Characteristics associated with Lipoprotein(a) concentrations in school children: Interim results from Hand aufs Herz Study

Background Lipoprotein(a) [Lp(a)] is a genetically determined variant of low-density lipoprotein (LDL), often referred to as "bad cholesterol," and is a well-established independent risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis. Despite its significance, there is limited data on the clinical and metabolic factors associated with Lp(a) levels in healthy school-age children. Purpose This study aims to profile Lp(a) levels in school children and identify the clinical and metabolic factors that contribute to variation in Lp(a), which remain poorly characterized in this population. Methods This study utilizes data from an ongoing study, an ongoing cardiovascular health study involving school children. Cross-sectional data were collected using standardized protocols and self-reported questionnaires, capturing variables such as Lp(a) levels, age, sex, fasting status, smoking frequency, and alcohol consumption. Statistical analyses included counts of available blood samples, scatterplots of Lp(a) by age, group comparisons using t-tests and ANOVA, and a multivariable linear regression model performed in R (v4.4.1). Results A total of 273 participants (139 boys and 139 girls) aged 8-19 years had available Lp(a) measurements. Scatterplots revealed significant variability in Lp(a) concentrations across ages, with no statistically significant difference between boys and girls (p = 0.607; 95% CI [-0.337, 0.197]). ANOVA analyses showed no significant difference in mean log-transformed Lp(a) levels between fasting and non-fasting groups (p = 0.161; 95% CI [−0.631, 0.107]). The multivariable linear regression model was not statistically significant (p = 0.355) and explained only a small portion of the variance in log-transformed Lp(a) (Adjusted R² = 0.051). Conclusion These findings suggest that Lp(a) levels in this cohort of school children are primarily influenced by genetic factors, with limited impact from modifiable behaviors or lifestyle factors such as alcohol intake and fasting status. The lack of significant associations with these factors supports the conclusion that Lp(a) levels are largely genetically determined. However, given the limited variance explained by the current analysis (adjusted R² = 0.051) and the absence of significant findings, more data are needed from larger population to better understand the full range of clinical, metabolic, and environmental factors that may contribute to variation in Lp(a) levels in children and adolescents.