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PubMed2024

An insight into the causal relationship between sarcopenia-related traits and venous thromboembolism: A mendelian randomization study.

BACKGROUND: As a geriatric syndrome, sarcopenia has a high prevalence in the old population and represents an impaired state of health with adverse health outcomes. A strong clinical interest in its relationship with venous thromboembolism (VTE), which is a complex trait disease with a heterogeneous annual incidence rate in different countries, has emerged. The relationship between sarcopenia and venous thromboembolism has been reported in observational studies but the causality from sarcopenia to VTE remained unclarified. We aimed to assess the causal effect of sarcopenia on the risk of VTE with the two-sample Mendelian randomization (MR) method. METHODS: Two sets of single-nucleotide polymorphisms (SNPs), derived from two published genome-wide association study (GWAS) meta-analyses and genetically indexing muscle weakness and lean muscle mass separately, were pooled into inverse variance weighted (IVW), weighted median and MR-Egger analyses. RESULTS: No evidence was found for the causal effect of genetically predicted muscle weakness (IVW: OR = 0.90, 95% CI = 0.76-1.06, p = 0.217), whole body lean mass (IVW: OR = 1.01, 95% CI = 0.87-1.17, p = 0.881) and appendicular lean mass (IVW: OR = 1.13, 95% CI = 0.82-1.57, p = 0.445) on the risk of VTE. However, both genetically predicted whole-body lean mass and appendicular lean mass can causally influence diabetes mellitus (IVW of whole-body lean mass: OR = 0.87, 95% CI = 0.78-0.96, p = 0.008; IVW of appendicular lean mass: OR = 0.71, 95% CI = 0.54-0.94, p = 0.014) and hypertension (IVW of whole-body lean mass: OR = 0.92, 95% CI = 0.87-0.98, p = 0.007; IVW of appendicular lean mass: OR = 0.84, 95% CI = 0.73-0.96, p = 0.013). CONCLUSIONS: Genetically predicted sarcopenia does not causally influence VTE directly, but it might still have an indirect effect on VTE incidence via diabetes mellitus and hypertension.

Humans↗
PubMed2026

Disentangling the association between chronic pain and sarcopenia-related traits: A bidirectional Mendelian randomization study.

ObjectiveThis study aimed to investigate the potential causal relationships between chronic pain and three key sarcopenia-related quantitative traits: (a) hand grip strength; (b) usual walking pace; and (c) appendicular lean mass, using bidirectional two-sample Mendelian randomization.MethodsWe conducted bidirectional two-sample Mendelian randomization using summary-level data from large-scale genome-wide association studies to assess the genetically predicted associations between chronic pain, including multisite chronic pain and chronic widespread musculoskeletal pain, and the aforementioned sarcopenia-related traits.ResultsMendelian randomization revealed that multisite chronic pain was significantly associated with an increased risk of low hand grip strength (odds ratio = 1.70; p&#x2009;<&#x2009;0.001) and decreased usual walking pace (odds ratio = 0.81; p&#x2009;<&#x2009;0.001); chronic widespread musculoskeletal pain was also significantly associated with decreased usual walking pace (odds ratio = 0.15; p&#x2009;<&#x2009;0.001). Additionally, higher left hand grip strength was significantly associated with a lower risk of multisite chronic pain (odds ratio = 0.90; p<&#x2009;0.001) and chronic widespread musculoskeletal pain (odds ratio = 0.99; p&#x2009;=&#x2009;0.002); higher right hand grip strength was significantly associated with a lower risk of multisite chronic pain (odds ratio = 0.91; p&#x2009;=&#x2009;0.002); and higher usual walking pace was significantly associated with a lower risk of multisite chronic pain (odds ratio = 0.49; p&#x2009;<&#x2009;0.001) and chronic widespread musculoskeletal pain (odds ratio = 0.92; p&#x2009;<&#x2009;0.001). No significant causal associations were detected for appendicular lean mass in either direction (all p&#x2009;>&#x2009;0.05).ConclusionThis study provides genetic evidence supporting potential causal links between chronic pain and key phenotypic components of sarcopenia.

Humans↗
PubMed2026

Genetically Predicted Muscle Mass and Function in Relation to Deep Vein Thrombosis: A Two-step Mendelian Randomization Study Highlighting the Mediating Role of BMI.

