What REALLY causes heart disease with Malcolm Kendrick

PS

Paul Saladino2h 4m · 2020-03-10

Claims Made

217

Claims Supported

125

Support Rate

58%

Support rate

125 of 217 claims supported

125 supported92 partial / not

Claims from this content

179

Not SupportedMetabolic health context is crucial for understanding atherosclerosis, not just LDL's direct injury to the endothelium.Well SupportedRotational bison grazing increased soil organic matter from 1% to 5% over 20 years at White Oak Pastures, improving water retention.Well SupportedIn a trial for sepsis and ARDS, patients receiving intravenous vitamin C had approximately 30% mortality, compared to over 46% in the placebo group.Well SupportedAtherosclerosis does not develop in veins, suggesting that endothelial damage is necessary for its initiation.Well Supported

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A. Volkovreader

4h

Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.

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N. Park

2d

Would love a "what would change this verdict" RSS feed. Sign me up if it exists.

LDL particles perform beneficial functions such as immunological function and cell membrane formation.

Partially SupportedStatins are HMG-CoA reductase inhibitors that interrupt the mevalonate pathway, critical for cholesterol synthesis.

Well SupportedStatins reduce LDL particles by upregulating LDL receptors on hepatocytes, increasing the catabolism of apoB-containing lipoproteins.

Not SupportedStatin trials often exclude participants who experience side effects during a pre-randomization period, leading to biased results that do not reflect real-world outcomes.

Not SupportedThe evidence directly implicating LDL cholesterol in the formation of atherosclerotic plaque or heart disease progression is weak.

Well SupportedVitamin K2 in animal products like eggs, meat, and liver may prevent heart disease by directing calcium deposition.

Well SupportedNative LDL does not initiate atherosclerosis and will not be taken up by macrophages in the sub-endothelial space.

Well SupportedLDL particles can bind to and neutralize lipopolysaccharide, lipotichoic acid, and viruses, playing an essential role in the innate immune system.

Not SupportedStatin trials often present cardiovascular risk reduction as a misleading relative risk rather than an absolute risk.

Well SupportedWhile the correlation between elevated LDL and improved outcomes in infection is not causal, LDL is beneficial to the immune system.

Well SupportedSunlight exposure, specifically ultraviolet light, stimulates nitric oxide production in the skin, which is essential for blood vessel health and dilation.

Well SupportedThe ox LDL assay measures the burden of oxidation within LDL particles.

Not SupportedInterventional trials show no benefit for higher doses of vitamin C.

Well SupportedScientific understanding requires constantly updating prior beliefs with new evidence, and changing one's mind based on new data is a strength, not a weakness.

Not SupportedStatin use is associated with an increased risk of diabetes, with relative increases up to 363% and an absolute risk increase of 2-3%.

Well SupportedEating carbohydrates, rather than dietary fat, leads to a spike in VLDL and consequently raises LDL levels.

Well SupportedGrass-fed, grass-finished desiccated organ supplements are a convenient way to consume nutrient-dense organs.

Not SupportedThere is insufficient solid data directly indicting LDL and apob-containing particles as the cause of endothelial injury leading to atherosclerosis.

Well SupportedThe amount of vitamin C required to prevent scurvy is significantly lower than the Recommended Daily Intake (RDI).

Not SupportedBeing myopically focused on LDL can lead to unnecessary statin prescriptions and removal of nutrient-rich foods.

Not SupportedStatins may worsen diabetes by inhibiting the formation of heme and coenzyme Q10.

Partially SupportedNutritional adequacy is important for a healthy immune system, especially in the context of coronavirus.

Not SupportedLDL has potential immunologic functions.

Not SupportedLipophilic statins that cross the blood-brain barrier may increase dementia risk by inhibiting cholesterol production in the brain.

Partially SupportedVitamin C deficiency is not the complete explanation for atherosclerosis, although it is supported by knowledge of scurvy.

Partially SupportedUsing a personal trainer via the Future app on an Apple Watch provides accountability and is less expensive than traditional personal training.

Partially SupportedHighly oxidized LDL particles are removed by scavenger receptors on endothelial cells like CD36, LOX1, and Sortilin.

Partially SupportedIn a state of abundance after a high-fat meal, the body may reduce VLDL release due to sufficient energy intake.

Partially SupportedIngested fructose is converted to approximately 41% glucose and 25% lactate in humans.

