Cholesterol Myths Update

Cardiovascular Care

Jan 13
Red Tree looks like a heart

What are “normal” cholesterol levels? Before the invention of cholesterol lowering drugs, a total cholesterol level of 300 was considered normal.

Since the mid-fifties when television (the newest way to advertise) was in its infancy, the “lipid hypothesis” hit the airways. It was big news. Eat fat and fat will build up in your arteries and you’ll either stroke out or have a massive heart attack mowing your lawn. It made perfect sense.

This conclusion was not, however, universal. We knew that CVD (cardiovascular disease) was a killer; it was the number one killer throughout most of the world. But many doubted this conclusion; that fats clogged our blood vessels just because they existed.

High cholesterol was associated with CVD, but one side said cholesterol was the cause of CVD and the other asked, what if it’s the result of CVD?

We were so concerned about this number one killer that the Framingham Study was begun in 1948.

On the Framingham’s list of Research Milestones, we see that in 1961 when they connected cholesterol levels to the other risk factors:

By the late sixties, researchers were creating tests to determine lipid values in the blood. In 1974, a group discovered a method of measuring serum cholesterol, triglycerides, and LDL:

Abstract: A method for estimating the cholesterol content of the serum low-density lipoprotein fraction (Sf0-20) is presented. The method involves measurements of fasting plasma total cholesterol, triglyceride, and high-density lipoprotein cholesterol concentrations, none of which requires the use of the preparative ultracentrifuge. Comparison of this suggested procedure with the more direct procedure, in which the ultracentrifuge is used, yielded correlation coefficients of .94 to .99, depending on the patient population compared. [Ref]

Meanwhile, in 1971, both JAMA and the Annals of Internal Medicine published  articles reflecting Framingham’s findings, which were that cholesterol was a risk factor, and that “Risk of coronary heart disease in men can be estimated using any of the lipids evaluated: however, none proved more useful than an accurate total serum cholesterol.”

But by 1978 it was confirmed that lowering cholesterol did not decrease heart disease nor did it prevent premature death.

PREVENTION of premature vascular disease is the major goal in the treatment of hyperlipemia. Epidemiologic studies provide convincing evidence that hypercholesterolemia is a major risk factor for coronary heart disease (CHD).1 In fact, clinical manifestations of CHD parallel the serum cholesterol levels even within the “normal range” of serum cholesterol. Although no studies have proved that reduction of serum cholesterol levels decreases CHD or increases longevity, the overwhelming evidence linking hypercholesterolemia with premature CHD suggests that we should initiate efforts to lower serum cholesterol levels while we await final proof of beneficial effects. [Ref]

Did you catch that last part? “. . . we should initiate efforts to lower serum cholesterol levels while we await final proof of beneficial effects.” This is utterly amazing. The assumption is that the result of lowering serum cholesterol will be beneficial. Since when has medical intervention always proved to be beneficial? Is there no one to worry that lowering cholesterol levels could be harmful?

The very next year, 1979, the “mind-set” that had carried everyone this far was blown apart by a little discovery concerning the difference between LDL and HDL:

Prospective data at Framingham and elsewhere have shown conclusively that risk of coronary heart disease in persons younger than age 50 is strikingly related to the serum total cholesterol level. Within so-called normal limits risk has been found to mount over a five-fold range. The impact has been found to be augmented by other risk factors. The contribution of the serum total cholesterol to risk has also been found to be determined by its partition in the various lipoprotein fractions. A relatively large amount of cholesterol in the low-density lipoprotein fraction is atherogenic, whereas that in the high-density fraction appears protective. The independent contribution of very-low-density lipoprotein and its triglyceride or cholesterol content has, on the other hand, not been established. The previous position that virtually all of the lipid information pertaining to coronary heart disease resided in the serum total cholesterol must be accordingly modified. [Ref]

What they did not know back then, and even refuse to admit now, is that LDL is not atherogenic (meaning,  promoting the formation of fatty plaques in the arteries) in itself, but lays down a layer where the blood vessel has been damaged by cardiovascular disease already. In other words, LDL is patching a spot where damage exists already (as we point out in our first cardiovascular article, The Heart of the Matter).  It is CVD that promotes the formation of fatty plaques and it is oxidation that forms calcified plaques.

