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Abstract <p>Observational studies link handgrip strength (HGS, a key sarcopenia sign) and visual impairment (VI), but their causality is unknown. We used bidirectional Mendelian Randomization (MR)—a genetic method to test causality—to explore if VI affects HGS, and if body mass index (BMI) plays a role. We used genetic data from large groups: FinnGen (218 792 people, VI), UK Biobank (461 089 people, HGS), and EBI/MRC-IEU (532 396 people, BMI). We focused on age-related VI (cataract, glaucoma, high eye pressure), used genetic markers linked to these traits to test causality, and did additional MR to check VI’s direct effect on HGS and BMI’s potential role as a middle factor. MR showed more severe VI tied to lower HGS: genetic predisposition to cataract reduced normal HGS chance by 48% (OR = 0.52, 95% CI 0.28–0.97, <i>P</i> = 0.04); genetic glaucoma susceptibility linked to a small but reliable HGS reduction (OR = 0.99, 95% CI 0.991–0.998, <i>P</i> &lt; 0.001)—small per person but meaningful for older adults due to glaucoma’s high prevalence. Further analyses confirmed glaucoma’s direct harm to HGS. BMI had a weak mediating role: it explained 11% of cataract’s effect and 44% of glaucoma’s effect, but its actual impact was very small. These confirm age-related VI is a modifiable risk factor for older adults’ functional decline. Age-related VI—especially cataract and glaucoma—causes lower HGS. Vision assessment should be part of geriatric care to prevent sarcopenia and frailty, key to older adults’ health.</p>

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Visual Impairment and Handgrip Strength in Aging: Evidence from Bidirectional Mendelian Randomization

  • 期刊论文

  • 发表日期：

    2025年9月1日

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  • Sh. Ran,
  • Y. Peng,
  • S. Wang,
  • Y. Li,
  • B. Liu

摘要

Abstract

Observational studies link handgrip strength (HGS, a key sarcopenia sign) and visual impairment (VI), but their causality is unknown. We used bidirectional Mendelian Randomization (MR)—a genetic method to test causality—to explore if VI affects HGS, and if body mass index (BMI) plays a role. We used genetic data from large groups: FinnGen (218 792 people, VI), UK Biobank (461 089 people, HGS), and EBI/MRC-IEU (532 396 people, BMI). We focused on age-related VI (cataract, glaucoma, high eye pressure), used genetic markers linked to these traits to test causality, and did additional MR to check VI’s direct effect on HGS and BMI’s potential role as a middle factor. MR showed more severe VI tied to lower HGS: genetic predisposition to cataract reduced normal HGS chance by 48% (OR = 0.52, 95% CI 0.28–0.97, P = 0.04); genetic glaucoma susceptibility linked to a small but reliable HGS reduction (OR = 0.99, 95% CI 0.991–0.998, P < 0.001)—small per person but meaningful for older adults due to glaucoma’s high prevalence. Further analyses confirmed glaucoma’s direct harm to HGS. BMI had a weak mediating role: it explained 11% of cataract’s effect and 44% of glaucoma’s effect, but its actual impact was very small. These confirm age-related VI is a modifiable risk factor for older adults’ functional decline. Age-related VI—especially cataract and glaucoma—causes lower HGS. Vision assessment should be part of geriatric care to prevent sarcopenia and frailty, key to older adults’ health.