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Causal associations between hand grip strength and pulmonary function: a two-sample Mendelian randomization study

BACKGROUND: Several observational studies have reported an association between hand grip strength (HGS) and pulmonary function (PF). However, causality is unclear. To investigate whether HGS and PF are causally associated, we performed Mendelian randomization (MR) analyses. METHODS: We identified 11...

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Detalles Bibliográficos
Autores principales: Zhao, Xianghu, Xu, Wenyuan, Gu, Yanchao, Li, Zhanghua, Sun, Guiju
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10664596/
https://www.ncbi.nlm.nih.gov/pubmed/37990169
http://dx.doi.org/10.1186/s12890-023-02720-0
Descripción
Sumario:BACKGROUND: Several observational studies have reported an association between hand grip strength (HGS) and pulmonary function (PF). However, causality is unclear. To investigate whether HGS and PF are causally associated, we performed Mendelian randomization (MR) analyses. METHODS: We identified 110 independent single nucleotide polymorphisms (SNPs) for right-hand grip strength (RHGS) and 103 independent SNPs for left-hand grip strength (LHGS) at the genome-wide significant threshold (P < 5 × 10(−8)) from MRC-IEU Consortium and evaluated these related to PF. MR estimates were calculated using the inverse-variance weighted (IVW) method and multiple sensitivity analyses were further performed. RESULTS: Genetical liability to HGS was positively causally associated with forced vital capacity (FVC) and forced expiratory volume in one second (FEV1), but not with FEV1/FVC. In addition, there was positive causal association between RHGS and FVC (OR=1.519; 95% CI, 1.418-1.627; P=8.96E-33), and FEV1 (OR=1.486; 95% CI, 1.390-1.589; P=3.19E-31); and positive causal association between LHGS and FVC (OR=1.464; 95% CI, 1.385-1.548; P=2.83E-41) and FEV1 (OR=1.419; 95% CI, 1.340-1.502; P=3.19E-33). Nevertheless, no associations were observed between RHGS and FEV1/FVC (OR=0.998; 95% CI, 0.902-1.103; P=9.62E-01) and between LHGS and FEV1/FVC (OR=0.966; 95% CI, 0.861-1.083; P=5.52E-01). Similar results were shown in several sensitivity analyses. CONCLUSION: Our study provides support at the genetic level that HGS is positively causally associated with FVC and FEV1, but not with FEV1/FVC. Interventions for HGS in PF impairment deserve further exploration as potential indicators of PF assessment. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12890-023-02720-0.