For the past six decades, the U.S. dietary advice has warned against eating cholesterol-rich foods, claiming dietary cholesterol promotes arterial plaque formation that leads to heart disease. We now have overwhelming evidence to the contrary, yet dogmatic thinking can be persistent, to say the least.
After decades’ worth of research failed to demonstrate a correlation between dietary cholesterol and heart disease, the 2015-2020 Dietary Guidelines for Americans1,2 finally addressed this scientific shortcoming, announcing “cholesterol is not considered a nutrient of concern for overconsumption.”
To this day, the evidence keeps mounting, showing there’s no link between the two. Similarly, the evidence supporting the use of cholesterol-lowering statin drugs to lower your risk of heart disease is slim to none, and is likely little more than the manufactured work of statin makers — at least that’s the implied conclusion of a scientific review3 published in the Expert Review of Clinical Pharmacology in 2018.
Cholesterol myth kept alive by statin advocates?
The 2018 review4 identified significant flaws in three recent studies “published by statin advocates” attempting “to validate the current dogma.” The paper presents substantial evidence that total cholesterol and low-density lipoprotein (LDL) cholesterol levels are not an indication of heart disease risk, and that statin treatment is of “doubtful benefit” as a form of primary prevention for this reason. According to the authors:5
“According to the British-Austrian philosopher Karl Popper, a theory in the empirical sciences can never be proven, but it can be shown to be false. If it cannot be falsified, it is not a scientific hypothesis. In the following, we have followed Popper’s principle to see whether it is possible to falsify the cholesterol hypothesis.
We have also assessed whether the conclusions from three recent reviews by its supporters are based on an accurate and comprehensive review of the research on lipids and cardiovascular disease (CVD) …
Our search for falsifications of the cholesterol hypothesis confirms that it is unable to satisfy any of the Bradford Hill criteria for causality and that the conclusions of the authors of the three reviews are based on misleading statistics, exclusion of unsuccessful trials and by ignoring numerous contradictory observations.”
As reported by Reason.com:6
“A comprehensive new study on cholesterol, based on results from more than a million patients, could help upend decades of government advice about diet, nutrition, health, prevention, and medication …
The study … centers on statins, a class of drugs used to lower levels of LDL-C, the so-called ‘bad’ cholesterol, in the human body. According to the study, statins are pointless for most people …
The study also reports that ‘heart attack patients were shown to have lower than normal cholesterol levels of LDL-C’ and that older people with higher levels of bad cholesterol tend to live longer than those with lower levels.”
No evidence cholesterol influences heart disease risk
Indeed, the authors of the Expert Review of Clinical Pharmacology analysis point out that were high total cholesterol in fact a major cause of atherosclerosis, “there should be exposure-response in cholesterol-lowering drug trials.”7 In other words, patients whose total cholesterol is lowered the most should also see the greatest benefit. Alas, that’s not the case.
A review of 16 relevant cholesterol-lowering trials (studies in which exposure-response was actually calculated), showed this kind of exposure-response was not detected in 15 of them. What’s more, the researchers point out that the only study8 showing a positive exposure-response to lowered cholesterol used exercise-only as the treatment.
Patients with high total cholesterol should also be at increased risk of death from CVD, but the researchers found no evidence of this either, not-so-subtly pointing out that this is “an idea supported by fraudulent reviews of the literature.” They provide the following example of how research has been misrepresented:9
“The hypothesis that high TC [total cholesterol] causes CVD was introduced in the 1960s by the authors of the Framingham Heart Study. However, in their 30-year follow-up study published in 1987, the authors reported that ‘For each 1 mg/dl drop in TC per year, there was an eleven percent increase in coronary and total mortality’.
Three years later, the American Heart Association and the U.S. National Heart, Lung and Blood Institute published a joint summary concluding, ‘a one percent reduction in an individual’s TC results in an approximate two percent reduction in CHD risk’. The authors fraudulently referred to the Framingham publication to support this widely quoted false conclusion.”