Partially SupportedDietary fat is packaged into triglycerides in the gut and then into chylomicron particles for transport in the bloodstream.

Partially SupportedAncestral Supplements' 'Mofo' contains testicle, bone marrow, liver, and prostate and may support sexual health and arterial/venous health.

Partially SupportedElevated LDL may offer protection against viral infections.

Partially SupportedIn many individuals with familial hypercholesterolemia, there is no clear correlation between LDL levels and heart disease incidence.

Partially SupportedLipoprotein little A (LPA) is the primary genetically inherited lipoprotein that increases the risk of early cardiovascular disease.

Well SupportedStatins increase diabetes risk, and this risk is often presented as an absolute difference to minimize its perceived severity.

Partially SupportedThe glycocalyx is damaged at arterial branch points due to turbulence, impairing nitric oxide signaling and vasodilation.

Partially SupportedSevere hypolipidemia is clinically associated with bacterial pneumonia.

Partially SupportedInsulin resistance negatively affects the glycocalyx and impairs nitric oxide synthesis, damaging the endothelium.

Not SupportedStatins should generally not be considered for individuals without a history of heart attack, unless they experience no adverse effects.

Not SupportedLowering cholesterol with statins may be detrimental to nerve cells.

Not SupportedThere is a reported 50x increased risk of Amyotrophic Lateral Sclerosis (ALS) with statin use.

Not SupportedLow-density lipoprotein (LDL) is a vital immunologic molecule and is not inherently atherogenic.

Partially SupportedAtherosclerosis may be a normal repair process for arteries, and problems arise when the repair process is too great or too slow.

Well SupportedStatins are more effective than ezetimibe at lowering apolipoprotein B (ApoB).

Partially SupportedThe majority of statin trials are sponsored by industry, with the ALLHAT trial being a notable exception showing no significant benefit for pravastatin in primary prevention.

Well SupportedApproximately 75% of people stop taking statins within two years, with 63% citing adverse effects as the reason.

Partially SupportedThe mevalonate pathway is involved in the synthesis of both cholesterol and ketones, with statins inhibiting a step in this shared pathway.

Partially SupportedStatins are an inexpensive tool for managing cardiovascular disease, but they are frequently discontinued.

Partially SupportedThe French paradox describes lower heart disease and obesity rates in France despite higher saturated fat consumption.

Partially SupportedA traditional explanation for high heart disease rates in Scotland was a poor diet including deep-fried Mars bars.

Not SupportedRecommendations to consume vegetable oils because they lower LDL are suspect and potentially harmful, given that LDL is not the primary villain in heart disease.

Not SupportedMedications like proton pump inhibitors (PPIs) can inhibit nitric oxide and should not be used to treat symptoms; root causes of problems should be identified instead.

Partially SupportedHigh lipoprotein(a) levels may indicate a state of hypercoagulability, suggesting individuals with high LPA should avoid actions that damage arteries.

Partially SupportedStatin-induced mitochondrial dysfunction leads to insulin resistance and an increased risk of diabetes.

Partially SupportedVitamin C deficiency leads to a loss of collagen, causing blood vessels to disintegrate, leading to bleeding and potentially death (scurvy).

Partially SupportedThe role of a substance like LPA in heart disease depends on damage or increased blood clotting, not its structure alone.

Well SupportedMaintaining a healthy body composition and checking visceral adipose tissue are important for health.

Partially SupportedLipoprotein A (LPA) attaches to the artery wall and is difficult to remove, contributing to higher concentrations in areas of plaque or clot formation.

Partially SupportedA paper suggests that high LDL is not associated with increased mortality in individuals over 60 years old.

Partially SupportedAtherosclerosis is a multi-step process that begins with endothelial damage, and factors like LPA and LDL do not directly cause this initial damage.

Partially SupportedThe brain is composed of approximately 25% cholesterol by dry weight, and myelin sheaths are made of cholesterol.

Partially SupportedHigher LDL cholesterol levels are associated with slightly improved mortality, and lower LDL levels are associated with the highest mortality rates.

Partially SupportedDoctors have faced professional repercussions for advocating for low-carb or against high-carb diets.

Partially SupportedLDL cholesterol does not directly damage the endothelium, challenging the 'response to injury' hypothesis.

