Seed Oils & Heart Disease: Oxidized LDL, Cholesterol, Fat & Cardiology  archive

https://mindandmatter.substack.com/p/seed-oils-and-heart-disease-oxidized 

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I. Atherosclerosis is a major component of cardiovascular disease, often described as a pus-filled infection in the artery wall that can burst and cause a heart attack.

Mind and Matter Podcast, Nick Norwitz

• The podcast describes atherosclerosis as an inflamed, pus-filled lesion in the artery that can rupture, sending material into the bloodstream and potentially causing a myocardial infarction.

• This process is a significant contributor to heart disease, which is noted as the number one killer globally.

II. Plaques in atherosclerosis are primarily composed of cholesterol, fats, dead cells, and macrophages.

• These plaques contain cholesterol, fats, endothelial cells, smooth muscle cells, and macrophages, which are white blood cells acting as a cleanup crew.

• The accumulation of these components in the artery wall forms the gruel or pus characteristic of atherosclerotic lesions.

III. Macrophages in plaques act as a cleanup crew, ingesting damaged tissue and bacteria but can overconsume fats and cholesterol.

• Macrophages, described as "big eaters," ingest bacteria and damaged tissue to protect the body and aid in healing, such as after a scrape.

• When macrophages ingest excessive fats and cholesterol, they can become foam cells, a key early sign of atherosclerosis.

IV. Foam cells are macrophages that have ingested so much fat and cholesterol that they appear foamy and can die, contributing to plaque formation.

• Foam cells form when macrophages overconsume fats and cholesterol, leading to a foamy appearance and potential necrosis.

• This process results in the leakage of incompletely digested material, forming the gruel or pus in atherosclerotic plaques.

V. Cholesterol in plaques led to the initial hypothesis that dietary cholesterol causes atherosclerosis, but this is not strongly supported in humans.

• Early observations of cholesterol in plaques prompted the idea that dietary cholesterol directly causes atherosclerosis, as studied in rabbits and chickens.

• Ancel Keys, a prominent cholesterol researcher, noted in 1952 and 1997 that dietary cholesterol has little to no relationship with atherosclerosis in humans.

VI. Rabbits, as herbivores, develop atherosclerosis when fed cholesterol, unlike humans or carnivores.

• Rabbits, not adapted to process cholesterol, quickly develop high cholesterol levels and atherosclerosis when fed cholesterol-rich diets.

• This makes rabbit studies less applicable to humans, who do not show a strong correlation between dietary cholesterol and atherosclerosis.

VII. Dietary cholesterol intake has a minimal impact on blood cholesterol levels in most humans due to a negative feedback mechanism.

• The body regulates cholesterol levels through a feedback loop where increased dietary cholesterol reduces endogenous production, and vice versa.

• A case study of a man eating 25 eggs daily showed normal cholesterol levels, indicating dietary cholesterol does not significantly elevate blood cholesterol in humans.

VIII. Cholesterol is an essential component of the human body, critical for cell membranes and hormone production.

• Cholesterol is a precursor to steroid hormones and a key structural component of cell membranes, regulating their fluidity.

• Genetic conditions impairing cholesterol synthesis or transport lead to severe health issues, such as retardation, highlighting its essential role.

IX. Cholesterol is chemically neutral, making it a safe building block for biological systems.

• Cholesterol’s neutral nature prevents it from reacting harmfully with other bodily components, making it ideal for structural roles.

• This neutrality contrasts with oxidized cholesterol, which is toxic and contributes to plaque formation.

X. Mainstream cardiology initially focused on cholesterol as the cause of atherosclerosis but shifted to lipoproteins, particularly LDL.

• Early research targeted cholesterol due to its presence in plaques, but later studies focused on lipoproteins like LDL as key players.

• This shift occurred as treatments to lower cholesterol levels showed limited impact on heart disease rates.

XI. LDL (low-density lipoprotein) is a major carrier of cholesterol and fats in the blood, packaged in apolipoprotein B (ApoB).

• LDL particles, containing ApoB, transport cholesterol and fats, with most of the payload being fat, including linoleic acid.

• About 95% of ApoB in the bloodstream is associated with LDL particles, making it a significant focus in cardiovascular research.

XII. LDL levels alone are not a strong predictor of heart disease, as shown by some risk calculators excluding LDL.

• In 2013, discussions considered removing LDL from heart disease risk calculators due to its weak predictive power.

• Studies like the Jupiter trial found no significant relationship between LDL levels and cardiovascular disease rates.

XIII. Familial hypercholesterolemia (FH) results in high blood LDL levels due to dysfunctional LDL receptors, reducing cholesterol uptake into artery walls.

• FH patients have impaired LDL receptors, leading to elevated blood LDL but reduced cholesterol in artery walls.

• This condition highlights that high blood LDL does not necessarily translate to increased atherosclerosis.

XIV. PCSK9 mutations increase LDL receptor activity, lowering blood LDL levels and reducing heart disease rates.

• PCSK9 inhibitors increase LDL receptor numbers, enhancing LDL clearance from the blood and lowering heart disease risk.

• People with PCSK9 mutations have more LDL receptors, resulting in lower blood LDL and reduced atherosclerosis.

XV. FH patients historically did not show increased heart disease rates before modern industrial diets, suggesting environmental factors.

• Historical records, as noted by Castellane, show FH patients had normal mortality rates in pre-modern eras, despite high LDL.

• Increased heart disease in FH populations emerged in industrial societies, correlating with dietary changes.

XVI. Oxidized LDL, not native LDL, is a key driver of atherosclerosis by causing macrophages to form foam cells.

• Native LDL does not induce foam cell formation in macrophages, as shown in Brown and Goldstein’s in vitro studies.

• Oxidized LDL, particularly with oxidized linoleic acid, causes macrophages to overconsume, leading to foam cell formation and atherosclerosis.

XVII. Linoleic acid, a polyunsaturated fatty acid (PUFA), is highly susceptible to oxidation and is a major component of LDL particles.

• Linoleic acid, found in high amounts in LDL, is prone to oxidation due to its chemical structure, unlike more stable fats like oleic acid.

• The body cannot synthesize linoleic acid, making dietary intake the sole source of this oxidizable fat in LDL.

XVIII. Antioxidants in LDL particles are insufficient to prevent oxidation of polyunsaturated fatty acids like linoleic acid.

• LDL particles contain antioxidants, but the high PUFA content, particularly linoleic acid, overwhelms their protective capacity.

• This imbalance, noted by Steinberg and Witztum, makes LDL susceptible to oxidation, contributing to atherosclerosis.

XIX. Reducing dietary linoleic acid lowers the susceptibility of LDL to oxidation, decreasing atherosclerosis risk.

• Experiments replacing linoleic acid with oleic acid in diets reduced LDL oxidation, as shown in rabbit and human studies.

• Lowering linoleic acid intake decreases the oxidizable substrate in LDL, reducing foam cell formation.

XX. Scavenger receptors, unlike LDL receptors, take up oxidized LDL in an unregulated manner, contributing to foam cell formation.

• Scavenger receptors in macrophages recognize oxidized LDL, leading to excessive uptake and foam cell formation.

• This unregulated pathway contrasts with the controlled uptake of native LDL via LDL receptors, exacerbating atherosclerosis.

XXI. Oxidized LDL is toxic to both bacteria and human cells, serving as an antibiotic but also causing harm when excessive.

• Oxidized LDL disrupts bacterial quorum sensing, aiding infection prevention, as noted in its role against biofilms.

• Excessive oxidized LDL in the body is toxic, contributing to atherosclerosis by damaging artery walls.

XXII. Sterile inflammation, driven by oxidized LDL, contributes to atherosclerosis without infectious causes.

• Oxidized LDL triggers inflammation in artery walls, leading to plaque formation, as discussed in standard cardiovascular literature.

• This sterile inflammation is a key mechanism in atherosclerosis, independent of bacterial infection.

XXIII. ApoB48, produced in the gut, delivers oxidized fats directly from the diet to the bloodstream, bypassing the liver.

• ApoB48-containing particles, like chylomicrons, transport dietary fats, including oxidized fats, into circulation near the heart.

• This direct delivery of oxidized fats to the heart muscle increases atherosclerosis risk, as noted by Borén (2020).

XXIV. Periodontal disease increases oxidized LDL levels, which decrease with treatment, indicating external sources of oxidation.

• Periodontal disease generates oxidized LDL, contributing to atherosclerosis, as shown by reduced levels after treatment.

• This suggests that oxidation can occur outside the artery wall, challenging the idea that it primarily happens in plaques.

XXV. Most heart attacks occur postprandially, potentially due to a surge of oxidized fats from meals high in seed oils.

• Consuming foods like French fries, high in seed oils, delivers oxidized fats directly into circulation, increasing heart attack risk.

• This postprandial surge of oxidized lipids aligns with the timing of most heart attacks, as noted in the literature.

XXVI. The Maasai population exhibits non-pathological atherosclerosis, with arteries adapting to maintain blood flow despite fat buildup.

• The Maasai, consuming a diet of milk, blood, and beef, develop atherosclerosis but maintain flexible arteries, avoiding heart attacks.

• This adaptation suggests that atherosclerosis does not always lead to pathological outcomes like heart disease.

XXVII. Industrial diets, particularly high in seed oils, correlate with increased heart disease rates globally.

• Epidemiological studies show heart disease rates rose in industrial societies with increased consumption of seed oils.

• Autopsy data reveal higher heart attack rates in populations consuming industrial diets compared to traditional ones.

XXVIII. African-Americans in the 1960s had half the heart disease rate of white Americans, but now have the highest rates in the U.S.

• In the 1960s, African-Americans had a 12.5% heart attack rate compared to 21% for white Americans, as shown in autopsy studies.

• Modern data indicate African-Americans now face the highest heart disease rates, correlating with dietary shifts toward industrial foods.

