Difference between revisions of "Cholesterol denialism"

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{{DenialismSide}}
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Statin denialism is supported by the literature since currently available studies do not support the use of statins for most individuals.
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{{pseudosciencenav}}
 
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{{hatnote|For the polar opposite fallacy, see [[dietary cholesterol myth]].}}
 
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{{hatnote|For Stalin Denialism, see [[Stalin apologetics]].}}
 
  
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'''Statin denialism''' (also known as '''cholesterol denialism''') is a form of [[pseudoscientific]] [[denialism]] that asserts that blood LDL cholesterol levels do not increase the risk of cardiovascular disease and/or 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 [[LCHF]] conspiracy theorists and has a presence on [[social media platforms]] such as [[Twitter]].
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https://pubmed.ncbi.nlm.nih.gov/29427042/ :
  
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Statin or cholesterol 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 blood cholesterol levels and the risk of heart disease and other cardiovascular diseases.<ref name="The Guardian">[https://www.theguardian.com/lifeandstyle/2018/oct/30/butter-nonsense-the-rise-of-the-cholesterol-deniers Butter nonsense: the rise of the cholesterol deniers]</ref> This view is contradicted by scientific evidence and has been described as bad science and dangerous.<ref name="The Guardian"/>
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'' Results: RORs for ALS were elevated for all statins, with elevations possibly stronger for lipophilic statins. RORs ranged from 9.09 (6.57-12.6) and 16.2 (9.56-27.5) for rosuvastatin and pravastatin (hydrophilic) to 17.0 (14.1-20.4), 23.0 (18.3-29.1), and 107 (68.5-167) for atorvastatin, simvastatin, and lovastatin (lipophilic), respectively. For simvastatin, an ROR of 57.1 (39.5-82.7) was separately present for motor neuron disease.
  
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The leading advocates of 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."<ref name="denialism">[https://www.csicop.org/si/show/statin_denialism Statin Denialism]</ref> Statin denialists are known to exaggerate the side effects of statins and utilize scaremongering tactics.<ref>[https://sciencebasedmedicine.org/the-movie-cholesterol-the-great-bluff-is-an-exercise-in-denialism/ The Movie “Cholesterol: The Great Bluff” Is an Exercise in Denialism]</ref>
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Conclusion: These findings extend previous evidence showing that significantly elevated ALS reporting extends to individual statin agents, and add to concerns about potential elevated occurrence of ALS-like conditions in association with statin usage. ''
  
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==Criticism from the medical community==
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https://www.tandfonline.com/doi/full/10.1080/17512433.2018.1519391 LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature :
  
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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]].<ref>Lansberg ''et al'' 2018. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5973378/ ''Nonadherence to statins: individualized intervention strategies outside the pill box'']. Vasc Health Risk Manag 14: 91–102.</ref>
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'' Introduction: For half a century, a high level of total cholesterol (TC) or low-density lipoprotein cholesterol (LDL-C) has been considered to be the major cause of atherosclerosis and cardiovascular disease (CVD), and statin treatment has been widely promoted for cardiovascular prevention. However, there is an increasing understanding that the mechanisms are more complicated and that statin treatment, in particular when used as primary prevention, is of doubtful benefit.
  
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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".<ref>Demasi, M; Lustig R. H; Malhotra A. (2017). [http://www.pharmaceutical-journal.com/opinion/insight/the-cholesterol-and-calorie-hypotheses-are-both-dead-it-is-time-to-focus-on-the-real-culprit-insulin-resistance/20203046.article "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.</ref> 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."<ref>[http://www.sciencemediacentre.org/expert-reaction-to-new-report-on-statins-and-the-cholesterol-hypothesis/ Expert reaction to new report on statins and the cholesterol hypothesis]</ref>
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Areas covered: The authors of three large reviews recently published by statin advocates have attempted to validate the current dogma. This article delineates the serious errors in these three reviews as well as other obvious falsifications of the cholesterol hypothesis.
  
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Cardiologist Steven E. Nissen, has described statin denialism as an "internet-driven cult with deadly consequences."<ref>Nissen SE. (2017). [https://theskepticalcardiologist.files.wordpress.com/2017/08/aimed.pdf "Statin Denial: An Internet-Driven Cult With Deadly Consequences"]. Ann Intern Med. 2017 Aug 15;167(4): 281-282.</ref> 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."<ref>[https://www.medpagetoday.com/cardiology/cardiobrief/66863 Nissen Calls Statin Denialism A Deadly Internet-Driven Cult]</ref>
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Expert commentary: 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. ''
  
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Professor of Medicine and Epidemiology Rory Collins has compared statin denialism to [[flat earth]]ism, 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."<ref name="The Guardian"/>
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https://bmjopen.bmj.com/content/6/6/e010401 Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review :
  
