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For the polar opposite fallacy, see dietary cholesterol.

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]

Low-density lipoprotein cholesterol (LDL-C) is an important causal risk factor for atherosclerotic cardiovascular disease.[5] Global deaths attributable to high LDL-C increased from 3 million in 1990 to 4.4 million in 2019.[6] Disability-adjusted life years (DALYs) attributable to high LDL-C also increased from 69.7 million in 1990 to 98.6 million in 2019.[6] In 2021, the World Heart Federation reported that elevated LDL-C contributed to 3.8 million CVD deaths.[7] High LDL-C levels are also associated with increased dementia risk.[8][9]

## Contents

* 1 Criticism from the medical community
* 2 "But they're measuring the wrong things!"
* 3 Lipoproteins
* 3.1 LDL-C and ApoB
* 3.2 Lipoprotein (a)
* 3.3 Remnant cholesterol
* 3.4 Total cholesterol
* 4 Other chronic disease risks
* 4.1 Dementia risk
* 4.2 Peripheral Artery Disease
* 5 List of notable cholesterol denialists
* 6 See also
* 7 External links
* 8 References

## 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.[10]

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".[11] 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."[12]

Cardiologist Steven E. Nissen, has described statin denialism as an "internet-driven cult with deadly consequences."[13] 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."[14]

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."[15] 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.[16][17][18]

## "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.[19]

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.[20] 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.

In recent years cholesterol denialists such as Eric Berg and Ben Bikman now accept that "small dense" LDL-particles cause heart disease but claim that high LDL-C is perfectly fine and there is only a concern if the LDL-particles are small. They both advocate LDL-P (particle number) testing. Eric Berg goes as far as calling large LDL particles "good".[21] Whilst small dense LDL particles are considered "more" atherogenic than large buoyant LDL particles; all LDL particles are atherogenic.[22][23] All LDL particles are equally able to cause atherosclerosis but this is ignored by cholesterol denialists. For example the 2020 European Atherosclerosis Society Consensus Panel states that "All LDL particles exert atherogenicity to variable degrees, which can be influenced by the proteome, lipidome, proteoglycan binding, aggregability, and oxidative susceptibility".[24] Cholesterol denialists do not mention that medium size LDL particles increase CVD risk.[25]

Large fluffy LDL particles, while less easily retained in the artery wall, deposit more cholesterol per particle so they are not "good". In reality it doesn't matter if LDL particles are small dense or large, what matters is the total number of LDL particles (total number of ApoB-containing lipoproteins, which includes all forms of LDL).[22][24][26][27] To reduce cardiovascular risk, the LDL-C needs to be lowered overall.[28][24] Cholesterol denialists advice of promoting high LDL-C is potentially dangerous and likely to increase CVD events.

## Lipoproteins[edit]

Lipoproteins are particles that transport cholesterol and other lipids through the bloodstream. Plasma lipoprotein particles are commonly divided into five main classes. They are, HDL, LDL, IDL, VLDL and chylomicrons.

### LDL-C and ApoB[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 and ApoB-containing lipoproteins as much as possible reduces cardiovascular events.[29][30] Apolipoprotein B (ApoB) is the primary apolipoprotein of chylomicrons, VLDL, Lp(a), IDL, and LDL particles. Higher levels of ApoB and LDL shorten healthspan in humans.[31]

By 2012, many clinical trials had been done.[32] 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%.[33]

The European Atherosclerosis Society have stated in 2017:

> Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C.[28]

The medical consensus to reduce heart disease risk is that optimal LDL-c should be less than 100mg/dl and those with heart disease or many risk factors, below 70 mg/dL.[34][35]

Cholesterol denialists ignore the fact that normal LDL-c is actually 20-40 mg/dl and that 50 to 70 mg/dl is normal for native hunter-gatherers, healthy human neonates, free-living primates, and other wild mammals.[36][37] The LDL levels of healthy newborns are in the 30 to 70 mg/dl range.[37] Reports of atherosclerosis in individuals with lifelong low LDL-C levels are extremely rare. No known adverse events have been linked to very low LDL-C levels.[38]

A 2022 review in the American Journal of Preventive Cardiology reported:

> Humans were never meant to harbor the low-density lipoprotein cholesterol (LDL-C) levels that are now commonplace. In one series of 147 full-term neonates, the average LDL-C was 20 ± 10 mg/dL. Despite the extraordinary rate of development and need for myelination, even neonates need very little LDL-C. The fact that animals, non-human primates, and humans who maintain low cholesterol levels from early in life have very little atherosclerosis all suggest that a ‘normal’ non-atherogenic LDL-C level is 20–40 mg/dl. That is of course difficult to achieve in a modern society and, as described herein, is not necessary for most people.