XXIX. African populations in the 1960s had near-zero heart attack rates, despite genetic similarities to African-Americans.

• A study of 4,500 autopsies in Africa found only one heart attack, contrasting with a 12.5% rate among African-Americans in the U.S.

• This discrepancy highlights the role of environmental factors, particularly diet, in heart disease prevalence.

XXX. The Kitavans and Tsimane populations have no heart disease, despite high ApoB levels, due to low seed oil consumption.

• These populations consume high-carbohydrate, non-industrial diets and exhibit no heart disease, despite elevated ApoB.

• Their low intake of seed oils, rich in linoleic acid, likely prevents the oxidation driving atherosclerosis.

XXXI. Industrial foods, particularly seed oils, are linked to obesity, diabetes, and heart disease in traditional populations adopting modern diets.

• A Kitavan who moved to a neighboring island and adopted an industrial diet became obese, mirroring trends in other populations.

• The Tsimane’s obesity rates correlate with access to industrial foods via motorboats, indicating dietary influence.

XXXII. Egyptian mummies showed atherosclerosis, but this is not representative due to sampling bias toward elites.

• Only high-status individuals were mummified, skewing data and making it unrepresentative of the broader population.

• Modern epidemiological methods, applied to current populations, provide more reliable insights into heart disease causes.

XXXIII. The Minnesota Coronary Experiment found that lowering cholesterol with polyunsaturated fats increased heart disease mortality.

• The experiment, designed by Ancel Keys, showed higher heart disease rates in those with greater cholesterol reduction via seed oils.

• Results were buried until 1989, 16 years after the study ended, due to conflicting with established dietary guidelines.

XXXIV. The Lyon Diet Heart Study successfully reduced heart disease by lowering linoleic acid and increasing omega-3 fats.

• This study reduced linoleic acid and increased alpha-linolenic acid, leading to lower heart disease rates.

• The dietary shift increased omega-3 fats like EPA in LDL, which is now an FDA-approved treatment for heart disease prevention.

XXXV. Statins lower LDL by inhibiting cholesterol synthesis and may have antioxidant effects, reducing oxidized LDL.

• Statins block the mevalonate pathway, reducing cholesterol production and thus LDL levels in the blood.

• Their potential antioxidant effects, possibly via upregulated LDL receptors, may contribute to their heart disease prevention benefits.

XXXVI. The American Heart Association promotes omega-6 PUFAs as heart-healthy but advises against fried foods, creating a contradiction.

• Omega-6 fats are labeled heart-healthy due to their LDL-lowering effect, yet fried foods, high in oxidized omega-6s, are discouraged.

• This inconsistency arises because frying oxidizes PUFAs, producing toxic lipids that contribute to atherosclerosis.

XXXVII. Oxidized cholesterol, often bound to linoleic acid, is toxic and found in atherosclerotic plaques.

• Linoleic acid’s high oxidation potential can oxidize cholesterol in LDL, making it toxic and contributing to plaque formation.

• This process explains the presence of both oxidized fats and cholesterol in atherosclerotic lesions.

XXXVIII. Smoking increases LDL oxidation, contributing to atherosclerosis.

• Smoking creates an oxidative environment that promotes LDL oxidation, increasing atherosclerosis risk.

• Avoiding smoking is a key strategy to reduce oxidized LDL and subsequent heart disease risk.

XXXIX. Pollution, such as leaded gasoline, historically increased LDL oxidation and heart disease risk.

• Environmental pollutants like lead increased oxidative stress, leading to higher oxidized LDL levels.

• Reducing exposure to pollution can lower the oxidative burden on LDL particles.

XL. Increasing omega-3 fat intake can replace omega-6 fats in LDL, reducing oxidation and atherosclerosis risk.

• Omega-3 fats, like EPA, displace omega-6 fats in LDL, making them less susceptible to oxidation.

• This dietary shift, as shown in the Lyon Diet Heart Study, lowers heart disease risk.

XLI. The liver avoids secreting VLDL particles containing oxidized PUFAs, which explains why seed oils lower LDL levels.

• Polyunsaturated fats impair VLDL production in the liver, reducing LDL levels because oxidized fats are not secreted.

• This mechanism, described by Ronald Krauss, highlights why seed oils lower blood cholesterol but may not reduce heart disease risk.

XLII. The Seven Countries Study by Ancel Keys suggested oxidized lipids, not cholesterol, as a potential cause of heart disease.

• The study’s concluding remarks noted that oxidized lipids might be the true culprit in atherosclerosis, not cholesterol itself.

• Keys did not sign the final paper, possibly due to its conflict with his earlier cholesterol hypothesis.

XLIII. Native LDL does not cause foam cell formation, unlike oxidized or modified LDL.

• In vitro studies by Brown and Goldstein showed that native LDL does not induce macrophages to become foam cells.

• Only modified LDL, such as oxidized or acetylated forms, triggers the overconsumption leading to atherosclerosis.

XLIV. The Borén (2020) paper emphasizes oxidized LDL as the initiating step in atherosclerosis.

• The European Atherosclerosis Society’s consensus statement identifies oxidized LDL as a key driver of plaque formation.

• This aligns with the standard cardiology model, focusing on oxidation rather than native LDL levels.

XLV. Aggregated LDL, linked to saturated fats in some models, requires linoleic acid for aggregation to occur.

• Studies cited by Borén (2020) show that LDL aggregation, induced by saturated fat-based signaling, depends on linoleic acid presence.

• Replacing linoleic acid with oleic acid prevents aggregation, highlighting linoleic acid’s role in atherosclerosis.

XLVI. Heart disease rates increased in the 20th century, correlating with industrial diet adoption, particularly seed oils.

• Epidemiological data show a rise in heart disease as industrial foods, including seed oils, became prevalent.

• This trend was observed across countries, with higher rates in industrialized nations consuming more processed foods.

XLVII. The National Diet-Heart Study failed to show benefits from replacing animal fats with PUFAs, leading to its discontinuation.

• This large-scale study, involving multiple stakeholders, found no significant heart disease reduction with PUFA-rich diets.

• Its lack of results led to its termination, with the Minnesota Coronary Experiment being its most rigorous component.

XLVIII. The Minnesota Coronary Experiment’s results were suppressed due to conflicting with dietary guidelines promoting PUFAs.

• The experiment’s finding that PUFA-induced cholesterol reduction increased heart disease mortality was not published until 1989.

• This delay reflects the influence of established dietary dogmas favoring seed oils over animal fats.

XLIX. ApoB48 particles deliver oxidized fats directly to the heart, increasing atherosclerosis risk.

• ApoB48, found in chylomicrons, bypasses the liver, delivering dietary oxidized fats directly to the heart muscle.

• This pathway, noted by Borén, is understudied but a significant contributor to atherosclerotic plaque formation.

L. The visceral fat around the gut may act as a filter for dietary fats before they enter circulation.

• Dietary fats absorbed in the intestine pass through the lymph system and visceral fat, potentially filtering harmful lipids.

• This process suggests a protective mechanism that may be overwhelmed by high seed oil consumption.

LI. Genetic variation in linoleic acid conversion to longer-chain PUFAs influences heart disease risk.

• Individuals with faster conversion of linoleic acid to arachidonic acid, often linked to agricultural ancestry, may face altered risks.

• African-Americans, slower converters, have high heart disease rates, possibly due to high omega-6 intake in modern diets.

LII. Indian women show higher conversion of short-chain to long-chain PUFAs, likely due to historical dietary pressures.

• A lack of animal foods in traditional Indian diets created selection pressure for efficient PUFA conversion.

• This genetic adaptation highlights how dietary history shapes metabolic responses to PUFAs.

LIII. ApoB48 is found across all lipoprotein sizes, not just chylomicrons, challenging traditional models.

• Frank Sacks’ research shows ApoB48 in various lipoproteins, contradicting the idea that it’s exclusive to chylomicrons.

• This finding underscores the role of ApoB48 in delivering oxidized fats throughout the body.

LIV. The presence of undigested ApoB48 in atherosclerotic plaques confirms its role in disease progression.

• Studies have identified ApoB48 molecules in the gruel of plaques, linking dietary oxidized fats to atherosclerosis.

• This direct evidence supports the hypothesis that gut-derived lipids contribute to plaque formation.

LV. The standard cardiology model overemphasizes LDL and cholesterol, ignoring the critical role of oxidation.

• Mainstream cardiology focuses on LDL levels as a primary risk factor, despite evidence pointing to oxidized LDL.

• This misemphasis leads to dietary recommendations that may not address the root cause of atherosclerosis.

LVI. Ancel Keys’ hypothesis that saturated fats cause heart disease was based on their effect on raising LDL levels.

• Keys believed saturated fats increased LDL, which he initially linked to heart disease, influencing dietary guidelines.

• Later findings, including his own, suggested oxidized lipids, not LDL levels, were more critical.

LVII. Seed oils lower LDL levels but increase oxidized LDL, potentially worsening heart disease outcomes.

• Polyunsaturated fats in seed oils reduce VLDL production, lowering LDL but increasing oxidized lipid content.

• This paradox explains why seed oil consumption may not reduce heart disease risk despite lower LDL.

LVIII. The liver’s refusal to secrete oxidized PUFAs protects the body but masks the underlying issue of oxidation.

• The liver avoids exporting oxidized lipids, reducing circulating LDL but not addressing the toxicity of oxidized PUFAs.

• This mechanism, described by Krauss, highlights a protective but incomplete response to dietary PUFAs.

LIX. The cardiovascular literature acknowledges oxidized LDL’s role but often downplays dietary sources like seed oils.

• Papers like Borén (2020) confirm oxidized LDL’s role in atherosclerosis but avoid emphasizing seed oils as a source.

• This selective emphasis may reflect biases or political pressures within the field.

LX. The 2017 European Atherosclerosis Society paper overstated LDL’s role by selectively citing studies showing a positive correlation.