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James Stein, a Professor of Cardiovascular Research has stated that "many lives have been lost or impaired because of statin non-compliance."<ref>[https://www.medicine.wisc.edu/vital-signs/dr-james-stein-speaks-out-against-statin-denialism Dr. James Stein Speaks Out Against "Statin Denialism"]</ref>
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'' Results We identified 19 cohort studies including 30 cohorts with a total of 68 094 elderly people, where all-cause mortality was recorded in 28 cohorts and CV mortality in 9 cohorts. Inverse association between all-cause mortality and LDL-C was seen in 16 cohorts (in 14 with statistical significance) representing 92% of the number of participants, where this association was recorded. In the rest, no association was found. In two cohorts, CV mortality was highest in the lowest LDL-C quartile and with statistical significance; in seven cohorts, no association was found.
  
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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.<ref>[https://vascularnews.com/editors-in-chief-of-major-cardiovascular-journals-claim-medical-misinformation-puts-lives-at-stake/ Editors-in-chief of major cardiovascular journals claim medical misinformation puts “lives at stake”].</ref><ref>Hill JA, ''et al''. [https://academic.oup.com/ehjcvp/article/5/2/62/5301294 ''Medical misinformation: vet the message!'']. European Heart Journal - Cardiovascular Pharmacotherapy 5 (2): 62-63.</ref><ref>[https://www.ahajournals.org/circ/medical-misinformation Medical Misinformation: Vet the Message!]. List of the journals that have published the editorial.</ref>
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Conclusions High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic). Since elderly people with high LDL-C live as long or longer than those with low LDL-C, our analysis provides reason to question the validity of the cholesterol hypothesis. Moreover, our study provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies. ''
  
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== "But they're measuring the wrong things!" ==
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https://bmjopen.bmj.com/content/5/9/e007118 :
  
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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.<ref>[https://www.docsopinion.com/2019/02/23/ldl-cholesterol/ LDL-Cholesterol – The “Bad” Cholesterol Explained], Sigurdsson, ''Doc's Opinion'', 24-Mar-2019</ref>
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'' Abstract
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Objective To estimate the average postponement of death in statin trials.
  
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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.<ref>[https://chriskresser.com/the-diet-heart-myth-why-everyone-should-know-their-ldl-particle-number/ The Diet-Heart Myth: Why Everyone Should Know Their LDL Particle Number], Chris Kresser, 17-March-2019</ref>  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.
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Setting A systematic literature review of all statin trials that presented all-cause survival curves for treated and untreated.
  
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==List of notable statin denialists==
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Intervention Statin treatment compared to placebo.
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{{collist|4|
 
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*[[Mike Adams]]<ref name="denialism"/>
 
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*[[Leonard Coldwell]]<ref name="denialism"/>
 
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*[[Zoë Harcombe]]
 
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*[[Malcolm Kendrick]]<ref name="denialism"/>
 
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*[[Aseem Malhotra]]<ref name="The Guardian"/>
 
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*[[Joseph Mercola]]<ref name="denialism"/>
 
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*[[Tom Naughton]]
 
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*[[Tim Noakes]]<ref>[https://www.health24.com/Medical/Heart/Foods-diet-and-your-heart/Tim-Noakes-called-a-cholesterol-denialist-20130210 Tim Noakes called a 'cholesterol denialist']</ref>
 
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*[[Uffe Ravnskov]]<ref name="The Guardian"/>
 
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*[[Marika Sboros]]
 
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*[[Gary Taubes]]
 
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*Nina Teicholz
 
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}}
 
  
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==See also==
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Primary outcome measures The average postponement of death as represented by the area between the survival curves.
  
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*[[Saturated fat and cardiovascular disease]]
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Results 6 studies for primary prevention and 5 for secondary prevention with a follow-up between 2.0 and 6.1 years were identified. Death was postponed between −5 and 19 days in primary prevention trials and between −10 and 27 days in secondary prevention trials. The median postponement of death for primary and secondary prevention trials were 3.2 and 4.1 days, respectively.
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*[[Dietary cholesterol myth]]
 
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*[[Institute for Natural Healing]]
 
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*[[Vaccine denialism]]
 
  
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==References==
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Conclusions Statin treatment results in a surprisingly small average gain in overall survival within the trials’ running time. For patients whose life expectancy is limited or who have adverse effects of treatment, withholding statin therapy should be considered. ''
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{{reflist|2|80%}}
 
