Although a staggering amount of money has been spent on research to conclusively prove the link between saturated fat, cholesterol and Coronary Heart Disease (CHD), there exists a massive volume of scientific evidence published in peer-reviewed journals that completely absolves dietary cholesterol, saturated fat and elevated blood cholesterol of any harmful role in CHD.

Despite the fact that this research, contradicting the orthodox hypothesis, has been published in prestigious journals for decades, and despite the complete failure of the massive low-fat, anti-cholesterol campaign to lower the overall incidence of CHD, the cholesterol/saturated fat theory of CHD enjoys almost unanimous acceptance among health authorities. And yet the amount of cholesterol formed by the liver is controlled according to the needs of the body. If dietary cholesterol is increased, a healthy liver responds by making less cholesterol. However, if the cholesterol in the diet is decreased, the liver makes more. In this way the body regulates how much cholesterol is produced for its needs.

Yet at the drop of a hat, no few cardiologists will convince unsuspecting patients that because they have "high cholesterol" they should be subjected to an angiogram -- a very expensive and not completely safe procedure in which a catheter is injected into an artery in the groin and then pushed all the way up through the aorta into the region of the heart, where dye is injected into the blood so that an X-ray machine can see if there might be any blood flow blockages (blockages that are caused by excessive homocysteine in the blood). Evidence suggests that high levels of homocysteine in the blood promotes atherosclerosis (fatty-cholesterol-plaque deposits in blood vessels) by damaging the inner lining of arteries thereby causing plaque build up at various points inside arteries, often near the heart. Fortunately, folic acid, in combination with vitamins B-6 and B-12, helps break down homocysteine in the body, as shown in several studies. Other studies show that low blood levels of folic acid are linked with a higher risk of fatal coronary heart disease and stroke.

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The cholesterol  heart disease myth and why it is promulgated

All the clinical studies cited below are referenced here.

Already in 1936, Kurt Lande and Walter Sperry concluded "After thorough and methodical post-mortem investigation in victims of heart attacks, it was clear that no relationship was evident. It is concluded that the incidence and severity of atherosclerosis are not directly affected by the level of cholesterol in the blood serum. (Archives of Pathology 1936;22)

In 1961, researchers studied the levels of cholesterol and the degree of atherosclerosis seen at autopsy. No correlation could be observed between the blood cholesterol levels and the amount or severity of atherosclerotic plaque within the arteries  cholesterol levels, whether high or low, had no impact on the growth of atherosclerotic plaque, the major cause of Coronary Artery Disease (CAD). (Mathur et al 1961;Circulation: 23)

In 1962 autopsy studies by Polish researchers found that 2/3 of those who died from confirmed CAD, had serum cholesterol in normal to low ranges. They could find no correlation between blood cholesterol content and the cholesterol content of arterial plaque. (Marek et al 1962; American Heart Journal). Subsequent autopsy studies from the USA and Gautemala confirmed these findings.

Utilising EBCT technology, researchers at the Beth Israel Medical Centre in New York set out to determine if increased cholesterol levels, specifically LDL cholesterol, led to plaque build up. Looking at 182 individuals who may develop CAD, over 1-2 years of treatment with cholesterol lowering drugs, it was discovered that despite lower cholesterol levels there were ZERO differences in the development of atherosclerotic plaque. The researchers concluded "with respect to LDL cholesterol-lowering, 'lower is better' is not supported by changes in calcified plague progression." (American J. of Cardiology 2003; 92:3)

Human atherosclerotic plaque has all the hallmarks of an inflammatory response to infection, and there is considerable evidence to support such an etiology. For many years scientists have suspected that viruses and bacteria, in particular cytomegalovirus and Clamydia pneumonia participate in the development of artherosclerosis. A protein secreted by the liver during infection, named C-reactive protein, is a much stronger risk factor for CHD than cholesterol. Research within this area has exploded during the last decade, and by 2004, at least 200 reviews of this issue have been published in medical journals.

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