The purpose of this study is to investigate the relationship between early-life growth deficits, estimated using the Height-Gap metric, and lung function, cardiovascular health, and related biomarkers in adulthood. Height-Gap is defined as the difference between an individual's genetically predicted height (based on polygenic risk scores) and their actual measured height. We hypothesize that a greater Height-Gap—indicating a shorter stature than genetically expected—is associated with lower lung function (FVC, FEV₁, FEV₁/FVC), increased risk of airflow obstruction, and higher atherosclerotic burden (measured by coronary artery calcium score, CACS). Furthermore, we hypothesize that proteomic and metabolomic biomarkers will provide insights into the biological mechanisms linking early-life growth deficits with respiratory and cardiovascular disease risk. We will also assess how psychosocial factors and reproductive health indicators (e.g., parity, preeclampsia, gestational diabetes) influence Height-Gap’s association with inflammation, lung function, and cardiovascular outcomes. CT-derived heart measures (aortic diameter, aortic valve calcification, etc,) will also be analyzed to assess structural cardiovascular changes related to early growth deficits. This study will utilize data from the Swedish CArdioPulmonary bioImage Study (SCAPIS) to explore these associations in a large population-based cohort of adults aged 50-64 years.