Cholesterol on an Animal Based Diet, with Dave Feldman

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Paul Saladino1h 47m · 2021-11-02

Claims Made

175

Claims Supported

121

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Support rate

121 of 175 claims supported

121 supported54 partial / not

Claims from this content

143

Well SupportedGrass-fed, grass-finished, regeneratively raised organs are preserved to maintain maximum nutrients.Well SupportedIncreasing saturated fat and decreasing polyunsaturated fat intake is associated with lower plasma concentrations of lipoprotein(a) and oxLDL-EO6.Well SupportedIndigenous populations studied typically consume diets where linoleic acid constitutes about 2% of fat intake, contrasting with 7-15% in Western diets.Well SupportedAtherosclerosis is caused by the inflammatory response to oxidized cholesterol accumulation in macrophages within the artery wall.Well Supported

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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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Pork fat from pigs fed corn and soy can contain 10-15% or more linoleic acid, compared to wild pigs with around 4-5%.

Not SupportedMetabolic health context is crucial for understanding atherosclerosis, not just LDL's direct injury to the endothelium.

Well SupportedSaturated fat might be a normal adaptive response to maintain cell membrane fluidity, even if it raises LDL cholesterol.

Partially SupportedPaul Saladino's current diet macros are approximately 20% carbohydrates (150g), 50% fat (150g+), and 30% protein (200g), totaling around 2750-3000 calories daily.

Well SupportedHigher intake of linoleic acid is likely worse for humans from an evolutionary perspective.

Not SupportedAtherosclerosis begins with damage to the endothelium lining blood vessels.

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

Well SupportedDesiccated organ supplements, such as bone marrow and liver from Heart & Soil, preserve the most nutrients and are an easier way for many people to consume organ meats.

Well SupportedThe term 'hyper responder' was coined to describe individuals whose LDL cholesterol, including particle count, increases significantly on low-carb diets.

Well SupportedApoB-containing lipoproteins deliver lipids for growth or repair, and excessive deposition without removal leads to atherosclerosis.

Well SupportedThe human body stores consumed polyunsaturated fatty acids, impacting fat cells, membranes, and the brain.

Well SupportedMetabolic health determines the atherogenicity of one's lipid profile.

Well SupportedHigh HDL, low triglycerides, and elevated LDL indicate little to no increased risk of cardiovascular disease.

Well SupportedInsulin resistance can increase apoE and proteoglycans, contributing to atherosclerosis.

Well SupportedIn a low-carbohydrate diet context, an increase in LDL alongside a rise in HDL and a decrease in triglycerides is often observed and associated with healthier metabolism.

Well SupportedCT coronary artery calcium scans are recommended for assessing calcified plaque in arteries and are available out-of-pocket for under $200.

Partially SupportedReceptor-mediated metabolism of lipoproteins, particularly involving macrophages and their receptors, is crucial in understanding atherosclerosis.

Well SupportedReducing linoleic acid intake and consuming meat and organs can lead to significant health improvements.

Well SupportedHigh HDL and low triglycerides are not strongly associated with atherosclerosis.

Well SupportedThe radiation dosage for a CT angiogram is approximately 2 millisieverts.

Well SupportedTendon xanthomas and eruptive xanthomas are strongly associated with high cholesterol, especially in monogenetic FH.

Partially SupportedAdult chimpanzees have higher LDL levels than humans but do not develop atherosclerosis.

Partially SupportedIndividuals on ketogenic or low-carb diets with elevated LDL, low triglycerides, and high HDL may not have concerning cardiovascular risk.

Partially SupportedIncreased monounsaturated or polyunsaturated fat intake can make cell membranes more fluid, prompting the body to lower cholesterol levels.

Well SupportedConsuming large amounts of omega-6 or omega-9 polyunsaturated fats can replace saturated fatty acids in cell membranes, potentially affecting membrane fluidity.

Partially SupportedThe atherogenicity of LDL is a more critical question than the mechanisms causing elevated LDL.

Well SupportedNon-HDL cholesterol may be more relevant than LDL cholesterol for individuals on a low-carb diet with higher triglyceride levels.

Partially SupportedIndividuals with glycogen storage disease 1a have elevated LDL levels but not elevated atherosclerosis.

Partially SupportedFasting insulin is the best metric for metabolic health and should be considered alongside LDL.

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

Partially SupportedPaul Saladino's LDL has been around 100-128 mg/dL, attributed to dietary fat composition rather than familial hypercholesterolemia.

Partially SupportedConsuming canola oil or other seed oils, which are high in polyunsaturated fatty acids, generally lowers LDL cholesterol.