Partially SupportedGrass-fed, grass-finished meat from regenerative farms is highly nutritious and supports overall health, including brain, muscle, libido, and organ function.

Partially SupportedAvastin, a VEGF inhibitor, increased the risk of heart disease death by 1200% over a two-year period in some trials.

Not SupportedLinus Pauling's theory that atherosclerosis is invariably vitamin C deficiency, curable with megadoses of vitamin C, is not supported by evidence.

Not SupportedSunscreen contains xenoestrogen compounds that can negatively affect the thyroid.

Partially SupportedNon-steroidal anti-inflammatory drugs likely negatively affect the endothelium and increase blood clotting.

Partially SupportedOxidized LDL may damage the arterial wall's glycocalyx more than other LDL forms.

Partially SupportedThe ideal amount of vitamin C for humans is unknown, but it is important not to get too little.

Partially SupportedLiving a natural existence with good social interactions, psychological well-being, and physical health in balance is essential for overall health.

Not SupportedThe psychiatric downsides of statins, including increased risk of suicide and homicide, are significant and often not disclosed.

Not SupportedThe benefit of statins for nitric oxide synthesis is questionable, as nitric oxide synthesis can be achieved through sun exposure and exercise.

Not SupportedThe mainstream explanation that saturated fat down-regulates LDL receptor function is illogical.

Partially SupportedIncreasing cholesterol in rats and mice makes them more resistant to infections.

Partially SupportedHigh blood sugar and smoking damage the arterial glycocalyx, impairing its ability to prevent blood clots.

Partially SupportedDamage to the artery wall, caused by factors like smoking or insulin resistance, can lead to the formation of a blood clot due to tissue factor.

Partially SupportedDiabetes and high blood pressure can damage artery walls, contributing to atherosclerosis.

Not SupportedProton pump inhibitors (PPIs) have been associated with increased rates of dementia.

Partially SupportedWithin the carnivore diet community, there are views that vegetables may not be as beneficial as commonly believed and that fiber may not be essential for humans.

Partially SupportedLow-carb, ketogenic, or carnivore diets can lead to elevated LDL cholesterol.

Partially SupportedTo prevent atherosclerosis and live healthfully, one should avoid air pollution, exercise, get sun exposure, reduce stress, and engage in practices like sauna and yoga.

Partially SupportedFactors that increase nitric oxide production, such as sunlight, exercise, and relaxation, reduce cardiovascular disease risk.

Not SupportedBenefits attributed to statins can be achieved through natural methods like sun exposure, exercise, heat exposure, sauna, and cold exposure.

Partially SupportedSickle-shaped red blood cells can damage the endothelium, leading to atherosclerosis.

Partially SupportedInterventions that increase nitric oxide reduce cardiovascular disease risk, while those that decrease it increase risk.

Partially SupportedNitric oxide is a potent anticoagulant and cardiovascular protective agent.

Partially SupportedBlood clotting is a necessary component of cardiovascular disease.

Partially SupportedLDL is involved in blood clot stabilization, which explains its presence within blood clots.

Partially SupportedIn vitro studies exposing cells to vastly high concentrations of substances may not accurately reflect in vivo conditions.

Partially SupportedChronic damage from smoking and diabetes can overwhelm the body's capacity to repair endothelial damage with endothelial progenitor cells.

Partially SupportedThe 'response to injury' hypothesis posits heart disease arises from damage to the endothelium, repair systems, and clot formation.

Partially SupportedInhibiting the production of endothelial progenitor cells from bone marrow may impair proper healing and turnover of arteries.

Partially SupportedPlaque buildup in arteries involves endothelial damage and repair, becoming unhealthy when damage outpaces repair.

Partially SupportedAtherosclerosis, the formation of plaque in artery walls, is a primary concern related to heart disease and heart attacks.

Partially SupportedAngiotensin receptor blockers (ARBs) like losartan are used to lower blood pressure.

Partially SupportedEndothelial cells produce more nitric oxide and protect themselves when subjected to higher pressure.

Partially SupportedTurbulent blood flow, rather than just pressure, causes damage to arterial walls.

Partially SupportedMaintaining better repair than damage can prevent or potentially reverse arterial plaque growth.

Partially SupportedVEGF inhibitors, such as Avastin, can reduce nitric oxide levels to virtually zero.

Partially SupportedTurbulent blood flow at artery branch points can damage the glycocalyx.

