The idea that fat and cholesterol cause heart disease has never been shown; indeed enormous numbers of scientists and medical personnel have disputed this theory since its inception in the mid - 1950’s. Without doubt, this idea is wrong, as has been proved in many detailed analyses. Just go to Google and type in “cholesterol myths” and you will have enough information to see what I am talking about.
The early evidence implicating disturbances in carbohydrate metabolism as a primary cause of heart disease arose from studies of diabetes. Observations of Type 1 diabetics whose lives were saved by insulin treatment showed that there was a dark side to insulin therapy. The replacement of the missing hormone seems also to have harmful effects, an understanding of which is instructive to anti - aging research involves replacing age - reduced production of vital hormones such as growth hormone, DHEA (an adrenal gland hormone), and estrogen.
The clinical evidence linking excess insulin levels to heart disease came from mid - 1960’s studies of non - diabetics. The discovery came only 10 years after the mid - 1950’s notion (myth) that fat and cholesterol were the causes of heart disease. Unfortunately, the fat and cholesterol juggernaut was fully - flowered by this time and the connection of insulin to heart disease was ignored.
Heart disease is primarily a disease of modern industrialized countries. A common characteristic of developed nations is an abundant, continuous supply of food and a lack of physical activity. Also common is the fact that this food supply is high in carbohydrates. The idea that “well - fed” people produce more insulin and more cholesterol is well establishes. Blood triglycerides are a product of fat production in a well - fed liver by the conversion of ingested carbohydrates.
Glycated proteins permanently glued into the vessel walls of the heart and vascular system are characteristic of glucose - consuming humans. They form cross - links among one another and trap cholesterol, a trapping effect that increases relative to the amount of cross - linking that’s present. Cholesterol trapping in vessel walls is, of course, directly proportional to increases in cholesterol levels, a response that’s also directly proportional to exposure to glucose and insulin in the liver.
Current theories argue that heart disease occurs because of an accumulation of fat in the vessel walls and also because of the growth of smooth muscle cells. Recent studies shed new light on the mechanisms of vessel wall fat, cholesterol accumulation and smooth muscle cell proliferation and growth. These processes, it seems, derive entirely from the process of Glycation- arising from exposure to glucose and insulin, which have their source solely in the consumption of carbohydrates.
And high levels of blood cholesterol are not the problem. This has been known from the start of the 'coronary epidemic'. For example:
"Blood cholesterol values are not found to be high in our adult cases who show arteriosclerosis. The group with the lowest average cholesterol is the group with the greatest arteriosclerosis. Neither can the cholesterol values in our series be definitely correlated with any impending or existing arteriosclerotic process."
That was in 1930. Nothing has changed since then to nullify that finding.
(Joslin EP. Arteriosclerosis in Diabetes. Ann Int Med 1930; 4:54-66)