> Based on the log-linear relationship of LDL-C to the hazard ratio for an acute ASCVD event, the LDL-C level where no excess risk occurs is approximately 38 mg/dL or 1 mmol/L [64] (Fig. 1). This value is consistent with the LDL-C levels observed among hunter-gatherer populations. In the Framingham Study, the average LDL-C of a man presenting with an Acute Coronary Syndrome (ACS) is approximately 150 mg/dL. In the Cooper Center Longitudinal Study, even when LDL-C at baseline was < 100 mg/dL, there was a continuous rise in risk for Coronary Heart Disease (CHD) mortality over a mean follow-up time of 26.5 yrs. Hence, it is crucial that exposure to atherogenic lipoproteins be dramatically reduced early and over the long-term.[36]

The lower the LDL-C, the lower the risk and fewer complications of atherosclerosis.[36][39] Studies have found that people with LDL-C of 150 to 160 mg/dl have a significant increased risk in the prevalence of atherosclerosis.[40]

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.[30]

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.[41]

LDL particle concentrations drive the majority of atherogenic lipoprotein risk because they represent the majority of all circulating apoB particles. The consensus is to keep ApoB-containing lipoproteins low to reduce atherosclerotic cardiovascular disease risk.

> An apoB particle is the basic unit of injury to the arterial wall. The more apoB particles within the lumen of the artery, the greater the trapping of apoB particles within the arterial wall, the greater the injury to the arterial wall. The more apoB particles are reduced by therapy, the less the injury to the arterial wall, the greater the opportunity for healing.[42]

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.[43][44][45][46][47][48][49] 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.[43][50][51][52] Typically they do not change after 5 years of age except during times of significant inflammation, liver disease or kidney disease.[43][53] It is recommended that LP(a) should be measured in everyone at least once in a lifetime.[54]

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.[55]

Recently, cholesterol denialists who deny that LDL-C increases cardiovascular disease risk now accept that Lipoprotein (a) increases risk.[56] 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.[57]

Currently there are no approved drug treatments to lower Lp(a). Clinical trials are currently being conducted on Lepodisiran and Muvalaplin.[58][59]

### Remnant cholesterol[edit]

Remnant cholesterol and total cholesterol

Remnant cholesterol is an atherogenic lipoprotein composed primarily of very low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL) with chylomicron remnants. It is calculated as total cholesterol minus HDL-C and LDL-C. Elevated remnant cholesterol is associated with increased risk of cardiovascular disease events and stroke.[60][61]

### Total cholesterol[edit]

Total cholesterol also known as serum cholesterol, refers to the overall amount of cholesterol the blood, which is carried by lipoproteins.[62] It is calculated by summing the HDL level, LDL level, and 20% of the triglyceride level present in a blood sample.[63][64][65] There is a broad consensus that serum cholesterol should be under 200 mg/dl.[66][67][68] There is over 40 years of consistent epidemiological research showing that high serum cholesterol is associated with an increased cardiovascular disease risk in both young and older persons.[69][70][71][72][73][74][75][76][77][78] Recent research supports the lipid hypothesis that lower serum cholesterol is associated with reduced coronary heart disease risk.[79]

## Other chronic disease risks[edit]

### Dementia risk[edit]

High LDL-C levels are associated with an increased dementia risk.[8][9][80][81][82] A 2025 study found that LDL-C levels below 70 mg/dL were associated with a 26% reduction in the risk of all-cause dementia and a 28% reduction in the risk of Alzheimer’s disease-related dementia.[9][83]

### Peripheral Artery Disease[edit]

High LDL-C levels are considered a risk factor for peripheral artery disease.[84][85] Lipid-lowering medication is recommended to patients with peripheral artery disease.[84]