• The paper’s graph showed a positive LDL-heart disease relationship, but including all cited studies flattened the correlation.

• This selective reporting suggests a bias toward maintaining the LDL-centric model.

LXI. The 2020 Borén paper focuses on mechanisms, identifying oxidized LDL as a key initiator of atherosclerosis.

• Unlike the 2017 paper, Borén (2020) details how oxidized LDL, not native LDL, drives plaque formation.

• This shift reflects growing recognition of oxidation as the critical factor in atherosclerosis.

LXII. Minimally modified LDL is still recognized by LDL receptors, but heavily oxidized LDL shifts to scavenger receptors.

• Minimally oxidized LDL can be taken up by LDL receptors, maintaining regulated uptake by macrophages.

• Heavily oxidized LDL, unrecognized by LDL receptors, is taken up by scavenger receptors, leading to foam cell formation.

LXIII. The oxidation of LDL occurs in the bloodstream, not solely in the artery wall, as previously thought.

• Factors like periodontal disease and dietary oxidized fats contribute to LDL oxidation outside the artery wall.

• This challenges the traditional model that oxidation primarily occurs within atherosclerotic plaques.

LXIV. FH patients have high blood LDL but lower arterial wall LDL, yet still face increased heart disease in modern diets.

• Dysfunctional LDL receptors in FH reduce cholesterol uptake into artery walls, yet heart disease rates rise with industrial diets.

• This suggests dietary factors, like PUFAs, drive oxidation and atherosclerosis in FH patients.

LXV. The increase in heart disease in FH populations coincided with the rise of industrial diets high in seed oils.

• Castellane’s analysis shows FH mortality rates rose in the late 1800s, aligning with increased seed oil consumption.

• This temporal correlation implicates dietary PUFAs as a key environmental factor.

LXVI. Non-pathological atherosclerosis, as seen in the Maasai, does not lead to heart attacks due to arterial flexibility.

• The Maasai’s arteries expand to accommodate fat buildup, maintaining blood flow and preventing heart attacks.

• This contrasts with pathological atherosclerosis in industrial populations, where rigid arteries cause blockages.

LXVII. Heart disease is primarily an environmental, not genetic, condition, driven by dietary changes.

• Populations like the Kitavans and Tsimane show no heart disease until exposed to industrial diets, despite genetic similarities.

• Historical data on FH patients further confirm that environmental factors, not genetics, drive heart disease.

LXVIII. Seed oils, high in linoleic acid, are a major component of industrial diets linked to heart disease.

• Industrial diets, rich in seed oils, correlate with increased heart disease rates across populations.

• The Kitavans and Tsimane, with low seed oil intake, have no heart disease, supporting this link.

LXIX. The American Heart Association’s promotion of seed oils as heart-healthy ignores their role in LDL oxidation.

• Seed oils are recommended for lowering LDL, yet their high linoleic acid content increases oxidized LDL, promoting atherosclerosis.

• This contradiction is evident in warnings against fried foods, which contain oxidized PUFAs from seed oils.

LXX. The Lyon Diet Heart Study’s success highlights the benefit of reducing linoleic acid and increasing omega-3 fats.

• The study’s dietary intervention lowered linoleic acid and increased alpha-linolenic acid, reducing heart disease rates.

• This approach increased EPA in LDL, a protective omega-3 fat, validated by later FDA approval.

LXXI. Statins may reduce heart disease risk partly through antioxidant effects, not just LDL reduction.

• Statins’ inhibition of cholesterol synthesis lowers LDL, but their antioxidant properties may also reduce oxidized LDL.

• This pleiotropic effect could explain their efficacy beyond simple LDL reduction.

LXXII. HDL protects against heart disease by removing oxidized lipids from circulation.

• HDL’s role is to clear oxidized lipids, reducing their toxic impact on artery walls.

• If HDL loses this ability, its protective effect against atherosclerosis diminishes.

LXXIII. The Minnesota Coronary Experiment’s failure to reduce heart disease with PUFAs challenges the cholesterol hypothesis.

• The experiment showed that replacing animal fats with PUFAs increased heart disease mortality, contradicting expectations.

• This finding, buried for 16 years, suggests PUFAs may exacerbate rather than prevent heart disease.

LXXIV. The Seven Countries Study hinted at oxidized lipids as a cause of heart disease, not cholesterol itself.

• The study’s final remarks suggested oxidized lipids, not cholesterol, were driving atherosclerosis, challenging Keys’ hypothesis.

• Keys’ refusal to sign the paper reflects discomfort with these findings conflicting with his earlier views.

LXXV. The liver’s regulation of VLDL secretion prevents oxidized lipids from entering circulation, lowering LDL levels.

• The liver avoids secreting VLDL with oxidized PUFAs, reducing circulating LDL but not addressing oxidation’s root cause.

• This mechanism explains why seed oils lower LDL but may not reduce heart disease risk.

LXXVI. ApoB48’s role in delivering dietary oxidized fats directly to the heart is understudied but significant.

• ApoB48 particles, carrying oxidized fats from the gut, contribute to plaque formation by bypassing liver regulation.

• Borén (2020) highlights triglyceride-rich lipoproteins, including ApoB48, as a major atherosclerosis risk factor.

LXXVII. Genetic conditions like FH show variable heart disease expression, influenced by diet.

• FH patients exhibit diverse heart disease outcomes, not directly tied to LDL levels, as shown by historical data.

• Dietary shifts toward high-PUFA industrial foods correlate with increased heart disease in FH populations.

LXXVIII. The Maasai’s diet of animal products results in atherosclerosis without heart attacks, due to arterial adaptation.

• Their high-fat diet leads to fat-lined arteries, but flexible vessels prevent blockages and heart attacks.

• This contrasts with industrial populations, where rigid arteries and oxidized lipids drive pathological outcomes.

LXXIX. Industrial foods, including seed oils, drive obesity and diabetes alongside heart disease.

• Traditional populations like the Kitavans develop obesity and diabetes when adopting industrial diets high in seed oils.

• The Tsimane’s correlation of obesity with motorboat access to industrial foods supports this link.

LXXX. The cardiovascular field’s focus on LDL overlooks the critical role of oxidized PUFAs.

• Despite evidence from Borén (2020) and others, mainstream cardiology emphasizes LDL over oxidized lipids.

• This focus leads to dietary recommendations that may inadvertently increase atherosclerosis risk.

LXXXI. Oxidized cholesterol in plaques results from linoleic acid oxidation, not direct cholesterol oxidation.

• Linoleic acid’s high oxidation potential in LDL oxidizes bound cholesterol, contributing to plaque toxicity.

• This process explains the presence of both oxidized fats and cholesterol in atherosclerotic lesions.

LXXXII. Reducing dietary linoleic acid is a key strategy to lower oxidized LDL and heart disease risk.

• Lowering linoleic acid intake reduces the oxidizable substrate in LDL, decreasing foam cell formation.

• The Lyon Diet Heart Study’s success in reducing linoleic acid supports this approach.

LXXXIII. Increasing omega-3 fats displaces omega-6 fats in LDL, reducing oxidation risk.

• Omega-3 fats like EPA replace linoleic acid in LDL, making them less prone to oxidation.

• This dietary shift, validated by the Lyon study, lowers atherosclerosis risk.

LXXXIV. Smoking and pollution increase LDL oxidation, exacerbating atherosclerosis.

• Environmental factors like smoking and pollution create oxidative stress, increasing oxidized LDL levels.

• Avoiding these factors is critical to reducing heart disease risk.

LXXXV. The American Heart Association’s dietary guidelines reflect historical biases from Ancel Keys’ cholesterol hypothesis.

• Keys’ advocacy for replacing animal fats with seed oils shaped guidelines, despite later evidence implicating oxidized lipids.

• These guidelines persist, despite contradictions like warnings against fried foods containing oxidized PUFAs.

LXXXVI. The Minnesota Coronary Experiment’s suppression reflects the influence of dietary dogmas.

• The experiment’s unfavorable results were delayed for 16 years due to their conflict with established PUFA recommendations.

• This highlights how scientific biases can delay the acceptance of contradictory evidence.

LXXXVII. The Lyon Diet Heart Study’s unique focus on reducing linoleic acid set it apart from other interventions.

• Unlike other studies, the Lyon study specifically lowered linoleic acid while increasing omega-3 fats, reducing heart disease.

• This approach directly addressed the oxidation issue, unlike PUFA-heavy interventions.

LXXXVIII. Statins’ antioxidant effects may contribute to their efficacy beyond LDL reduction.

• Statins’ potential to upregulate LDL receptors and reduce oxidized LDL may explain their heart disease benefits.

• This pleiotropic effect suggests a broader mechanism than simple cholesterol lowering.

LXXXIX. HDL’s protective role depends on its ability to clear oxidized lipids from circulation.

• HDL removes oxidized lipids, preventing their accumulation in artery walls and reducing atherosclerosis risk.

• Impaired HDL function diminishes this protective effect, increasing heart disease risk.

XC. The cardiovascular field’s reluctance to emphasize seed oils reflects political and historical influences.

• Despite evidence from Borén (2020) and others, seed oils’ role in LDL oxidation is downplayed in mainstream recommendations.

• This may stem from long-standing dietary guidelines rooted in Keys’ cholesterol hypothesis.

XCI. FH patients’ historical lack of heart disease suggests dietary PUFAs as a modern trigger.

• Before industrial diets, FH patients had normal heart disease rates, despite high LDL levels.

• The rise in heart disease with seed oil consumption implicates PUFAs as a key environmental factor.

XCII. The Maasai’s non-pathological atherosclerosis challenges the assumption that all atherosclerosis is harmful.

• Their fat-lined but flexible arteries allow normal blood flow, preventing heart attacks despite atherosclerosis.