Partially SupportedHigh ApoB levels in bears do not correlate with increased atherosclerosis risk, suggesting functional fat use is more important than LDL levels.

Partially SupportedHigh levels of polyunsaturated fatty acids (PUFAs) may reduce circulating LDL particles because they are modified faster and removed by scavenger receptors.

Partially SupportedMetabolic health can be assessed using a continuous glucose monitor, fasting insulin levels, or visceral adipose tissue measurement.

Partially SupportedApoB-containing lipoproteins can bind to pathogens and participate in host defense against oxidative stress.

Partially SupportedHyperlipidemia can occur without increased atherosclerosis in individuals with glycogen storage disease 1A.

Partially SupportedCell membranes maintain constant fluidity by inserting cholesterol molecules.

Partially SupportedLipoprotein entry into the subintimal space and interaction with immune cells can go wrong if the system is overwhelmed.

Partially SupportedCT coronary angiograms involve a radiation dose of approximately 2 mSv, equivalent to one year of natural background radiation.

Partially SupportedThe intima is the space below the endothelium where macrophages engulf LDL particles, initiating atherosclerotic plaque.

Partially SupportedEndothelial cells can separate to allow monocytes (macrophage precursors) to move into the subendothelial space for immune cleanup.

Partially SupportedDave Feldman's personal lipid profile includes triglycerides of 74 mg/dL, HDL of 87 mg/dL, and LDL of 216 mg/dL on a non-keto diet.

Partially SupportedA rise in LDL cholesterol on an animal-based diet with carbohydrates is primarily due to low carbohydrate intake and lipid metabolism according to lipid energy models.

Well SupportedApoB-containing lipoproteins, such as VLDL, distribute triglycerides to tissues and become LDL as they deplete.

Partially SupportedChanges in diet, such as increasing saturated fat and reducing seed oils, can lead to elevated LDL cholesterol in some individuals.

Well SupportedThe lipid hypothesis posits a dose-dependent relationship between LDL concentration and atherosclerosis.

Partially SupportedAtherosclerosis development requires a 'spark,' such as endothelial injury or dysfunction, in addition to LDL concentration.

Not SupportedFamilial hypercholesterolemia is not a suitable model for understanding elevated LDL in metabolically healthy individuals regarding atherosclerosis.

Partially SupportedCholesterol is essential for maintaining cell membrane fluidity.

Partially SupportedThere is no known group of people with functional lipid metabolism who also have high LDL and increased atherosclerosis.

Well SupportedCoronary CT angiography provides clarity about cardiovascular health at the cost of increased radiation and potential contrast risks.

Partially SupportedThe study aims to determine if metabolically healthy individuals with an LDL-C increase of over 50% due to dietary changes experience accelerated atherosclerosis.

Partially SupportedAll-cause mortality is the ultimate balance sheet for evaluating interventions because it accounts for all health factors.

Partially SupportedCholesterol levels may increase significantly in older individuals following ketogenic or hardcore low-carb diets.

Partially SupportedThere is no known experiment demonstrating that apob-containing lipoproteins are directly injurious to the endothelium in an otherwise metabolically healthy human.

Partially SupportedBefore LDL retention occurs in the subendothelial space, there is an expansion of the extracellular matrix and smooth muscle cells within the intima.

Partially SupportedApoB knockout models in mice and rats do not develop atherosclerosis, suggesting apoB is involved in plaque formation.

Partially SupportedElevated LDL cholesterol in individuals who feel well on an animal-based diet warrants further investigation.

Partially SupportedDave Feldman prefers to obtain organ nutrients from real food rather than supplements.

Partially SupportedIndividuals with rising LDL on an animal-based or lower-carbohydrate diet should research their health status and make independent decisions with their doctor and family.

Partially SupportedPhospholipids in cell bilayers contain saturated, unsaturated, and polyunsaturated fatty acids that impact membrane permeability and fluidity.

Partially SupportedIndividuals in the 'keto gains' group tend to have lower LDL levels compared to runners or cyclists.

Partially SupportedMetabolism is the constant counterbalancing between anabolism and catabolism of substances in the body, particularly in relation to fuel.

Partially SupportedMetabolic dysfunction, specifically the balance between anabolism and catabolism, may relate to changes in lipid profiles.

Partially SupportedInjury, such as denuding with a balloon catheter, can induce atherosclerosis.

Limited ResearchThe link between reduced LDL levels and a corresponding reduction in atherosclerotic severity is not strongly established.