## List of notable cholesterol denialists[edit]

* Mike Adams[3]
* Eric Berg
* Leonard Coldwell[3]
* James DiNicolantonio
* Jason Fung
* Zoë Harcombe
* Malcolm Kendrick[3]
* Chris Kresser
* Abd ul-Rahman Lomax
* Dwight Lundell
* Aseem Malhotra[2]
* Joseph Mercola[3]
* Jimmy Moore
* Tom Naughton
* Tim Noakes[86]
* David Perlmutter
* Ray Peat
* Matthias Rath
* Uffe Ravnskov[2]
* Marika Sboros
* Gary Taubes
* Paul Saladino
* Nina Teicholz
* Frank Mitloehner

## See also[edit]

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

## External links[edit]

* LDL Particle Size - Does Size Matter? Cardiologist Explains
* Low Cholesterol & Increased Mortality Risk?: Clarifying the Confusion

## References[edit]

1. ↑ Cholesterol Denialism is Pseudoscience. medscape.com.
2. ↑ 2.0 2.1 2.2 2.3 2.4 Butter nonsense: the rise of the cholesterol deniers
3. ↑ 3.0 3.1 3.2 3.3 3.4 Statin Denialism
4. ↑ The Movie “Cholesterol: The Great Bluff” Is an Exercise in Denialism
5. ↑ Low-Density Lipoprotein Cholesterol Is Predominantly Associated With Atherosclerotic Cardiovascular Disease Events in Patients With Evidence of Coronary Atherosclerosis: The Western Denmark Heart Registry. ahajournals.org.
6. ↑ 6.0 6.1 Global Burden Attributable to High Low-Density Lipoprotein-Cholesterol From 1990 to 2019
7. ↑ https://world-heart-federation.org/wp-content/uploads/World-Heart-Report-2023.pdf
8. ↑ 8.0 8.1 Cholesterol and the risk of dementia. alzheimers.org.uk.
9. ↑ 9.0 9.1 9.2 Low-density lipoprotein cholesterol levels and risk of incident dementia: a distributed network analysis using common data models. jnnp.bmj.com.
10. ↑ Lansberg et al 2018\. Nonadherence to statins: individualized intervention strategies outside the pill box. Vasc Health Risk Manag 14: 91–102.
11. ↑ Demasi, M; Lustig R. H; Malhotra A. (2017). "The cholesterol and calorie hypotheses are both dead — it is time to focus on the real culprit: insulin resistance". The Pharmaceutical Journal doi:10.1211/CP.2017.20203046.
12. ↑ Expert reaction to new report on statins and the cholesterol hypothesis
13. ↑ Nissen SE. (2017). "Statin Denial: An Internet-Driven Cult With Deadly Consequences". Ann Intern Med. 2017 Aug 15;167(4): 281-282.
14. ↑ Nissen Calls Statin Denialism A Deadly Internet-Driven Cult
15. ↑ Dr. James Stein Speaks Out Against "Statin Denialism"
16. ↑ Editors-in-chief of major cardiovascular journals claim medical misinformation puts “lives at stake”.
17. ↑ Hill JA, et al. Medical misinformation: vet the message!. European Heart Journal - Cardiovascular Pharmacotherapy 5 (2): 62-63.
18. ↑ Medical Misinformation: Vet the Message!. List of the journals that have published the editorial.
19. ↑ LDL-Cholesterol – The “Bad” Cholesterol Explained, Sigurdsson, Doc's Opinion, 24-Mar-2019
20. ↑ The Diet-Heart Myth: Why Everyone Should Know Their LDL Particle Number, Chris Kresser, 17-March-2019
21. ↑ You Have Good and Bad LDL. drberg.com.
22. ↑ 22.0 22.1 Apolipoprotein B Particles and Cardiovascular Disease: A Narrative Review. pubmed.ncbi.nlm.nih.gov.
23. ↑ Atherogenic Lipoprotein Particles in Atherosclerosis. ahajournals.org.
24. ↑ 24.0 24.1 24.2 Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel. academic.oup.com.
25. ↑ LDL particle size and composition and incident cardiovascular disease in a South-European population: The Hortega-Liposcale Follow-up Study. sciencedirect.com.
26. ↑ Does LDL Particle Size Matter?. dralo.net.
27. ↑ LDL size and Heart Disease (small dense vs large "fluffy") | Dr. William Cromwell. youtube.com.
28. ↑ 28.0 28.1 Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel
29. ↑ Effect of long-term exposure to lower low-density lipoprotein cholesterol beginning early in life on the risk of coronary heart disease: a Mendelian randomization analysis. pubmed.ncbi.nlm.nih.gov.