• This suggests that the nature of atherosclerosis, not its presence, determines its impact.

XCIII. Industrial diets’ spread correlates with global heart disease increases, particularly in developing nations.

• As industrial foods, including seed oils, spread to developing countries, heart disease rates rise.

• This trend, observed in epidemiological studies, underscores the environmental basis of heart disease.

XCIV. ApoB48’s direct delivery of oxidized fats to the heart bypasses protective liver mechanisms.

• Unlike ApoB100, ApoB48 delivers dietary fats, including oxidized PUFAs, directly to circulation, increasing plaque risk.

• This pathway, highlighted by Borén, explains postprandial heart attack risks.

XCV. Genetic variation in PUFA conversion influences individual heart disease risk in modern diets.

• Faster converters of linoleic acid to arachidonic acid may face altered risks due to dietary PUFA intake.

• This variation, linked to ancestry, explains differential heart disease outcomes in populations like African-Americans.

XCVI. The liver’s regulation of VLDL secretion protects against oxidized lipid circulation but does not address dietary sources.

• By avoiding secretion of oxidized PUFAs, the liver lowers LDL but does not prevent dietary intake of oxidizable fats.

• This highlights the need to reduce dietary linoleic acid to address the root cause.

XCVII. The Seven Countries Study’s acknowledgment of oxidized lipids was overshadowed by its cholesterol focus.

• The study’s suggestion that oxidized lipids drive heart disease was not emphasized due to Keys’ earlier cholesterol hypothesis.

• This reflects a broader tendency to prioritize cholesterol over oxidation in cardiovascular research.

XCVIII. The Borén (2020) paper’s focus on triglyceride-rich lipoproteins highlights ApoB48’s role in atherosclerosis.

• Triglyceride-rich lipoproteins, including ApoB48 particles, are identified as significant contributors to plaque formation.

• This underscores the importance of dietary oxidized fats in heart disease risk.

XCIX. The cardiovascular field’s selective emphasis on LDL reflects biases rather than mechanistic evidence.

• Despite evidence implicating oxidized LDL, mainstream cardiology continues to focus on LDL levels.

• This bias, rooted in historical guidelines, overlooks the critical role of dietary PUFAs.

C. Reducing seed oil consumption and increasing omega-3 fats is a practical strategy to lower heart disease risk.

• Lowering linoleic acid and increasing omega-3 fats reduces LDL oxidation, as shown in the Lyon Diet Heart Study.

• This dietary approach aligns with mechanistic evidence and offers a clear path to heart health.

The Influence of Diet on Cardiovascular Health: Insights from the Mind and Matter Podcast

McKinsey Health Institute Report

August 17, 2025

Executive Summary

Cardiovascular disease (CVD) remains the leading cause of mortality globally, with diet emerging as a critical modifiable risk factor. Drawing from the Mind and Matter podcast by Nick Norwitz, this report synthesizes evidence implicating dietary factors, particularly oxidized lipids from seed oils, in the development of atherosclerosis and subsequent CVD. The podcast challenges the conventional cholesterol-centric model, emphasizing the role of oxidized low-density lipoprotein (LDL) driven by dietary linoleic acid, a polyunsaturated fatty acid (PUFA) abundant in industrial seed oils. Key findings include:

• Oxidized LDL as a Primary Driver: Unlike native LDL, oxidized LDL, particularly containing oxidized linoleic acid, initiates atherosclerosis by promoting foam cell formation in artery walls.

• Dietary Linoleic Acid and Seed Oils: Industrial diets high in seed oils (e.g., soybean, corn, and canola oil) increase linoleic acid intake, elevating oxidized LDL and CVD risk.

• Historical and Population Insights: Populations like the Maasai and Kitavans, with low seed oil consumption, exhibit minimal CVD despite high LDL or atherosclerosis, highlighting environmental influences over genetics.

• Interventional Evidence: Studies like the Lyon Diet Heart Study demonstrate that reducing linoleic acid and increasing omega-3 fats significantly lowers CVD risk.

• Recommendations: Stakeholders in healthcare, food production, and policy should prioritize reducing dietary linoleic acid, promoting omega-3 fats, and aligning guidelines with mechanistic evidence.

This report outlines the science, historical context, and actionable strategies to address diet-related CVD risk, advocating for a shift from LDL-focused interventions to oxidation-centric approaches.

Table of Contents

1. Introduction

   • 1.1 Background on Cardiovascular Disease

   • 1.2 Objectives and Scope

2. The Science of Atherosclerosis

   • 2.1 Mechanisms of Plaque Formation

   • 2.2 Role of Oxidized LDL

   • 2.3 Linoleic Acid and Seed Oils

3. Historical Context and Population Studies

   • 3.1 Evolution of the Cholesterol Hypothesis

   • 3.2 Insights from Traditional Populations

   • 3.3 Industrial Diets and Rising CVD Rates

4. Evidence from Interventional Studies

   • 4.1 The Minnesota Coronary Experiment

   • 4.2 The Lyon Diet Heart Study

   • 4.3 Implications for Statins and Other Interventions

5. Current Dietary Guidelines and Challenges

   • 5.1 American Heart Association Recommendations

   • 5.2 Contradictions in PUFA Advocacy

   • 5.3 Influence of Historical Biases

6. Strategic Recommendations

   • 6.1 For Healthcare Providers

   • 6.2 For Food Industry Stakeholders

   • 6.3 For Policymakers

   • 6.4 For Consumers

7. Future Directions

   • 7.1 Research Priorities

   • 7.2 Innovation in Food Systems

   • 7.3 Leveraging Technology for Personalized Nutrition

8. Conclusion

9. References

10. Appendices

1. Introduction

1.1 Background on Cardiovascular Disease

Cardiovascular disease, encompassing conditions like myocardial infarction and stroke, accounts for approximately 17.9 million deaths annually, making it the leading global cause of mortality (World Health Organization, 2024). Atherosclerosis, the buildup of plaques in artery walls, is a primary driver of CVD, characterized by inflammation and lipid accumulation. Historically, cholesterol and LDL have been central to CVD research and treatment, but emerging evidence, as discussed in the Mind and Matter podcast by Nick Norwitz, shifts focus to oxidized lipids, particularly those derived from dietary PUFAs like linoleic acid. This report explores how dietary patterns, especially the rise of industrial seed oils, influence CVD risk and proposes strategies for stakeholders to address this public health challenge.

1.2 Objectives and Scope

This report aims to:

• Synthesize mechanistic insights from the podcast on how diet, particularly linoleic acid, contributes to atherosclerosis.

• Analyze historical and population-based evidence to contextualize dietary impacts on CVD.

• Evaluate interventional studies to assess dietary modification efficacy.

• Propose actionable recommendations for stakeholders to reduce CVD risk through dietary changes.

• Identify future research and innovation opportunities.

The scope focuses on dietary influences, particularly seed oils, while acknowledging other factors like genetics, smoking, and pollution, as discussed in the podcast.

2. The Science of Atherosclerosis

2.1 Mechanisms of Plaque Formation

Atherosclerosis involves the accumulation of cholesterol, fats, dead cells, and macrophages in artery walls, forming plaques that can rupture and cause heart attacks. Macrophages, acting as a "cleanup crew," ingest damaged tissue and bacteria but can overconsume fats and cholesterol, becoming foam cells—a hallmark of early atherosclerosis. These foam cells die, releasing undigested material that forms the "pus-filled" gruel in plaques, as described by Norwitz.

2.2 Role of Oxidized LDL

Native LDL, a carrier of cholesterol and fats, does not induce foam cell formation, as shown in Brown and Goldstein’s in vitro studies. However, oxidized LDL, particularly containing oxidized linoleic acid, is taken up unregulated by macrophage scavenger receptors, leading to foam cell formation. Borén (2020) identifies oxidized LDL as the initiating step in atherosclerosis, emphasizing its toxicity to both bacteria and human cells.

2.3 Linoleic Acid and Seed Oils

Linoleic acid, a PUFA abundant in seed oils (e.g., soybean, corn, canola), is highly susceptible to oxidation due to its chemical structure. Unlike monounsaturated fats like oleic acid, linoleic acid’s double bonds make it prone to forming toxic oxidized lipids in LDL particles. The podcast highlights that dietary linoleic acid, which the body cannot synthesize, is the primary source of oxidizable fats in LDL, directly linking seed oil consumption to increased CVD risk.

3. Historical Context and Population Studies

3.1 Evolution of the Cholesterol Hypothesis

The cholesterol hypothesis, championed by Ancel Keys, initially linked dietary cholesterol and saturated fats to CVD via elevated LDL levels. However, Keys himself noted in 1952 and 1997 that dietary cholesterol has minimal impact on blood cholesterol in humans due to a negative feedback mechanism. The Seven Countries Study, led by Keys, later suggested oxidized lipids as a potential cause, but this was overshadowed by the cholesterol focus.

3.2 Insights from Traditional Populations

Populations like the Maasai, Kitavans, and Tsimane provide critical insights. The Maasai, consuming a diet of milk, blood, and beef, develop non-pathological atherosclerosis, with flexible arteries preventing heart attacks. Similarly, the Kitavans and Tsimane, with high-carbohydrate, low-seed-oil diets, exhibit no CVD despite elevated ApoB levels. These cases suggest that atherosclerosis is not inherently pathological and that industrial diets drive adverse outcomes.

3.3 Industrial Diets and Rising CVD Rates

The rise of industrial diets, particularly high in seed oils, correlates with increased CVD rates. In the 1960s, African-Americans had half the heart attack rate of white Americans (12.5% vs. 21%), but today, they face the highest rates in the U.S., aligning with dietary shifts toward processed foods. African populations in the 1960s had near-zero heart attack rates, despite genetic similarities, underscoring environmental influences.

