Genetics
Lp(a) fully expresses by age 2, but guidelines only recommend testing children after stroke, a review of Lp(a) in pediatrics (J Clin Lipidol 2015)
Original title: Lipoprotein(a): Its relevance to the pediatric population
This review by McNeal examines Lp(a) relevance in the pediatric population. Unlike other lipoproteins, which reach adult levels only after adolescence, Lp(a) is fully expressed by age 1 or 2 in children, though its metabolism remains poorly understood despite decades of research. Current pediatric guidelines do not recommend routine Lp(a) screening except in youth with ischaemic or haemorrhagic stroke, or those with a parental history of atherosclerotic cardiovascular disease unexplained by classical risk factors, largely because no data show that lowering Lp(a) reduces cardiovascular risk independent of LDL cholesterol. Lifestyle modification studies in children have been largely inconclusive, though one study in obese children showed an Lp(a) decrease alongside favourable changes in other lipids. The most compelling pediatric evidence is Lp(a) association with arterial ischaemic stroke risk, comparable to that of antiphospholipid antibodies or protein C deficiency, and the author emphasises educating youth and families about this risk and avoiding additional lifestyle risk factors.
Original abstract
Lipoprotein(a) (Lp(a)) is a highly atherogenic and heterogeneous lipoprotein that is inherited in an autosomal codominant trait. A unique aspect of this lipoprotein is that it is fully expressed by the first or second year of life in children, a pattern that is distinctly different from other lipoproteins, which typically only reach adult levels after adolescence. Despite decades of research, Lp(a) metabolism is still poorly understood but what is abundantly clear is that it is an independent risk factor for atherosclerotic cardiovascular disease (ASCVD). The Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents does not recommend measuring Lp(a) levels as part of routine screening except in youth with an ischemic or hemorrhagic stroke or youth with a parental history of ASCVD not explained by classical risk factors. One of the reasons that both the pediatric and adult guidelines fail to include this lipoprotein as part of routine lipid screening is the absence of data to show that lowering Lp(a) will reduce current or future ASCVD risk independently of low-density lipoprotein cholesterol (LDL-C) lowering. The cholesterol carried by Lp(a) is included in the low-density lipoprotein cholesterol measurement, but a separate test is used to measure the lipoprotein mass and/or cholesterol carried only by Lp(a). Because levels seem to be largely under genetic control, studies of lifestyle modification have been inconclusive although one study in obese children showed a decrease in the Lp(a) level comparable with the favorable effect on other lipids. The most compelling data regarding the importance of Lp(a) in the pediatric population are the increased risk associated with arterial ischemic stroke, a risk that is comparable with that associated with antiphospholipid antibodies or protein C deficiency. Although no specific pharmaceutical treatments are recommended to lower Lp(a) levels in youth, it is vitally important to educate youth and their parents about the excessive risk associated with this lipoprotein and the need to avoid the acquisition of other lifestyle-related risk factors such as smoking, excess weight, and physical inactivity to preserve more ideal cardiovascular health in adulthood.
childrengeneticsguidelinesstroke
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.