Abstract 028: Infant Growth Trajectories and Lipid Levels in Adolescence: Evidence From a Chilean Infancy Cohort

Introduction: Growth in early infancy is hypothesized to affect chronic disease risk factors later in life. To date, most reports draw on European ancestry cohorts with few observations of early growth. To determine if previous findings generalize to diverse study populations and to accommodate more detailed growth estimates, we investigated the association between monthly infant growth from birth to 5 months and dyslipidemia in adolescents in a Hispanic/Latino cohort. Methods: We characterized infant growth in males (n=345) and females (n=308) from the Santiago Longitudinal Study (SLS) using three metrics: weight (kg), length (cm) and weight-for-length (g/cm). Nonlinear mixed effects (SITAR) and latent growth mixture models (LGMM) were two approaches to estimate infant growth characteristics. Growth functioned as an exposure and lipid levels at 17 years were the outcome, including HDL-C, LDL-C, and TG. We used a false discovery rate of 0.05 to report findings. Results: Height trajectories presented the strongest evidence for an effect on dyslipidemia in adolescence in both the SITAR and LGMM models. SITAR analyses demonstrated an inverse relationship between height velocity before six months of age and HDL-C levels in adolescence. LGMM models offered more nuanced findings. A two-class height trajectory model offered the best fit: one group (n~268) had shorter length at birth accompanied by lower velocity/higher acceleration; the other group (n~406) had higher length at birth and higher velocity/lower acceleration. The lower velocity/higher acceleration group had lower mean HDL-C (mg/dL) (35.4, se=0.9) than the higher velocity/lower acceleration group (43.8, se=0.7), χ2(1)=36.4, p-value=<0.001. Similarly, the best-fitting 3-class weight trajectory model indicated the lower velocity/medium acceleration group had a higher mean LDL-C (mg/dL) (97.7, se=1.6, n~441) than the highest velocity/lowest acceleration group (88.8, se=2.0, n~202), χ2(1)=15.2, p-value=<0.001. A similar pattern for LDL-C emerged for the weight-for-length trajectories, χ2(1)=8.6, p-value=0.003. Summary: This study provides evidence of associations between infant growth from 0 and 5 months and blood lipid profiles during adolescence. Based on two different analytic approaches, characteristics of infant length trajectories were associated with HDL-C at mean age 17 years. These findings align with the well-established relationship between height and CVD in adulthood. Furthermore, groups with higher acceleration in all three trajectory types were more likely to have adverse lipid outcomes. Future research can inform the role of infant body size change in the context of downstream effects and CVD risk.