4. Evidence from Interventional Studies

4.1 The Minnesota Coronary Experiment

Conducted by Ancel Keys, this study replaced saturated fats with PUFA-rich seed oils, expecting reduced CVD. Instead, greater cholesterol reduction correlated with higher heart disease mortality. Results were suppressed until 1989 due to conflicts with dietary guidelines promoting PUFAs, highlighting biases in nutritional science.

4.2 The Lyon Diet Heart Study

This study reduced linoleic acid and increased omega-3 fats (e.g., alpha-linolenic acid), significantly lowering CVD rates. The intervention increased EPA in LDL, a protective omega-3 fat now FDA-approved for CVD prevention. This success underscores the benefit of replacing omega-6 PUFAs with omega-3s.

4.3 Implications for Statins and Other Interventions

Statins lower LDL by inhibiting cholesterol synthesis and may reduce oxidized LDL through antioxidant effects. However, their efficacy is not solely due to LDL reduction, suggesting a need to focus on oxidation. HDL’s role in clearing oxidized lipids further supports targeting oxidation over LDL levels.

5. Current Dietary Guidelines and Challenges

5.1 American Heart Association Recommendations

The American Heart Association (AHA) promotes omega-6 PUFAs as heart-healthy for lowering LDL but advises against fried foods, which contain oxidized PUFAs. This contradiction reflects a failure to address the oxidative potential of seed oils, as noted in the podcast.

5.2 Contradictions in PUFA Advocacy

Seed oils lower LDL by impairing VLDL production in the liver, but they increase oxidized LDL, potentially worsening CVD outcomes. The AHA’s focus on LDL reduction overlooks this paradox, rooted in Keys’ cholesterol hypothesis.

5.3 Influence of Historical Biases

The persistence of PUFA-centric guidelines stems from historical biases, including Keys’ influence and the suppression of studies like the Minnesota Coronary Experiment. The 2017 European Atherosclerosis Society paper overstated LDL’s role, selectively citing studies to maintain the cholesterol narrative.

6. Strategic Recommendations

6.1 For Healthcare Providers

• Educate on Oxidation: Train providers to focus on oxidized LDL as a key CVD driver, emphasizing dietary sources like seed oils.

• Promote Omega-3 Diets: Recommend diets high in omega-3 fats (e.g., fish, flaxseed) to displace linoleic acid in LDL.

• Personalized Nutrition: Use genetic profiling to identify patients with high PUFA conversion rates, tailoring dietary advice.

6.2 For Food Industry Stakeholders

• Reduce Seed Oil Use: Reformulate processed foods to minimize linoleic acid, replacing it with stable fats like oleic acid.

• Innovate Healthier Alternatives: Develop products with clinically proven ingredients, aligning with consumer demand for science-backed solutions (McKinsey, 2024).

• Partner with Testing Kits: Collaborate with at-home testing providers to offer cholesterol and nutrient deficiency monitoring, driving demand for healthier foods.

6.3 For Policymakers

• Update Dietary Guidelines: Revise guidelines to prioritize reducing linoleic acid and increasing omega-3 fats, based on mechanistic evidence.

• Subsidize Healthy Foods: Incentivize production and consumption of omega-3-rich foods to make them more accessible.

• Regulate Seed Oil Marketing: Restrict claims promoting seed oils as heart-healthy, addressing their oxidative risks.

6.4 For Consumers

• Limit Seed Oils: Avoid processed foods high in soybean, corn, and canola oils, opting for olive oil or animal fats.

• Increase Omega-3 Intake: Incorporate fish, flaxseed, or walnuts into diets to reduce LDL oxidation.

• Use At-Home Testing: Leverage home cholesterol testing kits to monitor and adjust dietary habits (McKinsey, 2024).

7. Future Directions

7.1 Research Priorities

• Oxidized LDL Mechanisms: Conduct studies to quantify the contribution of dietary linoleic acid to oxidized LDL levels.

• Population-Specific Interventions: Investigate dietary impacts on high-risk groups, such as African-Americans with genetic predispositions to PUFA metabolism.

• Long-Term Omega-3 Effects: Expand research on omega-3 supplementation’s impact on CVD outcomes across diverse populations.

7.2 Innovation in Food Systems

• AI-Driven Personalization: Develop AI tools to recommend diets based on individual genetic and metabolic profiles, reducing reliance on seed oils (McKinsey, 2024).

• Sustainable Omega-3 Sources: Invest in algae-based omega-3 production to provide scalable, environmentally friendly alternatives to fish.

• Clean Label Reformulation: Create processed foods with stable, non-oxidizable fats to meet consumer demand for clinical efficacy.

7.3 Leveraging Technology for Personalized Nutrition

• Wearable Biomonitoring: Promote wearable devices to track cholesterol and oxidative stress markers, guiding dietary choices (McKinsey, 2024).

• Telehealth Integration: Pair at-home testing with telehealth to provide real-time dietary guidance, enhancing consumer engagement.

• Data Privacy: Ensure robust data protection in wearable and AI-driven nutrition platforms to build consumer trust.

8. Conclusion

The Mind and Matter podcast by Nick Norwitz highlights a paradigm shift in understanding CVD, moving from a cholesterol-centric model to one focused on oxidized LDL and dietary linoleic acid. Industrial diets, particularly high in seed oils, drive atherosclerosis by increasing oxidized lipids, while traditional diets low in PUFAs correlate with minimal CVD. Interventional studies like the Lyon Diet Heart Study validate the efficacy of reducing linoleic acid and increasing omega-3 fats. Stakeholders must align guidelines, reformulate foods, and leverage technology to address this public health crisis. By prioritizing oxidation over LDL levels, society can reduce CVD’s global burden and promote metabolic health for all.

9. References

• Borén, J., et al. (2020). Low-density lipoproteins cause atherosclerotic cardiovascular disease: Pathophysiological, genetic, and therapeutic insights. European Heart Journal.

• World Health Organization. (2024). Cardiovascular diseases (CVDs).

• McKinsey & Company. (2024). McKinsey Health & Wellness report shows consumers expect effective, science-backed solutions.

• McKinsey & Company. (2024). Consumers Demand Data-driven Wellness Products.

• Norwitz, N. (2025). Mind and Matter podcast transcript.

10. Appendices

Appendix A: Key Definitions

• Atherosclerosis: The buildup of plaques in artery walls, leading to CVD.

• Oxidized LDL: LDL particles containing oxidized lipids, particularly linoleic acid, driving foam cell formation.

• Linoleic Acid: An omega-6 PUFA found in seed oils, highly susceptible to oxidation.

Appendix B: Population Data

• Maasai: Non-pathological atherosclerosis with no heart attacks.

• Kitavans/Tsimane: No CVD despite high ApoB, low seed oil intake.

• African-Americans (1960s vs. today): Shift from low to high CVD rates with industrial diet adoption.

Appendix C: Interventional Study Summaries

• Minnesota Coronary Experiment: Increased CVD mortality with PUFA-rich diets.

• Lyon Diet Heart Study: Reduced CVD with lower linoleic acid and higher omega-3 fats.

This extensive podcast excerpt from "Seed Oils Heart Disease Oxidized LDL Cholesterol Fat Cardiology.mp3" features an in-depth discussion with an expert who holds a Ph.D. in neuroscience and specializes in molecular, developmental, and evolutionary genetics. The podcast aims to translate complex scientific information about how the body reacts to diet, focusing specifically on heart disease and the role of dietary fats. The host leverages his strong scientific background to critically examine conventional wisdom in cardiology, particularly regarding the widely held belief that high cholesterol, especially LDL, is the primary driver of heart disease. The discussion delves into the pathophysiology of atherosclerosis, emphasizing the critical distinction between "native" LDL and "oxidized" LDL (oxLDL), positing that the latter, laden with oxidized polyunsaturated fatty acids (PUFAs) like linoleic acid (abundant in seed oils), is the true culprit behind plaque formation and cardiovascular issues. The conversation also highlights historical and epidemiological data, including studies on familial hypercholesterolemia and various global populations, to argue that heart disease is primarily an environmental problem linked to the rise of industrial diets, particularly seed oils, rather than a purely genetic one. The overarching purpose is to challenge mainstream cardiological views and suggest that reducing dietary intake of seed oils and other sources of PUFAs is a crucial step in preventing heart disease. 

Discuss Cardiovascular Disease.

Cardiovascular disease (CVD), particularly atherosclerosis, is described as a major health concern and a leading cause of death globally12. However, the sources present contrasting views on its underlying causes, traditional treatments, and the role of dietary factors.

Mainstream vs. Alternative Views on Cardiovascular Disease

Traditional/Mainstream View:

• Atherosclerosis is commonly understood as a process where "boils" or "pus-filled infections" (atheromas/plaques) form on the inside of arteries3. These plaques, primarily composed of cholesterol and fats, can become inflamed, burst, and block blood flow, leading to events like heart attacks3....

• The conventional belief, influenced by historical studies (including those on rabbits), posits that dietary cholesterol directly causes atherosclerosis6....

• Low-density lipoprotein (LDL) is widely considered "bad cholesterol," and high LDL levels are thought to drive heart disease910. Mainstream cardiology often focuses on lowering LDL as a primary treatment goal1112.

• High blood pressure (hypertension) is defined by guidelines from organizations like the American Heart Association (AHA) and American College of Cardiology (ACC)13. For adults, normal blood pressure is less than 120/80 mmHg, while 130/80 mmHg or higher is considered elevated and prompts medical intervention, often involving drugs14.

Alternative Perspectives and Critiques: The sources strongly challenge the mainstream narrative, suggesting that current medical approaches are often "pseudoscientific and based on profit"13.

• Reinterpreting Blood Pressure:

    ◦ High blood pressure is argued not to be a "disease" itself, but rather a compensation mechanism or a symptom of underlying damage to the cardiovascular system, such as compromised blood vessels or plaque1516. It's the body's attempt to maintain adequate blood flow to tissues when the original flow is too weak1517.

