ArticleMedicine2026
Assessing the causal influence of biomechanical factors on osteoporosis risk: A multivariable Mendelian randomization investigation.
Article in Medicine, 2026. 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
6 authors.
Funding
Abstract
While observational studies indicate correlations between multiple biomechanical traits and osteoporosis, causal inference has been constrained, impeding the clinical application of these measures in risk stratification. This Mendelian randomization (MR) study examines causal associations of ankle spacing width (ASW), height, body mass index (BMI), grip strength, and usual walking pace with bone mineral density (BMD) across skeletal sites and age groups. Genetic proxies for the exposures were derived from the Medical Research Council Integrative Epidemiology Unit and UK Biobank resources. Genetic association estimates for the outcomes were acquired from the Genetic Factors for Osteoporosis Consortium. Two-sample and multivariable MR analyses were applied to infer causality. Genetically proxied ASW (encompassing left, right, and combined measures) and height showed an inverse association with estimated BMD (eBMD; Beta < 0, P. adjusted < .05). In contrast, genetically predicted BMI was associated with an increase in eBMD (Beta > 0, P. adjusted < .05). Moreover, genetically predicted ASW was linked to lower total body BMD, with the inverse association being most pronounced in the 0 to 15 years age group. Multivariable MR analyses confirmed that ASW remained independently associated with both eBMD and total body BMD after adjusting for confounding factors. Our findings offer genetic evidence indicative of a causal detrimental effect of ASW and height on BMD, especially during early life stages, whereas BMI demonstrates a potentially protective causal role.
Indexed as
Identifiers
What Socratic 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 Socratic graph.