30. ↑ 30.0 30.1 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk: The Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS). academic.oup.com.
31. ↑ Mendelian randomization reveals apolipoprotein B shortens healthspan and possibly increases risk for Alzheimer’s disease. nature.com.
32. ↑ The Lipid Hypothesis
33. ↑ Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170 000 participants in 26 randomised trials. ncbi.nlm.nih.gov.
34. ↑ Cholesterol Numbers and What They Mean
35. ↑ Lipid Panel
36. ↑ 36.0 36.1 36.2 There is urgent need to treat atherosclerotic cardiovascular disease risk earlier, more intensively, and with greater precision: A review of current practice and recommendations for improved effectiveness
37. ↑ 37.0 37.1 Optimal low-density lipoprotein is 50 to 70 mg/dl: Lower is better and physiologically normal. sciencedirect.com.
38. ↑ Lipidology update: targets and timing of well-established therapies. escardio.org.
39. ↑ How Low Can You Go? New Evidence Supports No Lower Bound to Low-Density Lipoprotein Cholesterol Level in Secondary Prevention
40. ↑ Normal LDL-Cholesterol Levels Are Associated With Subclinical Atherosclerosis in the Absence of Risk Factors
41. ↑ Treatment Guidelines Overview: European Society of Cardiology/European Atherosclerosis Society Guidelines Treatment Guidelines Overview: European Society of Cardiology/European Atherosclerosis Society Guidelines
42. ↑ Apolipoprotein B Particles and Cardiovascular Disease: A Narrative Review. pmc.ncbi.nlm.nih.gov.
43. ↑ 43.0 43.1 43.2 An Update on Lipoprotein(a): The Latest on Testing, Treatment, and Guideline Recommendations. acc.org.
44. ↑ Lipoprotein (a) and risk of cardiovascular disease--a systematic review and meta analysis of prospective studies. pubmed.ncbi.nlm.nih.gov.
45. ↑ Lipoprotein (a) and Stroke: A Meta-Analysis of Observational Studies. ahajournals.org.
46. ↑ Lipoprotein(a) and Risk of Ischemic Stroke in the REGARDS Study. ahajournals.org.
47. ↑ Elevated Lipoprotein(a) and Risk of Ischemic Stroke. jacc.org.
48. ↑ Lipoprotein(a) as a Risk Factor for Cardiovascular Diseases: Pathophysiology and Treatment Perspectives. ncbi.nlm.nih.gov.
49. ↑ Lipoprotein(a) and its Significance in Cardiovascular Disease: A Review. jamanetwork.com.
50. ↑ Lipoprotein (a), an independent cardiovascular risk marker. ncbi.nlm.nih.gov.
51. ↑ Lipoprotein(a): A Genetically Determined, Causal, and Prevalent Risk Factor for Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association. ahajournals.org.
52. ↑ Use of Lipoprotein(a) in clinical practice: A biomarker whose time has come. A scientific statement from the National Lipid Association. lipidjournal.com.
53. ↑ Lipoprotein(a) in Clinical Practice. acc.org.
54. ↑ Eight reasons why lipoprotein(a) should be measured in everyone at least once in a lifetime. academic.oup.com.
55. ↑ Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statemen. academic.oup.com.
56. ↑ For example, Paul Saladino https://www.youtube.com/watch?v=AYFb9o6kdmQ
57. ↑ Lipoprotein(a), Causality, and Checkmate on Low-Carb Cholesterol Denialism. alineanutrition.com.
58. ↑ Trial Shows a Single Dose of an Experimental Therapy Reduces Lipoprotein(a), an Important Heart Disease Risk Factor, More than 94% for Nearly a Year. newsroom.clevelandclinic.org.
59. ↑ First oral treatment for Lipoprotein(a) shows significant cholesterol reduction. news-medical.net.
60. ↑ Nordestgaard BG (2016). "Triglyceride-Rich Lipoproteins and Atherosclerotic Cardiovascular Disease: New Insights From Epidemiology, Genetics, and Biology". Circulation Research. 118 (4): 547–563\. doi:10.1161/CIRCRESAHA.115.306249. PMID 26892957.547-563&rft.date=2016&rft_id=info:doi/10.1161/CIRCRESAHA.115.306249&rft_id=info:pmid/26892957&rft.au=Nordestgaard+BG&rft_id=https://doi.org/10.1161%2FCIRCRESAHA.115.306249&rfr_id=info:sid/rationalwiki.org:Cholesterol+denialism" class="Z3988">