    ◦ Medications (like ACE-inhibitors, beta-blockers, diuretics, alpha-blockers) that lower blood pressure do not address the root problem; instead, they can slow down healing and give a false sense of health18.

    ◦ Historical data shows that "normal" blood pressure thresholds have changed drastically over the last 125 years, often influenced by economic interests like selling drugs19....

    ◦ Very low blood pressure (e.g., below 90/60 mmHg) is presented as potentially more acutely dangerous than moderately high blood pressure, as it indicates insufficient oxygen and nutrient delivery to tissues, risking organ damage23....

• Challenging the "Bad Cholesterol" Narrative:

    ◦ Dietary cholesterol, for humans, is stated to have little relationship to atherosclerosis826. Even in a case where a man ate 25 eggs a day, his cholesterol levels remained "normal"2728.

    ◦ The issue is not native LDL itself, but oxidized LDL10.... Native LDL particles do not cause foam cells, which are the first sign of atherosclerosis31. When LDL becomes sufficiently oxidized, the normal LDL receptor no longer recognizes it, and it is instead recognized by "scavenger receptors," leading to macrophages "gorging" on it and becoming foam cells29....

    ◦ Linoleic acid, a polyunsaturated fatty acid (PUFA) predominantly found in plants and seed oils, is highly susceptible to oxidation and is a "dominant influence" in determining susceptibility to atherosclerosis when present in LDL particles34.... An "excess of polyunsaturated fatty acids in LDL in relationship to the content of natural endogenous antioxidants" makes them easily oxidized3638.

    ◦ Studies like the Minnesota Coronary Experiment found that the more cholesterol was lowered (by replacing animal fats with PUFAs/seed oils), the worse the outcome of heart disease was3940. This information was reportedly "buried" for years4041.

    ◦ The reason PUFAs lower LDL levels is suggested to be that they impair the liver's production of VLDL (very low-density lipoprotein), which is a precursor to most LDL, because the liver "won't produce a VLDL particle to send out to the body if it contains oxidized polyunsaturated fats"4042.

    ◦ Saturated animal fats, while increasing LDL levels on average, are argued not to be the cause of the problem, as their aggregation effect is prevented if linoleic acid is removed from the LDL particle4344.

Contributing Factors to Cardiovascular Disease

• Dietary Choices:

    ◦ Modern diets high in carbohydrates, especially when combined with plant-based (seed) oils and unsaturated fats, are identified as a primary cause of cardiovascular disease1. Elevated blood glucose damages blood vessels, and glycated/oxidized fatty acids clog arteries1.

    ◦ Seed oils are presented as highly processed industrial foods that contribute to oxidized lipids4546. Fried foods are noted to be particularly harmful because the polyunsaturated vegetable oils they are made from become oxidized47.

    ◦ An animal-based (carnivore) diet is advocated as the only way to genuinely heal the cardiovascular system and restore normal blood flow, thereby naturally stabilizing blood pressure48.... This diet provides essential nutrients like cholesterol, saturated fats, amino acids, and specific vitamins, which are crucial for healing48. People on a strict carnivore diet frequently report blood pressure normalization51.

    ◦ Lowering linoleic acid intake and increasing omega-3 fats (especially long-chain omega-3s like EPA) is highlighted as the most successful dietary intervention for heart disease, shown to replace omega-6 fats in LDL particles and make them less toxic52....

• Immune System Impact (from COVID-19 "vaccines"):

    ◦ COVID-19 "vaccines" are described as "genetic weapons" that cause the body to produce toxic spike proteins55. These proteins induce inflammation, blood clotting, and damage blood vessel walls5657.

    ◦ The injections are claimed to lead to an "immune system collapse," making the body vulnerable to infections and cancers, and driving autoimmune diseases58. Myocarditis (heart inflammation, particularly in young males) is explicitly mentioned as a result of heart cells displaying spike proteins, prompting immune attack57.

    ◦ The modified messenger RNA (mRNA) in these injections is designed to persist, causing individuals to continue producing spike proteins and "effectively poisoning themselves long after injection"57. This leads to a "chronic health crisis" with rising cancers, autoimmune conditions, and sudden deaths5559.

• Environmental Toxins and Lifestyle:

    ◦ Exposure to lead, arsenic, and industrial pollutants can damage kidneys and endothelium, leading to oxidative stress and elevated blood pressure60.

    ◦ Tobacco use and alcohol consumption also contribute to vascular damage and increased blood pressure22....

    ◦ A sedentary lifestyle and excessive screen time can reduce lymphatic flow and muscle pumps, causing fluid stagnation and poor oxygenation, which the body compensates for with higher blood pressure16.

    ◦ Chronic emotional strain and unresolved psycho-emotional conflicts are suggested to activate biological programs that can elevate blood pressure (German New Medicine perspective)16....

The Endocannabinoid System and Energy Balance

The endocannabinoid (eCB) system is presented as an "exostatic" system, whose evolutionary purpose is to promote energy accumulation in anticipation of future periods of scarcity63.... This goes beyond immediate homeostatic regulation, driving an organism to "do a little bit more of what [it is] doing"65.

Mechanisms by which the eCB System Promotes Energy Accumulation:

• Increased Food Intake and Palatability: The system enhances the perceived palatability of food, especially combinations of sugar and fat66.... It can also enhance olfactory perception of food when hungry, making food smells more attractive6970.

• Enhanced Nutrient Absorption: CB-1 receptor activation can reduce gut motility, allowing food to remain longer in the intestine for greater absorption7172.

• Lipogenesis and Fat Storage: In the liver, CB-1 activation contributes to fat synthesis (lipogenesis), and in adipocytes (fat cells), it promotes lipid accumulation7374.

• Reduced Energy Expenditure: The eCB system can decrease mitochondrial activity, leading to less efficient energy usage and more energy accumulation. It also reduces glucose utilization by muscles, saving it for storage7275.

• Behavioral Modulators: The system acts as an anxiolytic (reducing anxiety) and analgesic (reducing pain)7677. By lessening anxiety and pain, it motivates an animal to "go out and look for food" and "expose [itself] to dangers" in the search for resources, even if it means taking risks7778.

Link to Diet and Obesity:

• Endocannabinoids like anandamide and 2-AG are derived from arachidonic acid, which is an omega-6 polyunsaturated fatty acid (PUFA)7980.

• Increasing dietary omega-6 intake directly leads to higher levels of endocannabinoids and increased behaviors associated with energy accumulation8182. This suggests a "self-perpetuating" cycle where consuming more omega-6 rich fats can potentiate the eCB system, leading to more fat consumption and accumulation83....

• The widespread abundance of calories and disproportionately high levels of omega-6 PUFAs in modern diets are considered potentially direct contributors to the obesity epidemic84.

Safety Mechanisms within the eCB System:

• The eCB system exhibits biphasic effects (opposite effects depending on dosage/context) and has built-in "safety systems" to prevent excessive activation86....

• Pregnenolone, a neurosteroid, acts as a natural, specific inhibitor of CB-1 receptors89.... It is synthesized in neurons in response to CB-1 activation and helps to limit excessive cannabinoid effects, such as psychotic-like effects9293. This "negative allosteric modulation" ensures that the system doesn't spiral out of control93....

Broader Sociopolitical Implications

Some sources also suggest broader geopolitical and systemic issues influencing health and conflict. For instance, the "balkanization" of the Middle East, including the destruction of Syria, is presented as an objective of organizations like MI6, CIA, and MSAD, aimed at controlling oil and gas reserves and keeping Arab states in fear of Israel backed by US military power96. The conduct of foreign policy in the region is seen as leading to ongoing conflict, with no peace in sight for Syria or Lebanon, and Israel having an "annexation plan that supports greater Israel"96. Additionally, there are claims that the COVID-19 "vaccine" campaign is part of a globalist agenda to "murder the population" and that "corrupt systems must be restored to legitimacy"5597.

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Discuss Oxidized LDL.

Oxidized Low-Density Lipoprotein (LDL) refers to LDL particles that have undergone oxidation, primarily involving the polyunsaturated fatty acids (PUFAs) they carry, particularly linoleic acid1.... This process is central to how lipids contribute to cardiovascular disease, contrasting with the mainstream view that all LDL cholesterol is inherently "bad"56.

Here's a breakdown of oxidized LDL:

• Formation and Mechanism

    ◦ LDL particles in the bloodstream transport cholesterol and fats, with a significant portion of their fat content being linoleic acid, an omega-6 PUFA that the body cannot synthesize and must be consumed through diet2....

    ◦ Linoleic acid is a fragile fat, highly susceptible to oxidative damage within the oxygen-rich environment of the body, especially in the arteries2....

    ◦ When LDL particles become sufficiently oxidized, they are no longer recognized by the normal LDL receptors on cells. Instead, they are recognized by "scavenger receptors," which are unregulated cleanup pathways11....

    ◦ Macrophages, a type of white blood cell, will excessively ingest these oxidized LDL particles, transforming into what are known as "foam cells"1....

    ◦ The accumulation of these foam cells, along with fats, cholesterol, and dead cells, forms the "atherosclerotic plaques" (also described as "grrul" or "pus") that can clog arteries15....

    ◦ Oxidized lipids, including oxidized cholesterol (which is often oxidized by the more easily oxidized linoleic acid it's bound to), are toxic to cells and serve as signaling molecules for repair1819. The body has systems to dispose of these toxic oxidized lipids quickly1820.

• Role in Atherosclerosis and Heart Disease

    ◦ Research indicates that oxidized LDL is the initiating step in the development of atherosclerosis, rather than native (unoxidized) LDL1.... Native LDL does not cause foam cells to form22.

    ◦ The problem arises when the amount of oxidizable PUFAs in LDL particles exceeds the capacity of the body's natural antioxidants423.