BackgroundSarcopenia is observationally linked to venous thromboembolism, but the causal architecture and underlying biological pathways remain largely unclear. This study investigated the causal effects of sarcopenia-related traits on lower extremity deep vein thrombosis (DVT) and quantified potential mediating mechanisms.MethodsWe performed two-sample bidirectional Mendelian randomization (MR) and two-step mediation MR using large-scale GWAS data from UK Biobank, EMBL-EBI, and FinnGen. Exposures included appendicular lean mass (ALM), leg fat-free mass (LFM), hand grip strength, and walking pace. Eighteen candidate mediators were screened for indirect pathways.ResultsGenetically predicted higher ALM was significantly associated with increased DVT risk (FinnGen: OR = 1.288, 95% CI: 1.215-1.365, P < 0.001). Similar positive associations were observed for LFM (OR = 1.920-1.954, P < 0.001). By contrast, muscle functional traits - grip strength and walking pace - demonstrated no consistent causal effects. Reverse MR confirmed a unidirectional relationship. Body mass index (BMI) emerged as a pivotal mediator, accounting for 7.58% - 10.50% of the ALM-DVT effect and 52.74% - 62.73% of the LFM-DVT effect. Notably, the independent effect of ALM was largely attenuated after adjusting for metabolic confounders in multivariable MR.ConclusionGenetic predisposition to high muscle mass, rather than functional strength, increases DVT risk. This relationship appears to be significantly driven by metabolic adiposity, suggesting that the "muscle-vascular-coagulation" interaction is partly explained by body-size-related metabolic burden. Risk stratification should integrate muscle mass evaluation with comprehensive metabolic health assessments.

Humans↗
PubMed2026

A bi-directional Mendelian randomization study of&#xa0;sarcopenia-related traits and&#xa0;renal function.

The association between sarcopenia and renal function has been reported in observational studies; however, the directionality and potential causal nature of these associations remain uncertain. We assessed whether genetically predicted sarcopenia-related traits are associated with renal function and vice versa using bidirectional Mendelian randomization (MR). We conducted a bidirectional two-sample MR analysis using publicly available European-ancestry GWAS summary statistics for appendicular lean mass (ALM), hand-grip strength (left and right), and walking pace, and for renal function (cystatin C-based estimated glomerular filtration rate [eGFRcystatin C] and urinary albumin excretion [UAE]). Causal estimates were primarily obtained using inverse-variance weighted (IVW) models, complemented by sensitivity analyses (MR-Egger intercept, weighted median/mode, MR-PRESSO, Radial MR, and leave-one-out). In forward MR, genetically predicted walking pace was positively associated with eGFRcystatin C. Genetically predicted ALM and grip strength (right and left) were inversely associated with UAE. In reverse MR, genetically predicted UAE was inversely associated with ALM and right-hand grip strength. Estimates were broadly consistent across sensitivity analyses, and outlier-robust analyses (MR-PRESSO/Radial MR) yielded similar results. These findings provide genetic evidence consistent with bidirectional relationships between sarcopenia-related traits and renal function (particularly UAE), under standard MR assumptions. Given potential limitations (e.g., heterogeneity, pleiotropy, and possible sample overlap), the results should be interpreted cautiously and complemented by other lines of evidence.

Humans↗
PubMed2026

Causal Associations and Potential Mediating Factors between Sarcopenia-Related Traits and Heart Failure Risk: A Mendelian Randomization Study.

INTRODUCTION: In this two-sample, two-step Mendelian randomization (MR) study, we aimed to elucidate the causal associations between sarcopenia-related characteristics and heart failure (HF) risk, and to identify the factors mediating these associations, with a particular focus on the mediating roles of obesity and sedentary habits. METHODS: Genetic instruments for appendicular lean mass (ALM), hand grip strength (HGS), walking pace (WP), and potential mediators were extracted from genome-wide association studies. Inverse-variance weighting (IVW) was used as the primary analytical method, supplemented by MR-Egger regression, weighted median, and weighted mode analyses. Sensitivity analyses including Cochran's Q test and MR-Egger intercept method were performed to assess heterogeneity and pleiotropy. Bidirectional MR was conducted to exclude reverse causation. RESULTS: IVW revealed that a faster genetically predicted WP was associated with lower HF risk (odds ratio [OR] 0.44, 95% confidence interval [CI] 0.33-0.60, p = 5.806 &#xd7; 10-7). The mediation analysis indicated that body mass index (BMI) accounted for 32% of this effect, while time spent watching television accounted for 14%. Elevated ALM showed a slight but significant positive association with HF risk (OR 1.06, 95% CI 1.03-1.09, p = 5.437 &#xd7; 10-4). However, multivariable MR adjusting for BMI completely attenuated this association (p = 0.693), suggesting ALM reflects overall body composition rather than isolated muscle mass. No significant associations were found between HGS and HF. Bidirectional MR showed no robust reverse effects. CONCLUSIONS: These findings suggest that genetically predicted increased WP exerts beneficial effects against HF, partially mediated by obesity and sedentary habits. Targeting weight management and anti-sedentary interventions may mitigate HF risk in individuals with sarcopenia-related characteristics.

Heart failure↗