The evidence for LDL cholesterol as a causal risk factor for cardiovascular disease and reduced longevity is very strong. Large randomized trials (e.g., statin studies) and Mendelian randomization consistently show that elevated LDL increases cardiovascular risk, and lowering it reduces events and extends life in high-risk populations. However, the effect on total lifespan is context-dependent. In primary prevention for low-risk individuals, the absolute benefit is smaller. In older adults (>70 years), observational data suggest a U-shaped relationship, where very low LDL may be associated with higher mortality – likely due to reverse causation or frailty, not a direct protective effect. Mechanistically, LDL particles promote atherosclerosis, but particle number (ApoB) and small dense LDL are more atherogenic than total LDL alone. Consumer tests like MyBody-X typically report total LDL, which is useful but incomplete. For longevity, maintaining LDL around 100 mg/dL (2.6 mmol/L) with low inflammation and blood pressure appears optimal. Evidence: human-strong. Caveat: Single LDL values do not predict individual lifespan; comprehensive risk assessment is needed.
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