Background: Improved understanding on how family history (FH) of disease and social determinants of health interacts and cause cardiovascular disease (CVD) during the life course can inform new treatments and reduce health inequity. Objective: To identify key genes, proteins, metabolic and mechanistic pathways for how FH of different diseases and trajectories of socioeconomic status (SES) during the life course cause CVD to find new drug target and important lifestyle habits in order to improve health equity. Work plan: The population-based EpiHealth, TwinGene and SCAPIS studies will be used with linkage to national registers. We will explore new pathways for how 1) FH of disease and 2) trajectories of SES during the life course relate to coronary atherosclerosis and incident CVD using proteomic, genetic and metabolomic biomarker platforms with a multi-omics approach. For significant proteins and metabolites, causal associations will be studied using two-sample mendelian randomization, their role in mediating atherosclerosis will be studied using structural equation modelling, independence of traditional risk factors and life-style factors will be studied. We will perform pathway enrichment analyses for identified genes and search druggability databases. Linkage to national registers have been performed for Epihealth, TwinGene and SCAPIS and genetic data together with relevant phenotypes has been delivered to the researcher. Significance: The project will answer important questions on how genes and environment cause CVD and will identify new and more precise targets for treatment to reduce CVD and reduce health inequity in CVD.