Partially SupportedLPA may have prevented blood vessels from breaking down in vitamin C deficiency but increased the risk of disease by making it harder to remove blood clots.

Partially SupportedLinus Pauling believed that all heart disease was due to subclinical vitamin C deficiency and could be prevented by sufficient vitamin C intake.

Partially SupportedThe speaker takes 10 grams of vitamin C per day when experiencing a cold or flu.

Partially SupportedHeart disease and heart attacks are significant causes of mortality.

Not SupportedStatin trials may not be truly double-blind because cholesterol levels reveal statin administration.

Not SupportedFactors that reduce nitric oxide production, such as smoking, diabetes, and proton pump inhibitors (PPIs), increase the risk of cardiovascular disease.

Not SupportedThe paradigm that LDL is the primary driver of heart disease is incorrect, especially when considering insulin sensitivity on a low-carb or ketogenic diet.

Partially SupportedDamage to the glycocalyx and endothelium is considered the first step in atherosclerosis.

Partially SupportedA study suggests a slight mortality improvement in individuals over 60 with higher LDL cholesterol levels.

Partially SupportedHumans lost the ability to synthesize vitamin C approximately 40-60 million years ago.

Partially SupportedLPA may have evolved as a genetic adaptation to humans' inability to synthesize vitamin C, which is critical for collagen production and blood vessel integrity.

Not SupportedLDL cholesterol levels should not be reduced to zero, as cholesterol is essential for brain development, myelin sheath production, and neuronal health.

Partially SupportedThe carnivore code argues against fearing elevated ldl and saturated fat in the context of ketogenic diets.

Partially SupportedSupplements like vitamin C, vitamin D, and magnesium may be beneficial for individuals developing atherosclerosis, with vitamin K2 being potentially quite beneficial.

Partially SupportedUltraviolet light is a nutrient for humans and cannot be substituted by vitamin D pills.

Partially SupportedCardiovascular disease is a multi-step process influenced by hundreds of factors, not a single cause.

Partially SupportedEndothelialization and repair is a healthy response to artery wall damage, but becomes unhealthy when damage outpaces repair.

Partially SupportedBlood clot breakdown involves TPA activating plasminogen into plasmin to break down fibrin.

Partially SupportedLead toxicity is a significant cause of cardiovascular deaths.

Partially SupportedSmoking introduces nanoparticles into the lungs that can be absorbed and kill endothelial cells, leading to microparticles in the bloodstream.

Partially SupportedViagra increases nitric oxide synthesis, which is used to treat erectile dysfunction and pulmonary hypertension by opening blood vessels.

Partially SupportedDamage to blood vessels is a prerequisite for plaque formation.

Partially SupportedEndothelial cells do not develop plaque under low stress conditions, regardless of other risk factors.

Partially SupportedConditions like Hughes syndrome are significant risk factors for mortality and cardiovascular disease.

Partially SupportedThalidomide caused birth defects by preventing blood vessel growth in developing limbs.

Partially SupportedDrugs that increase nitric oxide synthesis, like ACE inhibitors, may increase the risk of lung cancer by promoting angiogenesis.

Partially SupportedACE inhibitors may primarily work by increasing nitric oxide synthesis to lower blood pressure.

Partially SupportedNitric oxide is essential for cardiovascular health, acting as a potent anticoagulant and cardiovascular-resistant agent.

Partially SupportedNitric oxide is critical for producing endothelial progenitor cells, which are essential for cardiovascular health.

Partially SupportedWhen an artery wall is damaged, the clotting cascade is activated, leading to rapid clot formation.

Partially SupportedKeeping arteries healthy may make many factors that contribute to cardiovascular disease less problematic.

Partially SupportedIncreased risk of heart disease is associated with endothelial damage, the formation of larger clots, and damage to repair systems.

Partially SupportedStatins may increase nitric oxide synthesis, contributing to their cardiovascular benefits.

Partially SupportedTaking a statin for five years increases life expectancy by approximately three days for primary prevention and 4.1 days for secondary prevention.

Partially SupportedIn a specific statin trial, the reduction in fatal heart attacks was zero, despite a reported overall reduction in heart attacks.

Not SupportedIndividuals on statins may be at higher risk during sepsis because statins reduce LDL, which is needed to manage bacterial toxins.

Not SupportedDietary changes that improve insulin resistance can achieve cardiovascular improvements similar to statins.

