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229 ‒ Understanding cardiovascular disease risk, cholesterol, and apoB — Whalespan

Content›Video›229 ‒ Understanding cardiova…

229 ‒ Understanding cardiovascular disease risk, cholesterol, and apoB

Peter Attia1h 19m · 2022-10-31

Claims Made

112

Claims Supported

74

Support Rate

66%

Support rate

74 of 112 claims supported

74 supported38 partial / not

Claims from this content

77

✓Well SupportedIndividuals with a high burden of cardiovascular disease and lifetime exposure to ApoB should aim for ApoB levels of 30 mg/dL, even if it requires multiple medications.✓Well SupportedApolipoprotein B (ApoB) measurement captures total atherogenic burden, including high VLDL, which can be missed by LDL particle number or LDL cholesterol measurements.✓Well SupportedAtherosclerosis is caused by the inflammatory response to oxidized cholesterol accumulation in macrophages within the artery wall.✓Well SupportedApolipoprotein B (Apo B), LDL particle size, and particle number are better markers for heart disease than traditional markers.

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✓Well Supported

Apolipoprotein B (ApoB) is a meaningful biomarker for cardiovascular risk.

✓Well SupportedMendelian randomization studies found no causal link between genes that raise or lower HDL cholesterol and atherosclerotic cardiovascular disease.

✕Not SupportedNo judgment should be made on a person's cardiovascular risk based on their HDL cholesterol level, nor should changing this metric be a therapeutic goal.

✓Well SupportedPhysiological apob concentrations, likely under 50 mg/dL, are associated with the greatest cardiovascular risk reduction.

✓Well SupportedCholesterol is essential for cell membrane structure and is a substrate for vital hormone production.

✓Well SupportedApoB particles are involved in the pathophysiology of atherosclerosis.

✓Well SupportedThe majority of the body's cholesterol is located in red blood cells, peripheral cells, and steroidogenic tissues, not circulating in plasma lipoproteins.

✕Not SupportedCurrent global guidelines base statin prevention strategies on 10-year risk, which hinders the prevention of premature disease.

✕Not SupportedLabeling HDL as 'good' and LDL as 'bad' cholesterol indicates a lack of understanding of lipid principles.

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

✓Well SupportedBeyond particle concentration, the quality of lipoproteins, including other proteins and their complex lipidome, should be assessed to determine their atherogenicity.

✓Well SupportedSmoking, hypertension, and hyperbeta-lipoproteinemia are the leading modifiable causes of ASCVD.

✓Well SupportedCells are not deprived of cholesterol when plasma lipid levels are modulated, as they can synthesize cholesterol or obtain it from other sources.

✓Well SupportedAn LDL particle number to HDL particle number ratio less than 35 may carry increased risk.

◐Partially SupportedLipoproteins are categorized into families defined by apob (VLDL, IDL, LDL, Lp(a)) and apoa (HDLs).

◐Partially SupportedMeasuring triglycerides is valuable for reasons beyond assessing ApoB or LDL particle count alone.

◐Partially SupportedThe fifth percentile for ApoB from the Framingham Offspring Study is 62 mg/dL, the 10th is 70 mg/dL, the 20th is 78 mg/dL, the 50th is 97 mg/dL, the 80th is 118 mg/dL, and the 95th is 140 mg/dL.

✓Well SupportedApob levels measured at age 35 are highly predictive of future apob levels.

✓Well SupportedDietary cholesterol has a negligible effect on blood cholesterol levels for most people.

✓Well SupportedApoB is necessary but not sufficient for atherosclerosis; inflammation and endothelial damage are also required for ApoB particles to cause damage.

✓Well SupportedPCSK9 inhibitors effectively lower apob.

✓Well SupportedLowering apolipoprotein B lipoproteins earlier in life can help eradicate atherosclerotic cardiovascular disease.

✓Well SupportedThe body transports cholesterol through the circulatory system using lipoproteins, which are vehicles composed of both lipid and protein components.

✓Well SupportedCholesterol within very low-density lipoprotein (VLDL) particles is atherogenic, and a high number of these particles increases cardiovascular risk.

◐Partially SupportedCholesterol is essential for the production of bile acids, which are necessary for digesting food, particularly fatty foods.

◐Partially SupportedMendelian randomization uses genetic variations fixed at birth to assess associations with outcomes, reducing confounding compared to prospective observational studies.

✓Well SupportedThe causality of apob and hypertension as cardiovascular risk factors is undisputed.

◐Partially SupportedThe causal benefit model uses non-HDL or apob to project cardiovascular risk over 20-30 years.

◐Partially SupportedSmoking and hypertension are well-understood major risk factors for cardiovascular disease, primarily acting by weakening or injuring the endothelium.

◐Partially SupportedApob levels rise with age, but not significantly enough to be the sole indicator of risk.

◐Partially SupportedVLDL, IDL, LDL, and HDL refer to lipoprotein density, which determines their separation in a lab gel.

◐Partially SupportedA 30% chance of infarct or stroke before age 65 is a more meaningful risk number for a 35-year-old than a 10-year risk score.

✕Not SupportedThe concept of 'bad cholesterol' is a mischaracterization; information about cholesterol is more accurate.

