels weren't critical in the first place, thanks in part to the US government initiative to fortify grain with folate.

It could also be that raised homocysteine levels are yet another marker for heart disease, a theory that is supported by some research. Perhaps, after all, 'dunno' is the correct response when people want to know the cause of heart disease, but, if so, it's a 'dunno' of a far richer quality.

(Source: Journal of the American Medical Association, 2004; 291: 565-75).


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