High cholesterol may protect against infections and atherosclerosis

High cholesterol may protect against infections and atherosclerosis. High cholesterol predicts longevity rather than mortality in old people. It’s role in cardiovascular events must be trivial.
  • Excerpt

“High cholesterol may protect against infections and atherosclerosis” is the title of a challenging article written by the Danish physician and medical researcher Uffe Ravnskov. He is one of the world’s leading critics of the idea that cholesterol causes cardiovascular disease and that high to medium levels of cholesterol must be lowered by a daily dosage of statins. Based on numerous scientific studies, Ravnskov declares that high cholesterol predicts longevity rather than mortality in old people, which strongly suggests that cholesterol’s role in cardiovascular events must be trivial.

Table of contents

During several decades, now, we have been over-exposed to the dogma that cholesterol is a villainous and dangerous substance that must be avoided and “lowered,” even though 85% of the cholesterol we have in our body is continually produced by the body itself, in the liver. Year after year, the medical “standard” of what is an acceptable or risk-free level of cholesterol is arbitrarily lowered, so that more and more people will fall into the category of otherwise healthy “patients” to whom statins must be prescribed. All of a sudden, your doctor may tell you: “Better begin today than wait until tomorrow, because you are at risk !” Health pundits, doctors and researchers who, like Dr. Ravnskov, openly doubt the mainstream cholesterol ideology and the need for statins are being accused of putting millions of people at great risk. They must deal with being ridiculed, shut up, silenced, convicted and banned.

Well, to distinguish facts from propaganda, let the outcomes of well-performed clinical and scientific research be our judge. Not the propaganda disseminated by the paid servants of the statin-industry. In much of the research that is used by the pharmaceutical industry we encounter little or no mention of what medicines actually do to influence what should be their essential effect: prolonging a healthy life. In cases of mortal diseases, isn’t longevity what most people are, or should be, interested in ?! To be precise, we should always look for the percentage of the patients who survive due to taking a medicine compared to the percentage that survives without taking it !! Nothing other than that will show us the absolute benefit of a medicine. But quite often, the pharmaceutical industry uses a statistic sleight of hand to misrepresent marginal and negligible absolute benefits of certain medicines by framing the results in terms of “relative risk” or “relative benefit.” See my previous article Masquelier’s OPCs versus Aspirin® - Relative and Absolute Benefits.

According to the studies cited by Ravnskov in High cholesterol may protect against infections and atherosclerosis, a high level of cholesterol plays a “key role in the immune defence system. There is also a growing understanding that an inflammatory response of the arterial intima to injury is a crucial step in the genesis of atherosclerosis and that infections may be one type of such injury.” The arterial intima is the inner part of the vascular wall that is in contact with the blood. It’s role in atherosclerosis was explained in a previous article: Narrow Pipes, High Pressure and Vascular “Tumors.” Stress, deficient nutrition, poisons (alcohol, nicotine, drugs) and free radicals actually wound the inner layer of the arterial wall. When this wounding action is severe and long lasting, the organism has to react with a powerful over-healing effort, the multiplication of the media-muscle-cells. This vascular “tumor,” also known as “proliferative lesion,” attracts all sorts of fortifying agents such as fats, fiber-like collagen and cholesterol to form a solid plaster.

Most certainly, cholesterol is involved in atherosclerosis, but the question is whether a high level of cholesterol causes coronary heart disease. Since cholesterol supports the immune system, so says Ravnskov, it does not cause, but mitigates the process of atherosclerosis. To support his viewpoints, he cites a scientific assessment ‒ meta­analysis ‒ of 19 studies including 68.406 deaths. A correlation was found between low total cholesterol and mortality from respiratory and gastrointestinal diseases, most of which are of an infectious origin. Also, in a 15 year follow-up study of more than 120.000 individuals, researchers found a strong association between low total cholesterol and the risk of being admitted to hospital due to an infectious disease. Significant relationships were found between low total cholesterol and urinary tract infections, all kinds of viral infections in women, and musculo-skeletal infections and skin- and subcutaneous infections in men. In a similar study of more than 100.000 individuals followed for 15 years, a strong association was found between low cholesterol and the risk of being admitted to hospital because of pneumonia or  influenza, though not for chronic, obstructive pulmonary disease (COPD) or asthma.

In his article, Ravnskov makes an interesting observation. Admitting that pathological findings similar to those seen in people with a familiarly determined high level of cholesterol have been produced in experimental animal models, he notes that these pathological changes “are not identical with human atherosclerosis, and no experiment has hitherto succeeded in producing a heart attack in an animal by hypercholesterolemia alone. Besides, these experimental changes cannot be produced by pure cholesterol, but very easily by its oxidation products, and it appears that most studies of experimental atherosclerosis have had little control over the purity of the dietary cholesterol.” His conclusion boils down to the proposition that atherosclerosis is caused by the direct stimulation of the endothelium by a number of factors, including smoking, the metabolic consequences of diabetes, an overload of homocystein and iron overload, a deficiency in copper, micro-organisms and oxidized cholesterol.

“There is much evidence to support roles for these factors,” says Ravnskov, “but the degree to which each of them participates remains uncertain.” Yes, when framed in terms of the degree to which each of these factors play a role in atherosclerosis, one might say that there exists uncertainty about how each of them participates in the process. However, it is very certain that all these challenges do play a role in the onset and development of cardiovascular disease. Likewise, it is also very certain that compounds such as Masquelier’s OPCs have been shown to have a beneficial effect on cardiovascular health, not in the least because they prohibit or mitigate the oxidation of cholesterol. I have extensively written about OPCs and cholesterol in OPCs, Dr. Jack Masquelier’s Mark on Health. Perhaps, it can help you find your way in the cholesterol “jungle.”

Hyperlinks: https://www.masqueliersopcs.com/en/news/dr-masquelier-cholesterol-and-opc