ArticleScientific reports2025
Causal Association Between Genetically Predicted Ankle Spacing Width and Risk of Age-Related Bone Mineral Density.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
While observational studies suggest associations between ankle spacing width (ASW, defined as the horizontal distance between the medial malleoli under weight-bearing conditions) and osteoporosis (OP), fractures, and falls, causal evidence remains limited. This gap hinders the translation of ASW measurements into clinical risk stratification tools. This study aimed to investigate the causal relationships between ASW indicators and site-/age-specific bone mineral density (BMD), bone fracture and fall risks. Genetic exposure data for ASW indicators were retrieved from the MRC-IEU datasets, and the outcome data were all derived from the Genetic Factors for Osteoporosis Consortium (GEFO). Genome-wide associations of single nucleotides polymorphisms (SNPs) were served as instrumental variables (IVs) to infer causal effects using two-sample mendelian randomization (TSMR) and multivariable mendelian randomization (MVMR) analyses. The results of sites-specific TSMR analysis revealed that per unit increase in ASW (including left and right) were causally associated with lower estimated from quantitative heel ultrasounds BMD (eBMD, reflecting calcaneal bone density) and total-body BMD (TB-BMD, assessed via DEXA scans), with pronounced effects in individuals aged over 60 years. Age-stratified analyses revealed no significant associations between ASW and TB-BMD in younger age groups (age ≤ 15, 15 < age ≤ 30, 30 < age ≤ 45, 45 < age ≤ 60) or site-specific fractures/falls. MVMR adjustment for BMI, smoking, and alcohol consumption confirmed persistent causal associations between ASW and reduced eBMD and TB-BMD, particularly for TB-BMD in individuals aged over 60 years. Our study provides evidence that genetically predicted ASW is associated with reduced eBMD and TB-BMD, and a causal association between ASW and TB-BMD (aged over 60), suggesting ASW as a potential auxiliary biomarker for monitoring age-dependent bone loss.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.