86Thousand400: Fat Vs Heart Attacks

- The false idea that we should eat less saturated fat came from Ancel Keys

- We now know that saturated fat is unrelated to heart disease risk in individuals. Instead any relationship appears to be the reverse of what Keys supposedly found

- Keys' failed "plumbing model" of heart disease has proved too simple to be true

- Cholesterol is one of the most critical chemicals in the body and humans could not survive without it. Without cholesterol, human life is impossible. To provide its life-sustaining actions, cholesterol is transported to all the body's cells to supplement the cholesterol that each produces for its survival

- The first challenge to Keys' theory arose when early epidiological studies showed that those with higher concentrations of one form of cholesterol, HDL-cholesterol, had a lower, not a higher risk for developing heart disease. (Disturbing find)

- Soon "experts" came up with a simple explanation. Cholesterol would be classified as either "good" or "bad". (HDL - Good, LDL - Bad)

- Simplistic interpretation "artery clogging" LDL-cholesterol is the "bad" form in which cholesterol is produced by the liver and then transported to the arteries where it is free to do its "artery clogging" damage. In contrast the "good" HDL cholesterol removes some of the cholesterol from the arteries and returns it to the liver (where it can immediately be turned back into "artery clogging" LDL-cholesterol to be returned to the arteries in order to repeat the endless process of arterial damage and disease promotion

- The illogic of this explanation of how HDL-cholesterol can be "good" seems to have escaped the attention of those who prefer this explanation

- Cholesterol is neither "good" nor "bad". It is just cholesterol

- The truth is that cholesterol does not even exist in the blood as a fat. Instead cholesterol is insoluble in water (and blood) because it is a fat. So it can be transported in the blood only in a water-soluble form. This is achieved by covering the cholesterol with a protein lining. In this way cholesterol in the blood is in fact a protein, not a fat. The technical term is that cholesterol is transported in the blood as a class of proteins known as lipoproteins. Certain lipoproteins are indeed linked to an increased risk of heart disease and so some lipoproteins are indeed "bad"

- Only when we understand the contribution of the different lipoproteins to our risk of developing arterial damage and heart disease can we begin to understand which diet will ensure our optimum health and minimise our risk of developing heart disease

- It is biologically impossible for humans to convert saturated fat into "bad" LDL-cholesterol

- Keys' explanation that saturated fat causes heart disease by increasing LDL-cholesterol production should have been thrown out as a biological impossibility in the 1950s

- Instead it continues as the dominant teaching, because the pharmaceutical industry determines what is taught about heart disease in medical schools. Since cholesterol-lowering (statin) drugs are one of the most profitable groups of the pharmaceutical agents, the industry has no appetite for anything other than the simplistic "plumbing" model of heart disease should be taught to medical students of believed by all medical doctors

- "Bad" lipoproteins as well as all other risk factors for heart disease are affected to a far greater extent by the carbohydrate than by the fat content of the diet

If Fat's not to blame. What is?

- If bad cholesterol is not the direct cause of arterial damage and heart disease, then why is cholesterol found in diseased arteries?

- The alternate explanation is that arteries are damaged by the entry of only one form of lipoprotein, the small, dense LDL-cholesterol particles, and then only if those small, dense LDL-cholesterol particles have been damaged by becoming oxidised. It is proposed that oxidised small, dense LDL-cholesterol particles have the ability to enter damaged arteries where they become "stuck" within the arterial wall, inducing an inflammatory reaction that leads ultimately to the irreversible arterial damage recognised as arterial plaque