Adult Height, Cardiovascular Disease, and the Underlying Mechanism: A Comprehensive Epidemiological and Genetic Analysis
Bibliographic record
Abstract
BACKGROUND: Adult height measures the complete growth of an individual and influences the development of cardiovascular disease (CVD). Despite recent within-sibling studies that have suggested minimal effects from environmental confounders, biological mechanisms underlying the height-CVD relationship remain elusive. METHODS: Leveraging the large-scale UK Biobank data set and summary statistics from the latest genome-wide association studies, we reevaluated the effect of height on 8 major CVD subtypes. Phenotypic associations were determined using Cox proportional hazard analysis. Putative causal relationships were assessed using univariable Mendelian randomization. Mediation analysis and 2-step Mendelian randomization were further performed to investigate the mediation effect of 15 common cardiometabolic or pulmonary risk factors. RESULTS: Height was consistently associated with a decreased risk of coronary artery disease (CAD), confirmed in epidemiological (hazard ratio, 0.90; 95% confidence interval [CI], 0.88-0.91) and genetic (odds ratio, 0.89, 95% CI, 0.86-0.92) analysis. Forced vital capacity was identified as the most significant mediator for the height-CAD relationship in epidemiological (proportion-mediated, 65.6%; 95% CI, 53.1%-78.0%) and genetic (proportion-mediated, 46.2%; 95% CI, 5.0%-87.5%) analysis. Notably, obesity, and blood pressure, lipid, and C-reactive protein levels also exhibited significant mediatory effects. Despite a consistent risk effect of height on atrial fibrillation and venous thromboembolism, no promising mediator was identified. CONCLUSIONS: Our study confirms the health effects of height on CAD, atrial fibrillation, and venous thromboembolism and emphasizes forced vital capacity as the primary pathway that links height to CAD. Importantly, it indicates that the CAD risk associated with nonmodifiable height could be mitigated through enhanced lung function and cardiometabolic conditions.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.003 | 0.003 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.002 |
| Bibliometrics | 0.003 | 0.004 |
| Science and technology studies | 0.001 | 0.000 |
| Scholarly communication | 0.001 | 0.001 |
| Open science | 0.001 | 0.001 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.001 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".