A few related things were going on during this early period of cholesterol investigations. A government committee, often referred to as the McGovern Committee, started up in 1968. Its job was to come up with some healthy nutritional standards; the first time our nearly 200 year old government got involved in nutrition. And a year earlier, 1967, the sugar industry [Sugar Association] paid three Harvard scientists to lie to the American public and blame FAT on heart disease without ever mentioning sugar. [How the Sugar Industry Shifted Blame to Fat]

The McGovern Committee issued its findings in 1977:

  • Increase consumption of “complex carbohydrates” and “naturally occurring sugars;” and
  • Reduce consumption of refined and processed sugars, total fat, saturated fat, cholesterol, and sodium. [2015 Dietary Guidelines Advisory Committee]

As you can see from these recommendations, our government had bought into the utterly unscientific “lipid hypothesis” developed by Ancel Keys in his highly flawed Seven Countries Study.

First the American Heart Association bought into the lipid hypothesis in 1956 when television in America was just taking off. They flooded the airwaves with their recommendations, and by the time McGovern started up his committee, he and his colleagues had bought the hypothesis, lock, stock, and barrel of lard.

It was a simple idea: if you eat fat, you’ll get fat in your arteries, which causes heart disease. It was so simple that people who knew nothing about science could understand it. The trouble is this: it was unscientific. [Who Is the Father of Preventive Medicine?]

Looking back, we can see that this was the start of the low-fat craze that put mega-tons of weight on the American public, initiating the fastest growth in metabolic disorders in the history of earth. Metabolic Disorder is what we have called The Disease of Our Time.

What we have at this point in history, the late seventies and early eighties, is an accepted concept that high cholesterol, especially high LDL, contributes to heart disease, and intake of fatty foods increases our cholesterol levels.

This is pure bullshit and those who know it’s bullshit started pulling their hair out trying to tell the public that they’ve been handed a pile of bullshit.

For example, if this was even close to the truth, not eating cholesterol (saturated fats) would keep one’s cholesterol numbers down; it doesn’t; and lowering cholesterol levels with drugs would prevent heart attacks; it doesn’t.

From our advisor’s web site, The Cholesterol Myths, we found this:

Counting money and counting food

Even in the early 1950’s the Framingham study included dietary analyses. Almost one thousand individuals were ques­tioned in detail about their eating habits. No connection was found between the composition of the food and the cholesterol level of the blood. Wrote Drs. William Kannel and Tavia Gordon, authors of the report: These findings suggest a cautionary note with respect to hypotheses relating diet to serum cholesterol levels. There is a considerable range of serum cholesterol levels within the Framingham Study Group. Something explains this inter-indivi­dual variation, but it is not the diet.

The Framingham study initially published a connection between dietary fats and cholesterol levels, but after gathering more and more data, they retracted their earlier pronouncements and realized there were other factors affecting these levels. The medical industrial complex apparently didn’t get the memo, because there were some really horrible studies being conducted that disagreed with the folks up in Boston (23 miles from Framingham). From Scientific American we get the following:

Despite the rejection of the lipid hypothesis by several “old-schoolers,” many scientists and physicians began to see the link between blood cholesterol and human health. But, even more brazen was the idea that negative health effects stemming from high cholesterol could be treated and reversed. In the early 1950s, research from the laboratories of Laurance Kinsell (Institute for Metabolic Research, Highland General Hospital) and Edward H. Ahrens (The Rockefeller University) concluded that eliminating dietary saturated fats and replacing them with unsaturated fats has a profound effect on reducing blood cholesterol. This finding was strengthened by the results of three pre-1970s clinical studies: The Paul Leren Oslo Study (1966); The Wadsworth Veterans Administration Hospital Study (1969); and The Finnish Mental Hospitals Study (1968). [Ref]

Need I tell you that all this research has been debunked and the findings are now generally ignored?

