This is a truly impressive doctor and researcher; Dr Uffe Ravnskov is a doctor (MD in 1961, University of Copenhagen) and independent researcher (PhD in 1973, University of Lund) and a specialist in Internal Medicine and Nephrology. He has literally published a zillion of articles, scientific papers about cholesterol and cardiovascular disease and has been awarded many times in his life for his contribution to innovative medical research. For me Dr Ravnskov is another pioneer of medicine. He has the courage to go against the erroneous but yet popular cholesterol theory for atherosclerosis.
Dr Ravnskov has published an impressive amount of work where he knocks down one by one all the myths concerning this hot matter: whether cholesterol and fats are responsible for heart attacks and atherosclerosis more specifically. He has a solid background in biochemistry and internal medicine; also his medical knowledge allows him to review from a doctor’s perspective many publications that never make it to the front cover just because they inconveniently prove that the cholesterol myth is completely inconsistent. In his website you will find so much information about this subject; I truly encourage you to take a look.
Dr Ravnskov is straight to the point: cholesterol is certainly not responsible but on the contrary people with elevated cholesterol were found to live more years than people deprived of dietary fat. That’s a bold statement to make but research shows exactly that. As I said you won’t find these publications in any front page as they completely go against the most popular and pharma supported official cholesterol model for heart disease. Also, he knocks down the myth that the levels of blood cholesterol are correlated in any way with the level of atherosclerosis found in a patient’s arteries. He explains why cholesterol is necessary for the human (and all mammals really) body, a basic piece of info that most doctors and researchers seem to dismiss after their first undergraduate year in university.
In his own words: “One of the most surprising facts about cholesterol is that there is no relationship between the blood cholesterol level and the degree of atherosclerosis in the vessels. If a high cholesterol really did promote atherosclerosis, then people with a high cholesterol should evidently be more atherosclerotic than people with a low. But it isn´t so.
The pathologist Dr. Kurt Landé and the biochemist Dr. Warren Sperry at the Department of Forensic Medicine of New York University were the first to study that question. The year was 1936. To their surprise, they found absolutely no correlation between the amount of cholesterol in the blood and the degree of atherosclerosis in the arteries of a large number of individuals who had died violently. In age group after age group their diagrams looked like the starry sky.
Drs. Landé and Sperry are never mentioned by the proponents of the diet-heart idea, or they misquote them and claim that they found a connection or they ignore their results by arguing that cholesterol values in the dead are not identical with those in living people.
That problem was solved by Dr. J. C. Paterson from London, Canada and his team. For many years they followed about 800 war veterans. Over the years, Dr. Paterson and his coworkers regularly analyzed blood samples from these veterans. Because they restricted their study to veterans who had died between the ages of sixty and seventy, the scientists were informed about the cholesterol level over a large part of the time when atherosclerosis normally develops.
Dr. Paterson and his colleagues did not find any connection either between the degree of atherosclerosis and the blood cholesterol level; those who had had low cholesterol were just as atherosclerotic when they died as those who had had high cholesterol. ”
Dr Ravnskov also explains what statins are and gives plenty of information about how they actually work and why they are the wrong drug for atherosclerosis although contradicting data may show that they have some cardioprotective effect.
“A new type of cholesterol-lowering drugs, the so-called statins (for instance Zocor® and Pravachol®) have been succesful. For the first time cholesterol-lowering have shown significant improvement of mortality, both coronary mortality, stroke mortality and total mortality. These trials are therefore considered as strong arguments for the idea, that a high cholesterol is dangerous.
Have these trials really demonstrated that raised LDL cholesterol has importance for coronary heart disease, as the trial directors concluded in the reports?
There is reason to question that, because some of the results are not consistent with what we have learned about cholesterol.
First, old patients were protected from cardiovascular disease just as much (or as little) as young ones, although most studies have shown that a high cholesterol is a weak risk factor, or no risk factor at all, for old people. (Unfortunately, in the only trial that included old people only, the PROSPER trial, the lowering of heart mortality was smaller than the increase of cancer mortality).
Second, also the number of strokes was reduced after statin treatment, although no studies have shown that a high cholesterol is a risk factor for stroke.
Third, patients who had had a coronary were protected although most studies have shown that a high cholesterol is a weak risk factor, if any at all, for those who already have had a coronary. (In fact, this finding should have stopped all the previous, secondary preventive trials).
And finally, the statins protected against coronary heart disease whether the cholesterol was high or low although most studies have shown that a normal or low cholesterol is no risk factor for coronary disease.
How come that the statins are effective for old people, for patients who already have had a coronary, and even for those whose cholesterol is normal? If the cholesterol level for these people is no risk factor for coronary disease, how could a lowering of that cholesterol improve their chances to avoid a coronary? The only reasonable explanation is that the statins do more than just lower cholesterol. There is much evidence for that.
The statins inhibit the body’s production of a substance called mevalonate, which is a precursor of cholesterol. When the production of mevalonate goes down, less cholesterol is produced by the cells and thus blood cholesterol goes down as well. But mevalonate is a precursor of other substances also, substances with important biologic functions. The metabolic pathways are not known in all details, but less mevalonate may explain why simvastatin makes smooth muscle cells less active and platelets less inclined to produce thromboxane. One of the first steps in arteriosclerosis is the growth and migration of smooth muscle cells inside the artery walls; and thromboxane is a substance which promotes the clogging of blood. Thus, by blocking the function of smooth muscle cells and platelets, simvastatin may benefit cardiovascular disease by at least two mechanisms and both of these mechanisms are independent of the cholesterol level. In fact, up till now we have learned about eleven anti-atherosclerotic effects of statin treatment that have been found independent on their effect on cholesterol.”