    ◦ This understanding helps explain why high LDL levels in the bloodstream do not always correlate with increased cardiovascular disease risk. For instance, individuals with familial hypercholesterolemia (FH), a genetic condition resulting in very high blood LDL, did not show higher rates of heart disease in pre-modern eras when their diets contained fewer PUFAs24.... Their higher mortality rates only began to increase in the modern industrial era, concurrently with increased PUFA consumption2627.

    ◦ Conversely, populations like the Maasai, Katavans, and Chima, who historically consumed non-industrial diets, exhibited little to no heart disease, despite some having high levels of fats in their arteries or high Apo B levels29.... This suggests that the composition and oxidation state of fats, rather than just their presence or quantity, are critical30.

• Dietary and Environmental Factors

    ◦ The composition of PUFAs in LDL particles is entirely controlled by diet, as the body cannot synthesize linoleic acid8....

    ◦ Studies, such as the Minnesota Coronary Experiment, indicated that attempts to lower cholesterol by replacing animal fats with PUFAs resulted in worse heart disease outcomes34. This is because polyunsaturated fats lower LDL levels by impairing the liver's production of VLDL (very low-density lipoprotein), as the liver will not secrete oxidized PUFAs3536.

    ◦ A significant increase in heart disease rates observed in industrial countries during the 20th century is strongly linked to the increased consumption of industrial foods, particularly seed oils rich in linoleic acid37....

    ◦ Beyond diet, other factors contribute to LDL oxidation, including smoking and pollution, which create a more oxidizing environment in the body40.

• Addressing Oxidized LDL

    ◦ The most successful dietary intervention to reduce heart disease, like the Lyon Diet Heart Study, involved reducing linoleic acid and increasing alpha-linolenic acid (an omega-3 fat), which led to the replacement of omega-6 fats with less toxic omega-3 fats in LDL particles4142.

    ◦ Reducing dietary omega-6 intake can also increase omega-3 levels in the body4344.

    ◦ While statins lower LDL levels and may have an antioxidant effect, they don't directly address the underlying problem of dietary-induced oxidation4546.

    ◦ The endocannabinoid system, which utilizes lipids derived from omega-6 PUFAs (arachidonic acid) as its primary signaling molecules, plays a role in energy accumulation and is potentiated by high-fat diets47.... This suggests another pathway through which modern diets rich in these fats could influence bodily functions related to energy storage, potentially exacerbating issues like obesity.

In summary, the key takeaway is that oxidized LDL, not native LDL, is considered problematic in the context of cardiovascular disease. The oxidation of LDL is significantly driven by the dietary intake of highly susceptible polyunsaturated fatty acids like linoleic acid found in seed oils1....

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Discuss Dietary Fats.

Dietary fats play a crucial and often misunderstood role in human health, particularly concerning cardiovascular health and metabolic regulation1....

Here's a comprehensive discussion based on the provided sources:

• Atherosclerosis and the Role of Oxidized LDL

    ◦ Atherosclerosis, a major cause of heart disease and a leading global killer, involves the formation of plaques within the arteries45. These plaques are primarily composed of cholesterol and fats, along with dead cells and macrophages (white blood cells)6.

    ◦ The conventional view in cardiology suggests that high cholesterol levels, particularly LDL ("bad cholesterol"), directly cause these plaques78. However, this is critiqued in the sources, stating that native (unoxidized) LDL does not cause foam cells (a precursor to plaques)910.

    ◦ The problem arises when LDL particles become oxidized11. Oxidized LDL, unlike native LDL, causes macrophages to "gorge" on them, turning into foam cells, which are the first sign of atherosclerosis1112.

    ◦ The linoleic acid, a polyunsaturated fatty acid (PUFA) found in abundance in LDL particles, is highly susceptible to oxidation1314. The body cannot produce linoleic acid; it must be consumed through diet13....

    ◦ When LDL particles are oxidized to a certain degree, the normal LDL receptor no longer recognizes them, and they are instead taken up by "scavenger receptors," leading to unregulated ingestion by macrophages and subsequent problems17....

• Impact of Diet on LDL Oxidation and Heart Disease

    ◦ The composition of PUFAs in LDL particles is entirely controlled by diet1621. Diets high in linoleic acid make LDL particles more susceptible to oxidation15....

    ◦ Historically, populations like the Maasai, who consumed exclusively animal products, had massive atherosclerosis (arteries lined with fat) but no heart attacks, suggesting that not all atherosclerosis is pathological and that vessel flexibility is key2324.

    ◦ Studies have shown that heart disease rates increased massively in the 20th century, particularly in industrial countries consuming large amounts of "industrial foods," including seed oils24....

    ◦ The Minnesota Coronary Experiment, designed to prove that replacing animal fats with unsaturated fats would reduce heart disease, actually found the opposite: the greater the effect on lowering cholesterol, the worse the outcome of heart disease2728. This information was allegedly suppressed for 16 years2930.

    ◦ The reason polyunsaturated fats (seed oils) lower LDL levels is because they impair the production of VLDL (a precursor to LDL) in the liver31. This is because the liver "won't produce a VLDL particle to send out to the body if it contains oxidized polyunsaturated fats," as the fats oxidize in the liver2931. This highlights a difference in interpretation: lower LDL levels due to seed oil consumption may be a sign of toxicity rather than health32.

    ◦ The most successful dietary intervention in medicine for heart disease was the Leon diet heart study, which reduced linoleic acid content and increased omega-3 fats, leading to omega-3s replacing omega-6s in LDL particles, making them less toxic3334.

• Dietary Fats and Blood Pressure

    ◦ Elevated blood pressure is not inherently a disease but a compensation mechanism for reduced blood flow due to damage to the cardiovascular system35.

    ◦ This damage often results from continuous elevated blood glucose due to consuming carbohydrates, especially in combination with plant-based (seed) oils and other unsaturated fats, which become oxidized1.

    ◦ Medications that lower blood pressure (e.g., ACE-inhibitors, beta-blockers) only address the symptom, not the underlying problem of cardiovascular damage36.

    ◦ Healing the cardiovascular system by supplying essential nutrients (cholesterol, saturated fats, amino acids, specific vitamins from animal-based foods) is presented as the only way to truly fix high blood pressure3738.

    ◦ A carnivore diet, consisting only of animal-based foods, is suggested to result in optimal blood pressure levels (typically around 110-130 systolic / 70-80 diastolic mmHg) by healing the cardiovascular system and providing complete nourishment3839.

• The Endocannabinoid System (ECS) and Dietary Fats

    ◦ The ECS, composed of cannabinoid receptors (CB-1 and CB2) and endogenous cannabinoids like anandamide and 2-AG, are lipids derived from arachidonic acid, an omega-6 polyunsaturated fatty acid4041.

    ◦ The ECS functions as an "exostatic system," driving the body to accumulate energy for future needs, rather than just immediate "endostatic" needs42....

    ◦ This exostatic function manifests in several ways:

        ▪ Increased food intake and palatability: The ECS enhances the reward system associated with food, making palatable foods (especially those rich in sugar and fat) more desirable, which encourages overeating beyond immediate caloric needs to build reserves45....

        ▪ Enhanced nutrient absorption: CB-1 receptor activation can reduce gut motility, allowing more time for nutrient absorption in the intestines4950.

        ▪ Increased lipid accumulation: CB-1 in the liver contributes to lipogenesis (fat synthesis), and in adipocytes (fat cells), it promotes lipid accumulation5152.

        ▪ Reduced energy expenditure: The system can also decrease mitochondrial activity, leading to less efficient energy use and more energy accumulation5354.

    ◦ Direct evidence in experimental animals shows that increasing the amount or proportion of omega-6 fatty acids in the diet leads to higher overall levels of CB-1 receptor signaling via increased endocannabinoid production5556.

    ◦ This connection between the abundance of omega-6 PUFAs in the modern diet and the ECS's exostatic function is suggested as a direct link to the obesity epidemic5758.

• Inconsistencies and Recommendations

    ◦ Mainstream cardiology's advice is seen as inconsistent: while promoting omega-6 rich seed oils as "heart healthy" for lowering LDL, they also advise against fried foods31.... This is illogical, as frying oxidizes these very same polyunsaturated vegetable oils60.

    ◦ To improve cardiovascular health, it is recommended to lower omega-6 intake, and supplement with or increase consumption of long-chain omega-3 fats (which can replace omega-6s in membranes)6162.

    ◦ Avoiding smoking and polluted areas are also recommended, as they create an oxidizing environment that damages LDL61.

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Discuss Scientific Research.

Scientific research, as discussed in the provided sources, encompasses a wide range of fields, from health and biology to artificial intelligence. It involves diverse methodologies, aims to understand complex phenomena and develop solutions, but is also subject to human biases, economic interests, and the inherent challenges of scientific inquiry.

Nature and Goals of Scientific Research Scientific research fundamentally seeks to elucidate mechanisms and solve problems1.... In the realm of health, this includes understanding diseases like cardiovascular disease (CVD) and developing treatments7.... For instance, research explores how "toxic spike proteins" can induce inflammation and clotting related to COVID-19 "vaccines"211, or how atherosclerosis, a major cause of death, develops through the formation of plaques primarily composed of cholesterol and fats912. In artificial intelligence, the goal is to advance AI's capabilities, with predictions that it will surpass human intelligence in the coming decades1314.

A key aspect of scientific research is the continuous evolution of understanding. For example, blood pressure guidelines have been updated numerous times over 125 years due to new data and interpretations7.... The understanding of cholesterol's role in heart disease has also shifted, with early theories linking dietary cholesterol directly to atherosclerosis based on studies in species like rabbits18..., a view later challenged by researchers like Ancel Keys himself22. Basic research, such as the discovery of the LDL receptor or the identification of pregnenolone as a natural inhibitor of CB-1 receptors, can directly inform the development of pharmaceutical products and clinical applications23....