Research into Statin drugs (cholesterol lowering drugs) began in the early seventies. In his book, The Cholesterol Wars: The Skeptics vs. The Preponderance of Evidence, Daniel Steinberg tells us that the Coronary Primary Prevention Trial of 1984 demonstrated that lowering cholesterol could significantly reduce the risk of heart attacks and angina. He then added that physicians were largely unconvinced. [Steinberg, Daniel. The Cholesterol Wars: The Skeptics vs. The Preponderance of Evidence. Academic Press, 2007.]

One of them was a local Minnesota physician by the name of Dr. Robert E. Olson who said: “Even bright, intelligent people are now so brainwashed they think one egg will go straight to the heart.” In an interview published JUNE 16, 1980, he said, “What has been shown is that a high level of serum cholesterol in the blood can lead to coronary heart disease. But there’s no clear-cut evidence that reducing blood levels of cholesterol by changes in diet can prevent coronary disease. The human body needs cholesterol. It’s manufactured by the liver and is essential to producing certain hormones.”

This is Dr Uffe Ravnskov, our advisor’s, learned opinion too; that people with high cholesterol could be having heart attacks, but it wasn’t their cholesterol that was causing them. In fact, the high cholesterol might just be trying to stop the heart disease.

Sugar NOT Cholesterol is the Culprit

Five decades of “suppressed” studies out of Harvard show us that sugar is inflammatory, and inflammation is the culprit behind heart disease. Interestingly enough, cholesterol is anti-inflammatory. Could it be helping and hurting at the same time? I kinda doubt it.

Here is a paper by our advisors, Dr Uffe Ravnskov, MD, PhD, the author of the infamous book, The Cholesterol Myths (you can read the book online). He sent me this article after I had done some research on lipids and wrote to him asking if it was possible that cholesterol was an anti-inflammatory. He told me that I had hit upon something, and yes, and here’s this article: High cholesterol may protect against infections and atherosclerosis.

Cholesterol has a purpose in the human body. It’s part of every cell membrane. It’s part of the brain. Here’s a quotation from our first article entitled The Cholesterol Myths:

The connection between heart disease and high cholesterol levels is not causal (high cholesterol does not cause heart disease) but rather high cholesterol can be an indicating factor that your arteries are undernourished and need repairing. 

But in the seventies and eighties, pharmaceutical companies were clamoring to get a drug to market that lowered cholesterol. And right away we saw that lowering cholesterol was a joke. From an article published in JAMA 1987 [Anderson KM, Castelli WP, Levy D. Cholesterol and mortality. 30 years of follow-up from the Framingham study. JAMA 1987;257:2176-2180] Ravnskov writes:

It is not true either, that cholesterol has a strong power to predict the risk of a heart attack in men above 65. In the 30 year follow-up of the Framingham population for instance, high cholesterol was not predictive at all after the age of forty-seven, and those whose cholesterol went down had the highest risk of having a heart attack! To cite the Framingham authors: “For each 1 mg/dl drop of cholesterol there was an 11 % increase in coronary and total mortality.”

On top of that, low cholesterol increases risk of cancer:

Many cohort studies have found that low cholesterol is a risk factor for cancer. The usual explanation is that cancer causes low cholesterol because cholesterol is consumed by the cancer cells. However, in the Framingham project low cholesterol was a risk factor for cancer even after 18 years of follow-up [167], and as mentioned, cancer mortality in people with FH (Familial Hypercholesterolemia) is lower than in the general population. Many observations are also in better accord with the opposite interpretation that low cholesterol predisposes to cancer.

There are more fatal drawbacks from lowering cholesterol artificially, but now we come to the purpose, the raison d’être of this article and why, in April of 2017 it is important to get this information out.

The first formal cholesterol guidelines were introduced in 1989 [Cholesterol guidelines, lipoprotein cholesterol levels, and triglyceride levels: potential for misclassification of coronary heart disease risk.], and formally adopted by 1993.

Since then, they’ve been modified nearly enough to make every human being a patient requiring medication.

The image above is from the year 2001-2002. Those were the guidelines. Since heart attack rates weren’t significantly lowered at those guidelines, they’ve been lowered again.

Today, 2017, normal LDL levels are at about 70 mg per dL, although some professor out of Harvard Medical School wants them at 50.

