In the 1950’s, researchers came up with the “lipid hypothesis” that claim a direct relationship between the amount of saturated and cholesterol in our diet and the incidence of coronary heart disease.
Proponents of the “lipid hypothesis” claim that when our intake of cholesterol and saturated fat is high, the saturated fat is turned into cholesterol which accumulates in the arteries. This is called atherosclerosis. These deposits of cholesterol gets thicker, form a plague, and eventually breaks off and form a blood clot in a vessel triggering a stroke or heart attack. This is what the medical community believed for many years, and it is still what the majority of the public believes. This is a too simplistic view.
Scientist have since discovered that at every stage of atherosclerosis - from the start to the stage to where plague breaks off and cause a heart attack - inflammation is involved. Inflammation is the way our body reacts to injury. When a part of our body is inflammed, it becomes red, swollen and we cannot move it properly e.g. a sprain ankle. Inflammation can also occur inside our body and and we usually do not know it when it happens.
Inflammation can trigger the release of subtances into our bloodstream that can damage the inner lining of arteries. Cholesterol has a healing ability and it puts a large amount of it over the damage area. Over time as more cholesterol accumulates, the plague grows and our arteries narrow.
New research shows that an elevated level of C-Reactive Protein (CRP) and Homocysteine promotes inflamation in our bodies and are a major risk factor for heart disease, possibly much more than high cholesterol levels. The studies shows that those with high level of CRP are more likely to have a heart attack or stroke than those with a high level of LDL or Bad cholesterol!
Recent studies have also shown that high CRP levels increase the chance of an artery re-closing after it has been opened by baloon angioplasty.
High level of CRP is likely due to allegies, an autoimmune disease, infections, obesity, diabetes, consuming transfat, a diet high in sugar and refined carbohydrates, cigarette smoking and a lack of anti-oxidant. An elevated level of homocysteine is likely due to inadequate intake of folic acid, vitamin B6 or B12, stress, excessive coffee drinking, use of oral contraceptive, impaired kidney or a genetic defect.
While a high level of LDL cholesterol has always been thought of as the bad guy of atherosclerosis that leads to heart disease, other factors such as high blood pressure, cigarette smoking, diabetes, infections, allergies, consuming trans fatty acids, sugar, refined carbohydrates, high glycemic food and other factors that promote inflammation cannot be ignored.
The aim is not just to lower LDL cholesterol but rather in the first place to prevent damage to the artery wall. Cholesterol only deposit itself on damaged artery wall - for the purpose of repair. It does not deposit itself on healthy, smooth blood vessels.