  
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[[Category:Cholesterol and statin denialists| ]]
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5441126/ Small Dense Low-Density Lipoprotein as Biomarker for Atherosclerotic Diseases (2017) :
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[[Category:Denialism]]
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'' Abstract
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Low-density lipoprotein (LDL) plays a key role in the development and progression of atherosclerosis and cardiovascular disease. LDL consists of several subclasses of particles with different sizes and densities, including large buoyant (lb) and intermediate and small dense (sd) LDLs. It has been well documented that sdLDL has a greater atherogenic potential than that of other LDL subfractions and that sdLDL cholesterol (sdLDL-C) proportion is a better marker for prediction of cardiovascular disease than that of total LDL-C. Circulating sdLDL readily undergoes multiple atherogenic modifications in blood plasma, such as desialylation, glycation, and oxidation, that further increase its atherogenicity. Modified sdLDL is a potent inductor of inflammatory processes associated with cardiovascular disease. Several laboratory methods have been developed for separation of LDL subclasses, and the results obtained by different methods can not be directly compared in most cases. Recently, the development of homogeneous assays facilitated the LDL subfraction analysis making possible large clinical studies evaluating the significance of sdLDL in the development of cardiovascular disease. Further studies are needed to establish guidelines for sdLDL evaluation and correction in clinical practice. ''
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'' 4. Atherogenic Modifications of sdLDL
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The circulation time of sdLDL is longer than that of large LDL particles that are cleared from the bloodstream through the interaction with the LDL receptor [57, 58]. Lipid trapping and accumulation by foam cells in the arterial wall are the key processes that lead to the development and growth of the atherosclerotic plaque. LDL particles are the main source of cholesterol stored in the plaques and their atherogenic properties have been extensively studied. It was demonstrated that native LDL does not cause lipid accumulation in cultured cells, whereas modified particles, such as oxidized, desialylated, glycated, and electronegative LDL, are highly atherogenic [9, 59]. Modified forms of LDL also possess proinflammatory properties and are prone to aggregation and formation of complexes that further increase their atherogenicity. ''
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'' 6. Effects of Statins and Other Therapies on sdLDL
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As the accumulating evidence points to the important role of sdLDL in the development of atherosclerosis and CVD, many studies focus on improving the lipid profile. The predominance of sdLDL is associated with the elevated TG and decreased HDL levels [96]. Hence, the goals of the corrective therapy include lowering the proportion of sdLDL-C and/or raising the HDL-C content. Statins are widely used in clinical practice as lipid lowering agents for treatment of dyslipidemia in atherosclerosis and related disorders. Despite the large amount of information available to date, it is not yet clear whether statins are efficient for specific lowering of sdLDL-C. The results of clinical studies are sometimes contradictory in that regard [57, 82, 97]. In some studies, statins failed to decrease the sdLDL proportion because larger LDL fractions were also decreased and the ratio of sdLDL-C versus lbLDL-C was unchanged [90]. Therefore the outcome of the statin treatment should be evaluated by the absolute changes of sdLDL concentrations and not their relative content or size distributions. Lack of standardization in LDL fractionation methods and varying clinical characteristics hinder the objective comparison of the results of clinical studies. More intervention studies are necessary to draw the conclusion on the effect of statin therapy on sdLDL-C proportion and its relationship to CVD risk reduction [3]. ''

Revision as of 22:37, 16 August 2021

Statin denialism is supported by the literature since currently available studies do not support the use of statins for most individuals.

https://pubmed.ncbi.nlm.nih.gov/29427042/ :

Results: RORs for ALS were elevated for all statins, with elevations possibly stronger for lipophilic statins. RORs ranged from 9.09 (6.57-12.6) and 16.2 (9.56-27.5) for rosuvastatin and pravastatin (hydrophilic) to 17.0 (14.1-20.4), 23.0 (18.3-29.1), and 107 (68.5-167) for atorvastatin, simvastatin, and lovastatin (lipophilic), respectively. For simvastatin, an ROR of 57.1 (39.5-82.7) was separately present for motor neuron disease.

Conclusion: These findings extend previous evidence showing that significantly elevated ALS reporting extends to individual statin agents, and add to concerns about potential elevated occurrence of ALS-like conditions in association with statin usage.

https://www.tandfonline.com/doi/full/10.1080/17512433.2018.1519391 LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature :

Introduction: For half a century, a high level of total cholesterol (TC) or low-density lipoprotein cholesterol (LDL-C) has been considered to be the major cause of atherosclerosis and cardiovascular disease (CVD), and statin treatment has been widely promoted for cardiovascular prevention. However, there is an increasing understanding that the mechanisms are more complicated and that statin treatment, in particular when used as primary prevention, is of doubtful benefit.

Areas covered: The authors of three large reviews recently published by statin advocates have attempted to validate the current dogma. This article delineates the serious errors in these three reviews as well as other obvious falsifications of the cholesterol hypothesis.