61. ↑ Yang XH, Zhang BL, Cheng Y, Fu SK, Jin HM. (2023). "Association of remnant cholesterol with risk of cardiovascular disease events, stroke, and mortality: A systemic review and meta-analysis". Atherosclerosis. 371: 21–31\. doi:10.1016/j.atherosclerosis.2023.03.012. PMID 36966562.21-31&rft.date=2023&rft_id=info:doi/10.1016/j.atherosclerosis.2023.03.012&rft_id=info:pmid/36966562&rft.au=Yang+XH,+Zhang+BL,+Cheng+Y,+Fu+SK,+Jin+HM.&rft_id=https://www.sciencedirect.com/science/article/abs/pii/S0021915023001144&rfr_id=info:sid/rationalwiki.org:Cholesterol+denialism" class="Z3988">`{{cite journal}}`: CS1 maint: multiple names: authors list (link)
62. ↑ Understand your cholesterol test results. heartuk.org.uk
63. ↑ What Your Cholesterol Levels Mean. heart.org.
64. ↑ How to calculate total cholesterol. medicalnewstoday.com.
65. ↑ What is serum cholesterol?. medicalnewstoday.com.
66. ↑ Lipid Panel. hopkinsmedicine.org.
67. ↑ Patient education: High cholesterol and lipids (Beyond the Basics). uptodate.com.
68. ↑ Cholesterol Levels. medlineplus.gov.
69. ↑ Serum Cholesterol Levels and Risk of Cardiovascular Death: A Systematic Review and a Dose-Response Meta-Analysis of Prospective Cohort Studies. pubmed.ncbi.nlm.nih.gov.
70. ↑ Clarifying the direct relation between total cholesterol levels and death from coronary heart disease in older persons. pubmed.ncbi.nlm.nih.gov.
71. ↑ Effect of Change in Total Cholesterol Levels on Cardiovascular Disease Among Young Adults. pubmed.ncbi.nlm.nih.gov
72. ↑ Lifetime risk of coronary heart disease by cholesterol levels at selected ages. pubmed.ncbi.nlm.nih.gov.
73. ↑ Lipids and risk of coronary heart disease. The Framingham Study. pubmed.ncbi.nlm.nih.gov.
74. ↑ A Combination of Blood Pressure and Total Cholesterol Increases the Lifetime Risk of Coronary Heart Disease Mortality: EPOCH-JAPAN. pubmed.ncbi.nlm.nih.gov.
75. ↑ Ten-year mortality from cardiovascular disease in relation to cholesterol level among men with and without preexisting cardiovascular disease. pubmed.ncbi.nlm.nih.gov.
76. ↑ Beyond low-density lipoprotein cholesterol: respective contributions of non-high-density lipoprotein cholesterol levels, triglycerides, and the total cholesterol/high-density lipoprotein cholesterol ratio to coronary heart disease risk in apparently healthy men and women. pubmed.ncbi.nlm.nih.gov.
77. ↑ Serum total cholesterol and long-term coronary heart disease mortality in different cultures. Twenty-five-year follow-up of the seven countries study. pubmed.ncbi.nlm.nih.gov.
78. ↑ Total cholesterol as a risk factor for coronary heart disease and stroke in women compared with men: A systematic review and meta-analysis. pubmed.ncbi.nlm.nih.gov.
79. ↑ Serum Cholesterol and Impact of Age on Coronary Heart Disease Death in More Than 4 Million Veterans. ahajournals.org.
80. ↑ Blood cholesterol and risk of dementia in more than 1·8 million people over two decades: a retrospective cohort study. thelancet.com.
81. ↑ The relationship between midlife dyslipidemia and lifetime incidence of dementia: A systematic review and meta‐analysis of cohort studies. pmc.ncbi.nlm.nih.gov
82. ↑ Elevated serum LDL-C increases the risk of Lewy body dementia: a two-sample mendelian randomization study. lipidworld.biomedcentral.com.
83. ↑ Lowering bad cholesterol may cut risk of dementia by 26%, study suggests. theguardian.com.
84. ↑ 84.0 84.1 Lipid Management in Peripheral Artery Disease: A Focus on Recent and Evolving Data. acc.org.
85. ↑ Association of lipids and lipid-lowering drugs with peripheral arterial disease: A Mendelian randomization study. sciencedirect.com.
86. ↑ Tim Noakes called a 'cholesterol denialist'