Partially SupportedXanthelasmas can occur in individuals before elevated lipoproteins or before adopting a ketogenic diet.

Partially SupportedApoB-containing lipoproteins may function as non-nucleated immune cells, intentionally getting oxidized as part of their role in host defense.

Partially SupportedA whole foods diet containing meat and organs provides sufficient polyunsaturated fatty acids, including omega-3s, making deficiency unlikely.

Partially SupportedFlavored pork rinds are a very low-carb snack option.

Partially SupportedIncreased endocytosis is hypothesized for individuals engaging in significant anaerobic exercise due to greater membrane maintenance needs for muscle repair and growth.

Partially SupportedRunners and cyclists who do less resistance training may have higher LDL levels.

Partially SupportedIn a mixed diet with poor lipid regulation, HDL tends to decrease, triglycerides and LDL increase, and small LDL particles increase significantly.

Partially SupportedThe 'Triad' refers to elevated LDL with high HDL and low triglycerides, indicative of good metabolic health.

Partially SupportedAdipose cells require elasticity to expand and contract, necessitating more phospholipids and free cholesterol for expansion and shedding for contraction.

Partially SupportedHigher intake of polyunsaturated fatty acids can increase ketogenesis, potentially opposing triglyceride assembly and VLDL secretion.

Partially SupportedFat-adapted individuals require carrier proteins for fat metabolism, and lipid metabolism dysfunction can affect lipid levels.

Partially SupportedMetabolically healthy individuals are less likely to have excess proteoglycans in the subintimal space.

Partially SupportedEndothelial dysfunction is observed in hyperinsulinemia and metabolic dysfunction.

Partially SupportedIn individuals with familial hypercholesterolemia, immune cells like monocytes and macrophages may have upregulated LDL receptor related proteins, potentially leading to increased LDL uptake and accelerated atherosclerosis.

Partially SupportedRodent models may not accurately replicate human lipid systems for studying atherosclerosis due to differences in LDL levels and lipid metabolism.

Partially SupportedMoving fat around the body for energy requires carrier proteins like albumin and apolipoproteins.

Partially SupportedApoB-containing lipoproteins may function as non-nucleated immune cells that trap pathogens.

Partially SupportedIndividuals with LDL particle counts in the top 1% should exhibit signs of arterial injury if the lipid hypothesis is correct.

Partially SupportedSome researchers propose that apob has altered functional domains, affecting its binding to proteoglycans.

Partially SupportedThe lipid hypothesis is simple and testable but requires explanation for populations where it does not apply.

Partially SupportedMany reported cases of xanthomas are false positives, and a dermatologist should be consulted for accurate diagnosis of skin lesions.

Partially SupportedAssuming high LDL cholesterol is solely responsible for cardiovascular disease in homozygous FH patients may be premature.

Partially SupportedMacrophages are part of the causal pathway for atherosclerosis, and limiting their production would likely reduce atherosclerosis but impair the immune response.

Partially SupportedLDL particles may play a role in the immune system and are not solely responsible for initiating cardiovascular disease.

Partially SupportedArteries develop atherosclerosis due to higher pressure causing more endothelial damage.

Not SupportedThe physical dimensions of LDL particles make it improbable for them to directly penetrate the endothelium without causing damage.

Partially SupportedA study is being crowdfunded to investigate lean mass hyper-responders, aiming to recruit 100 individuals with specific lipid profiles (LDL >= 190, HDL >= 60, Triglycerides <= 80, with a >50% increase in LDL from baseline <160) and assess their cardiovascular system via CT angiograms over one year.

Partially SupportedThe study on lean mass hyper-responders is expected to show low to very low progression of atherosclerosis.

Partially SupportedIndividuals should understand their situation and make independent personal health decisions.

Partially SupportedPhospholipids in cell bilayers are partially derived from diet and delivered via lipoproteins.

Not SupportedThe argument that LDL geometrically increases atherosclerosis risk with increasing levels is questionable when data from glycogen storage disease type 1a exists.

Not SupportedIt is problematic to determine lifelong therapy based on a single lipid marker.

Partially SupportedPhysical measurements like CT angiograms and CAC scores may be prioritized over blood markers for assessing cardiovascular disease.

Partially SupportedIn a metabolically healthy state, LDL particles may not become stuck in proteoglycans.

Partially SupportedDave Feldman can manipulate his lipid levels and related enzymes within seven days.

Partially SupportedDesiccated organ supplements may reverse biological age and improve energy, joint mobility, and cognitive clarity.

Partially SupportedPhysical measurements like CAC and CIMT are considered the most powerful data for assessing cardiovascular disease.