Methodology and Approaches Scientific research employs a variety of empirical methods:

• In vitro studies were used to demonstrate how modified (acetylated or oxidized) LDL particles cause macrophages to become foam cells, a key step in atherosclerosis23....

• Epidemiological studies have investigated heart attack rates across different populations and countries, highlighting "massive discrepancies" and connections to industrial foods like seed oils28....

• Autopsy studies have been used to identify permanent damage (scarring) from heart attacks, allowing historical tracking of disease rates29.

• Genetic studies explore conditions like familial hypercholesterolemia (FH) and PCSK9 mutations to understand genetic predispositions to heart disease, though these predispositions are often shown to interact significantly with environmental factors like diet32....

• Animal models, such as mice, are used to investigate biological systems like the endocannabinoid system, including studies involving the deletion of specific receptors in different cell types38....

• Clinical trials for drugs like Remonabant (a CB-1 antagonist) against obesity and diabetes also contribute to research, although they can reveal unexpected side effects4344.

Theoretical frameworks guide research questions and interpretations. Examples include the "biological terrain perspective" which views high blood pressure as an adaptive response to a "degraded terrain" caused by biochemical imbalances, toxins, and deficiencies4546. "German New Medicine" interprets hypertension as a "meaningful biological special program" triggered by unresolved psycho-emotional conflicts4748. The concept of "exostasis" explains why organisms might accumulate energy beyond immediate needs (e.g., eating for future famine), driven by external stimuli and reward systems, with the endocannabinoid system potentially serving this function49.... Modern tools like the Lumen device measure CO2 levels to determine fat versus carbohydrate burning, aiding metabolic flexibility research5354.

Challenges and Biases in Scientific Research The sources raise several critical points about the integrity and objectivity of scientific research:

• Publication Pressure over Truth: One critique suggests that the "currency for success in science is papers published," not necessarily "truth per se," leading to potential issues like scientists not carefully reading literature or overlooking "blatant error"5556.

• Influence of Dogma and Profit: Blood pressure guidelines are described as being updated partly to "fit their agenda of diagnosing people and putting them on extremely expensive, dangerous and useless drugs," suggesting a "pseudoscientific and based on profit" approach715. The mainstream medical view on heart disease, particularly regarding the role of saturated fats and seed oils, is presented as "backwards" and influenced by a historical "indoctrination" promoted by organizations like the American Heart Association8....

• Suppression of Contradictory Data: The Minnesota Coronary Experiment, designed to prove that replacing animal fats with unsaturated fats would reduce heart disease, found the opposite: "the greater the effect on lowering cholesterol, the worse the outcome of heart disease was"5960. This critical finding was "buried" and not published until 16 years later, after the hypothesis had become "dogma" and part of dietary guidelines60.... This highlights how "scientists aren't saints" and can be influenced by "career ambitions and all of the same biases that everybody else has"62.

• Inconsistencies and Contradictions: Despite widespread belief that LDL (often called "bad cholesterol") drives heart disease, some risk calculators used by physicians do not even include LDL levels, as "no relationship was found between LDL and cardiovascular rates" in some studies63.... This indicates inconsistencies within the mainstream understanding itself66.

• Challenges in Studying Certain Molecules: Lipids, central to many biological processes, are described as "ephemeral," "constantly changing," and "difficult to label," making them experimentally challenging to study6768.

Specific Areas of Research Highlighted

• Cardiovascular Disease (CVD): While conventionally attributed to cholesterol and fat plaques912, alternative perspectives suggest that continuous elevated blood glucose from carbohydrates, especially combined with oxidized unsaturated fats (seed oils), is the primary cause5769. High blood pressure is seen as a "compensation mechanism" for damaged blood vessels, not a disease itself70. The oxidation of linoleic acid (a polyunsaturated fatty acid from plants) in LDL particles is highlighted as a critical factor in causing inflammation and plaque formation71....

• Endocannabinoid System (ECS): Research into the ECS, including CB-1 and CB2 receptors and endogenous cannabinoids like anandamide, reveals a complex system that impacts various physiological processes676. It is proposed as an "exostatic system" that promotes energy accumulation by enhancing food intake, nutrient absorption, lipogenesis (fat synthesis in the liver), and fat accumulation in fat cells39.... Increased dietary omega-6 fatty acids can directly lead to increased endocannabinoid production and activity40. Research also explores how the ECS modulates motivation, anxiety, and pain, all contributing to an organism's drive to seek and accumulate resources44.... The discovery of pregnenolone as a natural inhibitor of CB-1 provides insights into potential safety mechanisms within the system and avenues for drug development24....

• Artificial Intelligence (AI): Research in AI focuses on developing "superintelligent AI"1386. Key research questions include addressing the "alignment problem" – ensuring AI's goals align with humanity's best interests, with some experts proposing to program "maternal instincts" into AI to prevent it from harming humans8788. There is also an ongoing debate within the field regarding the necessity and extent of regulation for AI development8990.

Source91 (Douglas Macgregor: America and Israel Will Strike Iran Very Soon!) primarily discusses geopolitics and military strategy and does not contain information relevant to scientific research. Similarly, Source92 (George Mallory Faked his Death) focuses on historical revisionism and conspiracy theories regarding historical events rather than the methodologies or principles of scientific research.

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Discuss Seed Oils.

Seed oils are a category of industrial foods, primarily plant-based, that have become increasingly prevalent in modern diets. They are a significant source of polyunsaturated fatty acids (PUFAs), particularly linoleic acid, which is an omega-6 PUFA1.... The body cannot synthesize linoleic acid, meaning its presence in the body's tissues, including in LDL particles, is entirely controlled by diet2....

Here's a discussion of seed oils and their implications for health:

• Oxidation and Atherosclerosis

    ◦ Linoleic acid is a fragile fat, highly susceptible to oxidative damage in the oxygen-rich environment of the body, especially in the arteries89.

    ◦ When LDL particles, which carry cholesterol and fats (with linoleic acid being a major component), become sufficiently oxidized (oxidized LDL), they are no longer recognized by normal LDL receptors on cells10. Instead, they are taken up by "scavenger receptors" through an unregulated cleanup pathway1112.

    ◦ Macrophages, a type of white blood cell, excessively ingest these oxidized LDL particles, transforming into "foam cells," which are the initial sign of atherosclerosis1314. The accumulation of foam cells, fats, cholesterol, and dead cells forms atherosclerotic plaques1516.

    ◦ Research indicates that oxidized LDL is the initiating step in the development of atherosclerosis, not native (unoxidized) LDL1718. Oxidized lipids are toxic to cells and signal for repair19.

    ◦ The problem arises when the amount of oxidizable PUFAs in LDL particles surpasses the body's natural antioxidant capacity9. This is influenced by dietary intake, as well as other factors like smoking and pollution, which create an oxidizing environment2021.

• Impact on Cardiovascular Health

    ◦ The massive increase in heart disease rates observed in industrial countries during the 20th century is strongly linked to the increased consumption of industrial foods, including seed oils22....

    ◦ The Minnesota Coronary Experiment found that replacing animal fats with polyunsaturated fats (PUFAs) in an attempt to lower cholesterol actually resulted in worse heart disease outcomes; the greater the cholesterol lowering, the worse the heart disease outcome25. This study's findings were allegedly suppressed for 16 years2627.

    ◦ The reason polyunsaturated fats (like those in seed oils) lower LDL levels is because they impair the liver's production of VLDL (very low-density lipoprotein), a precursor to LDL. The liver "won't produce a VLDL particle to send out to the body if it contains oxidized polyunsaturated fats," as these fats oxidize in the liver2628. This suggests that lower LDL levels due to seed oil consumption may be a sign of toxicity rather than health29.

    ◦ Traditional populations, such as the Maasai, Katavans, and Chima, who historically consumed non-industrial diets, exhibited little to no heart disease, despite some having high fat levels in their arteries or high Apo B levels30.... This indicates that the composition and oxidation state of fats, rather than just their quantity, are critical factors3233.

    ◦ Industrial plant-based processed foods, including seed oils, are implicated in the degradation of biological terrain, leading to issues like vascular stiffness and elevated blood pressure. Continuous elevated blood glucose from carbohydrates, especially when combined with unsaturated fats, causes damage to blood vessels and leads to glycated and oxidized fatty acids clogging arteries3435.

    ◦ Mainstream cardiology's advice is seen as inconsistent, as it promotes omega-6 rich seed oils as "heart healthy" while simultaneously advising against fried foods, which are made from these same oils and become oxidized during frying3637.

• Connection to the Endocannabinoid System (ECS)

    ◦ The body's endogenous cannabinoids, such as anandamide and 2-AG, are lipids derived from arachidonic acid, an omega-6 polyunsaturated fatty acid3839.

    ◦ The ECS functions as an "exostatic system," which drives the body to accumulate energy for future needs, rather than just immediate needs40.... This system influences increased food intake and palatability, enhanced nutrient absorption, increased lipid accumulation, and reduced energy expenditure43....

    ◦ Experimental animal studies show direct evidence that increasing the amount or proportion of omega-6 fatty acids in the diet leads to higher overall levels of CB-1 receptor signaling via increased endocannabinoid production4849.

    ◦ This connection between the abundance of omega-6 PUFAs in the modern diet and the ECS's exostatic function is suggested as a direct link to the obesity epidemic5051.

• Recommendations

    ◦ To improve cardiovascular health, it is recommended to lower omega-6 intake and increase consumption of long-chain omega-3 fats, which can replace omega-6s in LDL particles, making them less toxic21....

    ◦ A carnivore diet, consisting only of animal-based foods, is suggested to result in optimal blood pressure levels and heal the cardiovascular system by supplying essential nutrients and avoiding plant-based oils and processed foods55....

    ◦ Apps like "Seed Oil Scout" are available to help consumers find restaurants and grocery store products that are free of seed oils, aiding in reducing their consumption159.

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