Under 50 nmol/L
Promoted by preventive cardiology and longevity platforms
The strongest case for it
Mendelian randomization supports a causal role for Lp(a) in atherosclerotic disease and aortic stenosis, and risk rises continuously rather than at a clean threshold. The lower cutoff reflects that continuity.
What it leaves out
Lp(a) is roughly 80–90% genetically determined and essentially unmodifiable by diet, exercise, or current standard therapy. Selling a target for a number you cannot change (without saying so) converts useful risk information into an anxiety product.