Not SupportedStatins may have positive effects, potentially through increasing nitric oxide, but these benefits are outweighed by their harms.

Not SupportedThe reporting system for statin adverse effects significantly underreports issues.

Not SupportedStatins can cause muscle pain and joint pain.

Not SupportedStatin use can lead to irritability, anger, and severe temper issues.

Not SupportedCorticosteroids and immunosuppressants can significantly increase heart disease risk by interfering with the body's healing systems.

Not SupportedProton pump inhibitors are associated with an increased risk of ischemic stroke and myocardial infarction, particularly with long-term use at high doses.

Not SupportedOxidized LDL is a minor factor in heart disease compared to factors like smoking.

Partially SupportedFamilial hypercholesterolemia patients with high LDL in the mid-19th century lived longer than the general population, suggesting a protective role during a time of high infectious disease mortality.

Not SupportedAvoiding sun exposure carries a risk equivalent to smoking 20 cigarettes a day due to nitric oxide creation.

Partially SupportedHigh LDL levels may be a consequence of having fewer LDL receptors, and the problem lies with the reduced number of LDL receptors.

Partially SupportedLDL particles serve as lipid surfaces on which fibrin is held and stabilized, contributing to the formation of blood clots.

Partially SupportedReduced LDL receptor numbers are associated with higher levels of Factor VIII, a key clotting factor.

Not SupportedThe pharmaceutical industry may exaggerate benefits using relative risk reductions and downplay harms using absolute risk increases.

Not SupportedStatin adverse effects are not solely a nocebo effect.

Partially SupportedMost ingested fat bypasses the liver and does not impact VLDL or LDL production.

Not SupportedAvoiding unnecessary medications and reducing polypharmacy may contribute to falling life expectancy.

Partially SupportedA diet promoting insulin sensitivity, including moderate carbohydrates and nutrient-dense animal foods, is important for avoiding endothelial damage and atherosclerosis.

Partially SupportedA diet that promotes insulin sensitivity and avoids insulin resistance is crucial for health.

Partially SupportedInhibiting vascular endothelial growth factor (VEGF) can prevent the formation of new blood vessels.

Partially SupportedAn ancestrally appropriate amount of sun exposure, resulting in a slight tan or color, is recommended and should not be feared, unless there is a history of skin cancer.

Partially SupportedLower sun exposure in women is associated with a risk equivalent to smoking.

Partially SupportedHigh blood pressure and arterial turbulence create stress on the endothelium, promoting atherosclerosis.

Partially SupportedAtherosclerosis is initiated by damage to the artery wall, leading to blood clot formation on the damaged site, which then gets covered and incorporated into the artery wall, potentially forming plaque.

Partially SupportedIn vitro studies exposing cells to vastly high concentrations of substances to test LDL's effect on endothelium are flawed because they remove supporting factors and repair systems present in the body.

Partially SupportedInhibiting vascular endothelial growth factor (VEGF) likely causes significant problems for cardiovascular health.

Partially SupportedNitroglycerin stimulates nitric oxide synthesis, causing vasodilation, lowering blood pressure, and acting as an anticoagulant.

Partially SupportedSickle cell disease significantly increases cardiovascular disease risk in young people by 50,000%.

Partially SupportedApolipoprotein A blocks TPA's action, preventing breakdown of certain blood clots.

Partially SupportedFactors like homocysteine damage artery walls but are not the sole cause of cardiovascular disease.

Partially SupportedIn the mid-1980s, Malcolm Kendrick believed he was the only person globally who did not link cholesterol and saturated fat to heart disease.

Partially SupportedThe prevailing understanding of the link between diet, cholesterol, and heart disease may be incorrect.

Not SupportedThe focus on saturated fat and high LDL as central to heart disease models is a forced fit that has led to complications like oxidized and small dense LDL.

Not SupportedFamilial hypercholesterolemia is a poor model for LDL causing atherosclerosis as it can involve LDL receptor defects and hypercoagulability.

Not SupportedThe assertion that LDL is the sole cause of cardiovascular disease is flawed due to statins' pleiotropic effects.

Partially SupportedMedications that only lower LDL-C through mechanisms other than statins, such as cholestyramine and bile acid sequestrants, do not show cardiovascular risk reduction.

Partially SupportedSevere abdominal pain may be caused by statins.