Expert commentary: 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.

https://bmjopen.bmj.com/content/6/6/e010401 Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review :

Results We identified 19 cohort studies including 30 cohorts with a total of 68 094 elderly people, where all-cause mortality was recorded in 28 cohorts and CV mortality in 9 cohorts. Inverse association between all-cause mortality and LDL-C was seen in 16 cohorts (in 14 with statistical significance) representing 92% of the number of participants, where this association was recorded. In the rest, no association was found. In two cohorts, CV mortality was highest in the lowest LDL-C quartile and with statistical significance; in seven cohorts, no association was found.

Conclusions High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic). Since elderly people with high LDL-C live as long or longer than those with low LDL-C, our analysis provides reason to question the validity of the cholesterol hypothesis. Moreover, our study provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies.

https://bmjopen.bmj.com/content/5/9/e007118 :

Abstract Objective To estimate the average postponement of death in statin trials.

Setting A systematic literature review of all statin trials that presented all-cause survival curves for treated and untreated.

Intervention Statin treatment compared to placebo.

Primary outcome measures The average postponement of death as represented by the area between the survival curves.

Results 6 studies for primary prevention and 5 for secondary prevention with a follow-up between 2.0 and 6.1 years were identified. Death was postponed between −5 and 19 days in primary prevention trials and between −10 and 27 days in secondary prevention trials. The median postponement of death for primary and secondary prevention trials were 3.2 and 4.1 days, respectively.

Conclusions Statin treatment results in a surprisingly small average gain in overall survival within the trials’ running time. For patients whose life expectancy is limited or who have adverse effects of treatment, withholding statin therapy should be considered.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5441126/ Small Dense Low-Density Lipoprotein as Biomarker for Atherosclerotic Diseases (2017) :

Abstract

Low-density lipoprotein (LDL) plays a key role in the development and progression of atherosclerosis and cardiovascular disease. LDL consists of several subclasses of particles with different sizes and densities, including large buoyant (lb) and intermediate and small dense (sd) LDLs. It has been well documented that sdLDL has a greater atherogenic potential than that of other LDL subfractions and that sdLDL cholesterol (sdLDL-C) proportion is a better marker for prediction of cardiovascular disease than that of total LDL-C. Circulating sdLDL readily undergoes multiple atherogenic modifications in blood plasma, such as desialylation, glycation, and oxidation, that further increase its atherogenicity. Modified sdLDL is a potent inductor of inflammatory processes associated with cardiovascular disease. Several laboratory methods have been developed for separation of LDL subclasses, and the results obtained by different methods can not be directly compared in most cases. Recently, the development of homogeneous assays facilitated the LDL subfraction analysis making possible large clinical studies evaluating the significance of sdLDL in the development of cardiovascular disease. Further studies are needed to establish guidelines for sdLDL evaluation and correction in clinical practice.

4. Atherogenic Modifications of sdLDL The circulation time of sdLDL is longer than that of large LDL particles that are cleared from the bloodstream through the interaction with the LDL receptor [57, 58]. Lipid trapping and accumulation by foam cells in the arterial wall are the key processes that lead to the development and growth of the atherosclerotic plaque. LDL particles are the main source of cholesterol stored in the plaques and their atherogenic properties have been extensively studied. It was demonstrated that native LDL does not cause lipid accumulation in cultured cells, whereas modified particles, such as oxidized, desialylated, glycated, and electronegative LDL, are highly atherogenic [9, 59]. Modified forms of LDL also possess proinflammatory properties and are prone to aggregation and formation of complexes that further increase their atherogenicity.

6. Effects of Statins and Other Therapies on sdLDL As the accumulating evidence points to the important role of sdLDL in the development of atherosclerosis and CVD, many studies focus on improving the lipid profile. The predominance of sdLDL is associated with the elevated TG and decreased HDL levels [96]. Hence, the goals of the corrective therapy include lowering the proportion of sdLDL-C and/or raising the HDL-C content. Statins are widely used in clinical practice as lipid lowering agents for treatment of dyslipidemia in atherosclerosis and related disorders. Despite the large amount of information available to date, it is not yet clear whether statins are efficient for specific lowering of sdLDL-C. The results of clinical studies are sometimes contradictory in that regard [57, 82, 97]. In some studies, statins failed to decrease the sdLDL proportion because larger LDL fractions were also decreased and the ratio of sdLDL-C versus lbLDL-C was unchanged [90]. Therefore the outcome of the statin treatment should be evaluated by the absolute changes of sdLDL concentrations and not their relative content or size distributions. Lack of standardization in LDL fractionation methods and varying clinical characteristics hinder the objective comparison of the results of clinical studies. More intervention studies are necessary to draw the conclusion on the effect of statin therapy on sdLDL-C proportion and its relationship to CVD risk reduction [3].

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