◐Partially SupportedThe body's ability to produce cholesterol is critical for survival.

◐Partially SupportedPreventing atherosclerotic cardiovascular disease requires reducing apoB particles, protecting the endothelium, and managing inflammation.

◐Partially SupportedCoronary disease incidence has increased in the last five years despite statin therapy, likely due to rising obesity and diabetes rates.

✕Not SupportedCurrent major global guidelines for statin prevention are based on a flawed 10-year risk of disease approach.

◐Partially SupportedSystolic hypertension in older adults may be caused by a loss of elastance in the proximal aorta, leading to stiffer arterial walls.

◐Partially SupportedAtherogenesis is multifactorial, and particle number is not always the sole determinant of atherosclerosis.

◐Partially SupportedASCVD is a disease state characterized by the deposition or buildup of sterols, including cholesterol and phytosterols, in the artery wall.

◐Partially SupportedCholesterol is synthesized by every cell in the body and is essential for cell creation, membrane fluidity, and transporter function.

◐Partially SupportedSmall VLDL cholesterol identified as remnants may not be pathological if particles are rich in ApoB and low in ApoC3, indicating rapid clearance.

◐Partially SupportedHypertension and lipid abnormalities are the two biggest behavioral risk factors for atherosclerotic cardiovascular disease, excluding smoking.

◐Partially SupportedUnderstanding the natural history of atherosclerosis is crucial for constructing an effective prevention strategy.

◐Partially SupportedIndividuals with Abetalipoproteinemia experience failure to thrive, fat malabsorption, vitamin deficiencies, and severe developmental issues due to the absence of ApoB-containing particles.

◐Partially SupportedA single HDL cholesterol measurement does not indicate an individual's metabolic health status because HDL functionality is what truly matters.

◐Partially SupportedStandard ldl cholesterol measurements in mg/dL represent weight per volume and do not indicate particle number.

◐Partially SupportedThe reduction in cardiovascular risk by starting interventions at age 35, or the losses incurred by starting at ages 45 or 55, can be calculated.

◐Partially SupportedApob levels can increase with menopause in women.

◐Partially SupportedStandard lipid panels report five numbers, but triglycerides may not be actionable by physicians when high.

◐Partially SupportedThe high absolute number of cardiovascular events before age 60 is due to a larger population size in younger age groups, not necessarily a higher individual event rate.

◐Partially SupportedMendelian randomization studies can be misleading when accounting for intermediate variables like triglycerides and non-HDL cholesterol or apob.

◐Partially SupportedCardiovascular risk calculation algorithms primarily use age and sex, with cholesterol and blood pressure contributing less significantly.

◐Partially SupportedAtherosclerosis begins in the first three decades of life, but clinically significant lesions typically develop in the fourth decade.

◐Partially SupportedThe probability for singular events, like having a heart attack in the next year, is challenging to predict accurately with current algorithms.

◐Partially SupportedEndothelial dysfunction is a state where the critically important endothelium functions abnormally.

✕Not SupportedThe pathophysiology of hypertension has not yielded clinically useful insights in the last 30-40 years.

◐Partially SupportedAtherosclerosis can be present in individuals as young as their 20s and 30s, characterized by oxidized ApoB-bearing particles within macrophages and thickened intima.

◐Partially SupportedApoB particles may induce endothelial dysfunction.

✕Not SupportedA 10-year risk threshold of 7.5% for treatment implies that 92.5% of the time, nothing will happen.

◐Partially SupportedDirectly measured LDL cholesterol assays have not been validated in disease patients and are not proven more accurate than calculated LDL for disease identification.

◐Partially SupportedMendelian randomization leverages genetic variants associated with exposures to infer causality and overcome confounding in observational studies.

◐Partially SupportedIndividualization of risk factor assessment and treatment is necessary for managing atherogenesis.

◐Partially SupportedSmoking and hypertension exacerbate cardiovascular risk more than ApoB alone.

◐Partially SupportedThe essential condition for atherosclerosis is the presence of cholesterol in the artery wall, which is not necessarily directly related to circulating cholesterol levels, although they often coexist.

◐Partially SupportedAtherosclerosis is an inevitable disease of the human species if people live long enough.

◐Partially SupportedSelecting individuals for cardiovascular prevention should incorporate causal measures like ApoB and non-HDL cholesterol, in addition to traditional risk factors.

◐Partially SupportedHypertension is a driving force that pushes apob particles into the arterial wall.

✕Not SupportedCardiovascular risk algorithms often classify individuals around age 40 as low risk, delaying preventative treatment until age 55-60, despite half of all heart attacks and strokes occurring before age 50.

✕Not SupportedCardiovascular disease is often well-advanced by the time 10-year risk assessments initiate prevention strategies.

◐Partially SupportedIn metabolic contexts with increased obesity, insulin resistance, and type 2 diabetes, there is greater discordance between apob and ldl-c, leading to underdiagnosis of risk.

◐Partially SupportedA significant reduction in plasma LDL cholesterol or total cholesterol does not equate to a significant reduction in total body cholesterol.

◐Partially SupportedQuantifying lipoproteins solely based on lipids is inadequate.