Adopt an aggressive and early approach to ApoB reduction, aiming for levels between 20-40 mg/dL (infantile levels), potentially starting in your 20s. This proactive strategy is suggested to potentially eliminate death from atherosclerotic causes, as evidence shows lower ApoB is better and pharmacologic lowering to these levels has no signal of harm.
Prioritize atherosclerotic cardiovascular disease (ASCVD) prevention when you are young (e.g., in your 30s and 40s), as the disease takes hold over decades and current guidelines often delay prevention until it’s well advanced. By your late 30s or early 40s, aim to lower ApoB to below 60 mg/dL (below the 5th percentile).
Insist on knowing your ApoB concentration as it is the most important biomarker for cardiometabolic risk, capturing the total atherogenic burden of lipoproteins (LDL, VLDL, IDL, Lp(a)). This metric is superior to LDL-C or even non-HDL-C for assessing risk and diagnosing specific conditions like Type 3 dyslipoproteinemia.
Recognize that standard LDL cholesterol (LDL-C) is often an estimation, not a direct measurement, and multiple calculation methods exist, leading to varying results. The number of LDL particles (LDL-P) or ApoB is a more accurate index of risk than LDL-C.
Refrain from using imprecise language like ‘good cholesterol’ or ‘bad cholesterol’ because the cholesterol molecules themselves are identical; the distinction lies in the lipoproteins (HDL and LDL) that transport them. Misusing these terms indicates a fundamental misunderstanding of lipid biology.
Do not rely solely on a high HDL cholesterol (HDL-C) level as an indicator of good health, as it doesn’t reflect the functionality of HDL, which is what truly matters. Efforts to pharmacologically raise HDL-C have largely failed to improve cardiovascular outcomes.
Beyond ApoB, actively address other primary modifiable risk factors for ASCVD, which unambiguously include smoking and hypertension, and examine other treatable factors that might injure the endothelium or arterial wall.
Recognize that the cholesterol consumed in food (e.g., eggs) has very little impact on the cholesterol levels measured in your bloodstream because most dietary cholesterol is in a form too large for gut absorption and is excreted.
Do not be concerned about very low plasma cholesterol levels resulting from lifestyle or pharmacological interventions, as they do not significantly deplete total body cholesterol. Cells can synthesize their own cholesterol, ensuring they have more than enough for essential functions.
Be skeptical of information sources, especially those discussing lipids and lipoproteins, if they use imprecise or incorrect terminology like ‘good’ or ‘bad’ cholesterol, as this indicates a fundamental lack of understanding of the subject.
Focus on understanding your long-term (20-30 year) risk projections for ASCVD, especially if you are young, as these numbers provide a more meaningful context for prevention strategies than short-term (10-year) risk calculations.
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