Partially SupportedRetrospectives on datasets like Copenhagen, UK Biobank, and Framingham should track the lipid triad and its correlation with all-cause mortality.

Partially SupportedAtherosclerosis progression is expected to be low at a population level, contrasting with rapid progression in populations with familial hypercholesterolemia (FH).

Partially SupportedBears experience significant increases in cholesterol during hibernation without developing rapid aortic plaque.

Partially SupportedPrimary hemostasis involves a platelet plug for minor vascular breaches, while secondary hemostasis involves fibrin for larger injuries.

Partially SupportedHemostasis, involving the balance between fibrinogen (fibrin) and plasminogen, is crucial for controlling bleeding and stabilizing vascular injury.

Partially SupportedBear apob likely still binds to proteoglycans, which is relevant to atherosclerosis models.

Partially SupportedPaul Saladino exhibits the lean mass hyper-responder phenotype with LDL of 216 mg/dL, HDL of 87 mg/dL, and triglycerides of 74 mg/dL.

Partially SupportedIndividuals with LDL around 700 should be monitored closely by a doctor.

Partially SupportedXanthelasmas occur in approximately 1 in 200 to 1 in 300 individuals in the general population.

Partially SupportedFamilial hypercholesterolemia is not a reliable proxy for elevated LDL in the general population.

Partially SupportedThe body adjusts LDL levels to maintain cell membrane fluidity.

Partially SupportedPaul Saladino's diet, with 20-25% of calories from carbohydrates, is technically low-carb but not ketogenic.

Partially SupportedThe lipid hypothesis, positing that high concentrations of apoB-containing lipoproteins drive atherosclerosis, has roots in 1970s work on the LDL receptor.

Partially SupportedA patient with homozygous familial hypercholesterolemia presented with extremely high LDL cholesterol (~780 mg/dL), xanthomas, stable angina at age three, and a heart attack at age six.

Not SupportedIf lipoproteins were the sole initiators of atherosclerosis, it would manifest uniformly throughout the vasculature.

Partially SupportedLipid metabolism is a strong model for cardiovascular risk.

Partially SupportedDifferences in cardiovascular outcomes are minimal between groups with low versus high LDL, even when LDL is as high as 170 mg/dL.

Partially SupportedHomozygous familial hypercholesterolemia (FH) is a rare genetic condition (1 in a million) characterized by extremely high LDL cholesterol (e.g., ~780 mg/dL), leading to xanthomas and early cardiovascular events like stable angina at age three and myocardial infarction at age six.

Partially SupportedThe endothelium, a single cell layer, lines arteries, the gut, and the blood-brain barrier, and its pathologies can be similar across these locations.

Partially SupportedInflammation involves endothelial cell separation, allowing apob-containing lipoproteins to penetrate the vessel wall.

Partially SupportedA study is examining arterial calcification in individuals on ketogenic and low-carb diets who are hyper-responders.

Partially SupportedWhen the body is fueled predominantly by fat, it builds up fat stores via anabolism, which are then broken down for energy between meals and during sleep.

Partially SupportedWhen the body is fueled predominantly by glucose, it builds up stored glucose as glycogen, which is then broken down for energy.

Not SupportedThe Hatle model suggests the body may increase lipoprotein uptake to compensate for an abundance of polyunsaturated fatty acids.

Partially SupportedTranscytosis is a major component of atherosclerosis, involving controlled movement of ldl particles.

Partially SupportedLDL does not accumulate and cause atherosclerosis in the avascular cornea of the eye where proteoglycans are present.

Partially SupportedInflammation, insulin resistance, and metabolic dysfunction are interconnected.

Partially SupportedChronically elevated inflammatory markers are strongly associated with disease outcomes, particularly atherosclerosis.

Partially SupportedTransient factors like stress or recent activity can temporarily affect blood lipid levels, making them less reliable than physical measurements.

Partially SupportedFunctional versus dysfunctional lipid metabolism may better explain physiological observations than the simple lipid hypothesis.

Partially SupportedXanthelasmas have been observed in approximately a dozen lean mass hyper-responders within a group of 7,000-8,000 individuals.

Partially SupportedMore research is needed to stratify lipid profiles to understand their outcome levels.

Partially SupportedA CT angiogram is considered the gold standard for observing cardiovascular disease.

Partially SupportedDave Feldman considers triglycerides and HDL more important than LDL.

Not SupportedPolyunsaturated fatty acids (PUFAs) in evolutionarily inappropriate amounts may be at the root of most metabolic disease.