Cholesterol denialism

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Cholesterol denialism is a form of pseudoscientific denialism that asserts that high blood LDL cholesterol levels do not increase the risk of cardiovascular disease.^[1] A related idea known as statin denialism holds that statin usage does not reduce the likelihood of cardiovascular disease. Proponents claim that statins should be avoided because they are sold by Big Pharma and cause adverse side effects. It is promoted by carnivore diet and LCHF conspiracy theorists and has a presence on social media platforms such as Twitter.

Cholesterol and statin deniers claim that saturated fat has wrongly been demonized by medical scientists and is healthy for dieting in very high quantities. They say that there is no link between LDL-c and total blood cholesterol levels and the risk of cardiovascular disease.^[2] This view is contradicted by scientific evidence and has been described as bad science and dangerous.^[2]

The leading advocates of cholesterol and statin denialism are associated with The International Network of Cholesterol Skeptics (THINCS). They have been accused of "cherry-pick[ing] the scientific literature to find studies that support their theses, ignore the flaws in those studies, and ignore the vast body of literature that contradicts them."^[3] Statin denialists are known to exaggerate the side effects of statins and utilize scaremongering tactics.^[4]

Global deaths attributable to high LDL-C increased from 3 million in 1990 to 4.4 million in 2019.^[5] Disability-adjusted life years (DALYs) attributable to high LDL-C also increased from 69.7 million in 1990 to 98.6 million in 2019.^[5] In 2021, the World Heart Federation reported that elevated LDL-C contributed to 3.8 million CVD deaths.^[6]

Criticism from the medical community[edit]

Cholesterol and statin denialism is not taken seriously by the medical community. Poor adherence to statin therapy is linked to significantly increased risk of cardiovascular events and death.^[7]

In 2017, cholesterol denialist Aseem Malhotra and colleagues published an article which disputed the link between blood cholesterol levels and occurrence of heart disease. The authors also suggested that "stopping statins may paradoxically save more lives".^[8] The article was criticized by the medical community. Cardiologist Tim Chico commented that "high cholesterol has been proven beyond all doubt to contribute to coronary artery disease and heart attack […] to say the cholesterol hypothesis is dead is simply incorrect."^[9]

Cardiologist Steven E. Nissen, has described statin denialism as an "internet-driven cult with deadly consequences."^[10] He has also written that "we have abundant scientific evidence demonstrating that treatment of high risk primary prevention patients substantially reduces the risk of cardiovascular morbidity." Whilst acknowledging that statins, like other drugs, have adverse effects, "the benefits are so well documented that every effort should be made to encourage use of these drugs in appropriate patients."^[11]

Professor of Medicine and Epidemiology Rory Collins has compared statin denialism to flat earthism, he has noted "the claims that blood LDL cholesterol levels are not causally related to cardiovascular disease (which is really in the same realm as claiming that smoking does not cause cancer) are factually false."^[2]

James Stein, a Professor of Cardiovascular Research has stated that "many lives have been lost or impaired because of statin non-compliance."^[12]

In 2019, a joint editorial was published in the top cardiovascular journals around the world to warn people about the medical misinformation of statin denialism found on social media.^[13][14][15]

"But they're measuring the wrong things!"[edit]

Blood levels of LDL cholesterol (the "bad" cholesterol correlated with heart disease) are typically calculated by measuring total blood cholesterol (in mg/dL in the U.S. and mmol/L elsewhere), subtracting the measured amount of HDL cholesterol, and further subtracting a constant fraction of the measured blood triglycerides.^[16]

While this is good enough for most people, cholesterol denialists aren't most people. They'll claim that it's the ratio of LDL cholesterol to HDL cholesterol, not the absolute amounts, that matter, and therefore cholesterol doesn't cause heart disease. They'll claim that the triglyceride-to-cholesterol ratio isn't always constant, which screws up the calculation for LDL cholesterol levels, therefore cholesterol doesn't cause heart disease. They'll claim that it's the LDL particle count (LDL-P), not the LDL cholesterol level (LDL-C) that matters, therefore cholesterol doesn't cause heart disease.^[17] They'll claim that there are two kinds of LDL cholesterol molecules -- large and fluffy, versus small and dense -- and that therefore cholesterol doesn't cause heart disease. I think you can see the pattern here.

Current consensus[edit]

There is a strong medical consensus from clinical trials and human Mendelian randomization studies that LDL-C is causally related to atherosclerotic cardiovascular disease, and that lowering LDL particles and other ApoB-containing lipoproteins as much as possible reduces cardiovascular events.^[18]

By 2012, many clinical trials had been done.^[19] The Cholesterol Treatment Trialists' Collaboration confirmed the LDL-C hypothesis after examining data from 26 trials involving 170 000 participants. According to their meta-analysis:

Further reductions in LDL cholesterol safely produce definite further reductions in the incidence of heart attack, of revascularisation, and of ischaemic stroke, with each 1·0 mmol/L reduction reducing the annual rate of these major vascular events by just over a fifth. There was no evidence of any threshold within the cholesterol range studied, suggesting that reduction of LDL cholesterol by 2–3 mmol/L would reduce risk by about 40–50%.^[20]

In 2019, the European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS) stated that the "LDL-C hypothesis" is no longer a hypothesis, it is an established fact:

