Analyzing 7,018 lipoprotein(a) measurements across 1,062 children at 10 age points — from 7 months to 15 years — the STRIP trial reveals that Lp(a) concentrations rise steadily through early adolescence, then diverge by sex: boys show a 15.1% decline after age 13 while girls' levels remain stable. Tracking correlations between age points were remarkably tight (Spearman's r = 0.854–0.956), meaning a child's Lp(a) rank position is largely fixed from infancy. By age 15, 16.2% of participants already exceeded the 30 mg/dL cardiovascular risk threshold. Critically, a heart-healthy dietary fat intervention produced no clinically meaningful Lp(a) reduction — a higher dietary fat quality goal was paradoxically associated with a modest 2.5% increase.
These findings carry significant implications. Lp(a) is now recognized as an independent, largely genetically determined cardiovascular risk factor, and emerging RNA-targeting therapies (pelacarsen, olpasiran) are in late-stage trials targeting adults. This preprint — not yet peer-reviewed — suggests that early childhood screening could identify high-risk individuals decades before clinical events, enabling longer monitoring windows. The dietary null finding reinforces the genetic primacy of Lp(a) regulation and argues against lifestyle modification as a mitigation strategy. Limitations include a predominantly Finnish cohort limiting generalizability, and the observational dietary analyses within an RCT framework. Still, the exceptionally strong tracking data represent a paradigm-confirming result: for Lp(a), cardiovascular destiny may be readable in infancy.