Why is this? Why would anyone call for out LDL levels to be lower than they’ve ever been before? Because people who have these so-called “normal” levels are dying of heart attacks.

Please note: These levels are abnormal. They have been achieved with drugs. The human body is supposed to have much higher cholesterol levels.

However, the thinking is thus: If your levels are low and people are still dying of heart attacks, we must lower them even more.

In this article: Minneapolis study finds most major heart attacks occur in people with normal cholesterol [April 2017] you will find the most recent guidelines for cholesterol won’t save you from a massive heart attack. So? What’s the solution?

“Lower the guidelines even further,” seems to be the solution. But this is insanity. Our heart attack rates have never been as high as they are today, and long ago people didn’t care about cholesterol.

And here we have an advertisement for Lipitor. I’ve blown up part of it to show you that … well, take a look yourself.


You see the really hysterical thing about all these studies by people who want us all to take Statin drugs is that, having manipulated the methodologies and statistics, they concluded that lowering LDL reduced the risk of heart attacks. On top of that they ignored other factors. The overall incidence of death on these drugs was never a consideration. It didn’t matter that people were committing suicide at higher than normal rates; it didn’t matter that people were being diagnosed with cancer (that’s a whole nother disease); and it didn’t matter that cholesterol is needed in the brain for proper brain biology, and that Statin drugs might just be affecting the brains of those taking these drugs.

And the really interesting thing about the Minnesota study is the word “normal.” What the hell are “normal” cholesterol levels according to the experts? They certainly aren’t the normal levels in human beings all over the planet.

Allow me to let you in on this so-called normal as far as this Minnesota study went: All of the people in the study had experienced and survived a STEMI, a ST-Elevation Myocardial Infarction, meaning a major artery had been blocked; something that happens (or is supposed to happen) when LDL cholesterol levels are high.

All of these people had “normal” cholesterol levels, or levels within the guidelines. In fact, 79% of the group met the newer, the tougher guidelines, while the rest met those older guidelines.

Lowering cholesterol levels with drugs does nothing except make a lot of money. Got that?

And if you want to save your life, here is our advisor Dr Uffe Ravnskov’s own words to us in an email:

If high LDL were the cause of atherosclerosis and coronary heart disease, those with the lowest values should live the longest, but it is just the opposite.  In a recent study we found that people above the age of 60 with the highest LDL-cholesterol live the longest! And remember that more than 95% of those who die from a heart attack are older than 60 years.

This is the purpose of this paper: Lowering cholesterol levels will do nothing to protect you from a heart attack or stroke.

An interesting study to read is the following in which everything conventional medicine knows about saturated fats is disproven (mainly because medicine, unlike the science of nutrition, seems to think all saturated fats are the same).

Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies:

Abstract: Two populations of Polynesians living on atolls near the equator provide an opportunity to investigate the relative effects of saturated fat and dietary cholesterol in determining serum cholesterol levels. The habitual diets of the toll dwellers from both Pukapuka and Tokelau are high in saturated fat but low in dietary cholesterol and sucrose. Coconut is the chief source of energy for both groups. Tokelauans obtain a much higher percentage of energy from coconut than the Pukapukans, 63% compared with 34%, so their intake of saturated fat is higher. The serum cholesterol levels are 35 to 40 mg higher in Tokelauans than in Pukapukans. These major differences in serum cholesterol levels are considered to be due to the higher saturated fat intake of the Tokelauans. Analysis of a variety of food samples, and human fat biopsies show a high lauric (12:0) and myristic (14:0) content. Vascular disease is uncommon in both populations and there is no evidence of the high saturated fat intake having a harmful effect in these populations. [Copyright © 1981 by The American Society for Clinical Nutrition, Inc]

We’ve been warned for decades that saturated fat is deadly and it is not. That is a horrible lie that has caused damage and ruined lives.

So, I will leave you with a link to a very important paper called The Skinny on Fats. This is good reading and it will tell you just how far off modern medicine really is when it comes to fats, nutrition, and cardiovascular disease.

The Skinny on Fats

Here is a must-see video.