Several recent placebo-controlled clinical studies have shown that the addition of either ezetimibe or anti-proprotein convertase subtilisin/kexin type 9 (PCSK9) monoclonal antibodies (mAbs) to statin therapy provides a further reduction in atherosclerotic cardiovascular disease (ASCVD) risk, which is directly and positively correlated with the incrementally achieved absolute LDL-C reduction. Furthermore, these clinical trials have clearly indicated that the lower the achieved LDL-C values, the lower the risk of future cardiovascular (CV) events, with no lower limit for LDL-C values, or ‘J’-curve effect... Human Mendelian randomization studies have demonstrated the critical role of LDL-C, and other cholesterol-rich ApoB-containing lipoproteins, in atherosclerotic plaque formation and related subsequent CV events. Thus, there is no longer an ‘LDL-C hypothesis’, but established facts that increased LDL-C values are causally related to ASCVD, and that lowering LDL particles and other ApoB-containing lipoproteins as much as possible reduces CV events.^[18]

The above is supported by current textbooks on lipidology. For example, Clinical Lipidology: A Companion to Braunwald's Heart Disease (third edition), published in 2024 states:

The first and most relevant update presented in the 2019 guidelines concerns the old concept of an “LDL-C hypothesis,” which is now replaced by the established causal role of elevated LDL-C levels in ASCVD. Besides this causal role, genetic studies have introduced the concept of exposure time, revealing that LDL-C also has a cumulative effect on the risk of ASCVD9, a longer-term exposure leads to a greater retention over time of LDL particles (or, more generally, proatherogenic apoB-containing particles) in the arterial wall. Thus, the overall effect of LDL-C level on ASCVD risk is determined by the combination of both plasma levels and time of exposure.^[21]

Cholesterol denialists are either unaware about any of these scientific developments or ignore all of the modern research from clinical trials and human Mendelian randomization studies.

Lipoprotein (a)[edit]

It is widely accepted in the scientific community that elevated Lipoprotein (a) is an independent risk factor for atherosclerotic cardiovascular disease and stroke.^{[22][23][24][25][26][27][28]} LP(a) can increase the risk of developing cardiovascular disease even when LDL-C levels are within the recommended range. Lp(a) levels are to a large extent genetically determined with little influence from environmental or lifestyle factors.^{[22][29][30][31]} Typically they do not change after 5 years of age except during times of significant inflammation, liver disease or kidney disease.^[22][32] It is recommended that LP(a) should be measured in everyone at least once in a lifetime.^[33]

In 2022, the European Atherosclerosis Society stated:

Similar to LDL, Lp(a) is an apoB-containing lipoprotein but the number of circulating particles is much lower. Given that risk associated with Lp(a) on a per particle basis may exceed that of LDL, cell signalling effects mediated by Lp(a) rather than Lp(a) accumulation per se may mainly contribute to atherogenicity. Imaging studies revealed that Lp(a) initiates inflammation in the arterial wall, and in advanced coronary artery disease, high Lp(a) levels were associated with accelerated progression of coronary calcium and the necrotic core volume. Similarly in AVS, high Lp(a) and proteins transported by Lp(a) (e.g. autotaxin) induces the expression of inflammatory and calcification genes in valvular interstitial cells and associates with increased incidence and progression of AVS.^[34]

Recently, cholesterol denialists who deny that LDL-C increases cardiovascular disease risk now accept that Lipoprotein (a) increases risk.^[35] This view from cholesterol denialists is contradictory as noted by Alan Flanagan:

The first thing to note is that Lp(a) contains an LDL particle. Which makes the “Lp(a) is causal but LDL-C isn’t” claim almost absurd from the outset.

[...]

Burgess et al. (JAMA Cardiology. 2018;3(7): 619-627) conducted a Mendelian randomization analysis involving >80,000 patients and>150,000 controls, where the genetic effect of lower Lp(a) levels was analysed and compared to the effects of lower LDL-C levels.

They demonstrated that the reduction in risk from lowering Lp(a) was proportional to the mass concentration, and that a reduction of 100mg/dL Lp(a) would be required to achieve a meaningful reduction in CHD risk. Now, here is where the rubber hits the road: the magnitude of this 100mg/dL reduction in Lp(a) was similar to the effect of lowering LDL-C by 38mg/dL.

And why is this interesting? Because although their mass concentrations may differ – 100mg for Lp(a) and 38mg for LDL – the cholesterol content of these respective masses is essentially similar: 30-40%.

This in effect tells us what is known: that the transport of cholesterol into the artery, and deposition of cholesterol therein, is the initiating process of atherosclerosis.

Thus, although the mass concentrations between 100mg Lp(a) and 38mg LDL differ, the effect of reducing either by those respective masses is to reduce circulating cholesterol by roughly the same amount. And reduce CHD risk by roughly the same, as a result of lowering the causal exposure.

So for LDL-C denialists to argue that Lp(a) is causal is the most self-defeating cockology ever witnessed.

It is literally them arguing for the exact position – the lipoprotein properties, the mechanism of action, all of it – that they otherwise deny.^[36]

Currently there are no approved drug treatments to lower Lp(a). Clinical trials are currently being conducted on Lepodisiran and Muvalaplin.^[37][38]

List of notable cholesterol denialists[edit]

See also[edit]

• Saturated fat and cardiovascular disease
• Dietary cholesterol
• Institute for Natural Healing
• Vaccine denialism

References[edit]