Observational studyMedicine2026
Body fat percentage and hypertension risk: A population-based observational and Mendelian randomization study.
Observational study in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
This study aimed to investigate the association and potential causal relationship between body fat percentage (BFP) and hypertension, with a focus on sex-specific thresholds and clinical implications for prevention. We integrated data from the National Health and Nutrition Examination Survey (1999-2018; n = 25,957) and summary-level genome-wide association studies (GWAS) from United Kingdom Biobank and Finnish Genetic Epidemiology Consortium. Multivariate logistic regression, restricted cubic spline, and threshold effect analyses were used to evaluate the nonlinear association between BFP and hypertension in the observational cohort. Two-sample Mendelian randomization (MR) employed single-nucleotide polymorphisms as instrumental variables, with inverse-variance weighted as the primary method; sensitivity analyses (MR-Egger, leave-one-out, heterogeneity tests) assessed robustness. Hypertension prevalence increased progressively from adipopenia (6.5%) to obesity (43.1%). Restricted cubic spline revealed a nonlinear positive association between BFP and hypertension in both sexes (P < .001 for nonlinearity). Sex-specific inflection points were identified: 31.32% in males and 41.82% in females. Below these thresholds, each 1% increase in BFP conferred higher odds of hypertension (males: odds ratio [OR] = 1.10; females: OR = 1.16); the effect attenuated above the thresholds. MR analyses confirmed a causal effect of genetically predicted BFP on hypertension (United Kingdom Biobank: OR = 1.003, 95% confidence interval: 1.001-1.005, P < .001; Finnish Genetic Epidemiology Consortium: OR = 1.846, 95% confidence interval: 1.587-2.146, P < .001), with no evidence of heterogeneity or horizontal pleiotropy. Higher BFP is robustly associated with and likely causally contributes to increased hypertension risk, with distinct sex-specific thresholds. These findings support incorporating BFP (beyond body mass index) into hypertension risk assessment and personalized prevention strategies.
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Registered trials
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