Cholesterol and CHD
For reasons still unknown, coronary heart disease suddenly took off during the 1920s throughout the industrialised world. By the 1940s it was becoming the major cause of premature death.
And nobody knew why.
( From my own research it was the introduction of Chlorine in tap water around the same time )
And nobody knew why.
( From my own research it was the introduction of Chlorine in tap water around the same time )
In 1950 an American doctor, John Gofman, hypothesised that blood cholesterol was to blame.
This was supported in 1951 when pathologists were sent to Korea to learn about war wounds by dissecting the bodies of dead soldiers.
To their surprise they discovered unexpected evidence of coronary heart disease: unexpected for they knew that death from heart disease was extremely rare under middle age and these men averaged only twenty-two years of age.
So the pathologists performed detailed dissections on the hearts of the next 300 corpses.
In thirty-five percent they found deposits of fibrous, fatty material sticking to the artery walls.
A further forty-one percent had fully formed lesions, and in three percent of the soldiers these lesions were sufficiently large that they blocked at least one coronary artery.
Thus, over three-quarters of all the men examined showed evidence of serious coronary heart disease - and they were barely out of their teens.
This was supported in 1951 when pathologists were sent to Korea to learn about war wounds by dissecting the bodies of dead soldiers.
To their surprise they discovered unexpected evidence of coronary heart disease: unexpected for they knew that death from heart disease was extremely rare under middle age and these men averaged only twenty-two years of age.
So the pathologists performed detailed dissections on the hearts of the next 300 corpses.
In thirty-five percent they found deposits of fibrous, fatty material sticking to the artery walls.
A further forty-one percent had fully formed lesions, and in three percent of the soldiers these lesions were sufficiently large that they blocked at least one coronary artery.
Thus, over three-quarters of all the men examined showed evidence of serious coronary heart disease - and they were barely out of their teens.
Doctors now had a problem.
As there are no symptoms with the partial blockage of the coronary arteries, how could they tell, without resorting to surgery, who was in danger?
They had to find what was different in those with the disease and those free of it.
As there are no symptoms with the partial blockage of the coronary arteries, how could they tell, without resorting to surgery, who was in danger?
They had to find what was different in those with the disease and those free of it.
To cut a long story short, they found cholesterol in the material that builds up on artery walls and causes them to become blocked;
People who died of heart disease often had high levels of cholesterol in their blood;
And those who suffered the rare hereditary disease, familial hypercholesterolaemia (hereditary high blood cholesterol), also suffered a higher incidence of CHD.
And so, not unnaturally perhaps, cholesterol and heart disease became linked.
People who died of heart disease often had high levels of cholesterol in their blood;
And those who suffered the rare hereditary disease, familial hypercholesterolaemia (hereditary high blood cholesterol), also suffered a higher incidence of CHD.
And so, not unnaturally perhaps, cholesterol and heart disease became linked.
But there are a number of significant points that the cholesterol theory overlooks.
For example, there is a marked difference between the build-up found in those with familial hypercholesterolaemia and those with coronary heart disease:
Hypercholesterolaemia causes large deposits at the mouths of the coronary arteries, often leaving the arteries themselves unblocked, and so does not reproduce the type of obstruction found in coronary heart disease.
People with myxoedema or nephrosis also have high blood cholesterol levels - yet in them, there is no increase in the incidence of CHD.
Neither is raised blood cholesterol a predictor of CHD in people over sixty.
It has also long been known that simple events, such as putting a cuff around the arm prior to taking a blood sample, or fear of the needle, can result in raised cholesterol values.
And, even where these are avoided, large fluctuations are known with peak to nadir variations of as much as twenty-three percent.
Lastly, cholesterol is only one of the constituents of an atheroma and, if you think about it, cholesterol is so necessary and so widespread in the body, it would have been surprising if it had not been found.
Nevertheless the lowering of blood cholesterol became the sole objective in the fight against CHD;
And the two principal methods used to achieve this are with diet and drugs.
For example, there is a marked difference between the build-up found in those with familial hypercholesterolaemia and those with coronary heart disease:
Hypercholesterolaemia causes large deposits at the mouths of the coronary arteries, often leaving the arteries themselves unblocked, and so does not reproduce the type of obstruction found in coronary heart disease.
People with myxoedema or nephrosis also have high blood cholesterol levels - yet in them, there is no increase in the incidence of CHD.
Neither is raised blood cholesterol a predictor of CHD in people over sixty.
It has also long been known that simple events, such as putting a cuff around the arm prior to taking a blood sample, or fear of the needle, can result in raised cholesterol values.
And, even where these are avoided, large fluctuations are known with peak to nadir variations of as much as twenty-three percent.
Lastly, cholesterol is only one of the constituents of an atheroma and, if you think about it, cholesterol is so necessary and so widespread in the body, it would have been surprising if it had not been found.
Nevertheless the lowering of blood cholesterol became the sole objective in the fight against CHD;
And the two principal methods used to achieve this are with diet and drugs.
References:
J W Gofman, et al. The role of lipids and lipoproteins in atherosclerosis .
Science. 1950; 111: 166.
Science. 1950; 111: 166.
J P Strong, H C McGill jr. The natural history of coronary atherosclerosis.
Am J Pathol. 1962; 40: 37.
Am J Pathol. 1962; 40: 37.
W F Enos, R H Holmes, J Beyer. Coronary disease among United States soldiers killed in action in Korea. Preliminary report.
JAMA 1953; 152: 1090.
JAMA 1953; 152: 1090.
Update
Friday, July 25, 2008 9:21 AM
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