Causal Roles of Lifestyle, Psychosocial Characteristics, and Sleep Status in Sarcopenia: A Mendelian Randomization Study

Abstract

Background Many studies reported that lifestyle, psychosocial characteristics, and sleep status related to sarcopenia, while few studies provided evidence of causal relationships between them. Methods The data used in our study were from UK Biobank, FinnGen Release 8, and large genome-wide association study meta-analyses. Two-sample MR was conducted to identify the causal associations of 21 traits of lifestyle, psychosocial characteristics, and sleep status with six traits of sarcopenia. Benjamini–Hochberg correction was performed to reduce the bias caused by multiple tests. Risk factor analyses were performed to explore the potential mechanism behind the exposures. Results MR analyses after adjustment proved the causal roles of coffee intake, education years, smoking, leisure screen time, and moderate-to-vigorous intensity physical activity during leisure time (MVPA) in sarcopenia was proven while providing no significant evidence for causal roles for carbohydrates intake, protein intake, alcohol, and sleep status in sarcopenia. Conclusions Our results strongly support that coffee intake, education years, smoking, leisure screen time, and MVPA played significantly causal roles in sarcopenia, which may provide new intervention strategies for preventing the development of sarcopenia.

Mapping the causal associations of cytokines with sarcopenia and aging traits: Evidence from bidirectional Mendelian randomization

“…Sensitivity analysis was performed to evaluate the strength of each IV in relation to the exposure of interest. The F statistics were calculated using the following formula: F = R 2 × ( N − 2)/(1 − R 2 ), where R 2 was obtained using the following formula 4 : R 2 = [2 × BETA2 × EAF × (1 − EAF)]/[2 × BETA2 × EAF × (1 − EAF) + 2 × SE(BETA)2 × N × EAF × (1 − EAF)]. In this formula, BETA represents the genetic effects on exposures, EAF represents the effect allele frequency, SE(BETA) represents the standard error of the genetic effects and N represents the sample size.…”

“…3 The aetiology of sarcopenia is multifactorial, involving a complex interplay of age-related changes in hormonal, inflammatory and metabolic pathways, as well as lifestyle factors such as smoking, physical inactivity and poor nutrition. 4 Chronic low-grade inflammation, known as inflammaging, has been identified as a key risk factor for the development and progression of sarcopenia, promoting muscle protein breakdown and impairing muscle regeneration. 5 In recent years, inflammaging has emerged as a key concept in the field of gerontology.…”

Standardizing trait selection in Mendelian randomization studies concerning sarcopenia

“…Though GWAS for overall sarcopenia trait may be unavailable, researchers always try to explore the causal factors for sarcopenia by using sarcopenia-associated traits. 1,2,4 The selection of sarcopenia-associated traits was various: Some studies may include only one trait, 5 and some may choose up to six or more 2 ; some may only select parts of sarcopenia trait, for example, only including muscle strength and muscle quantity traits while ignoring the physical performance traits. 6 The sarcopenia-associated trait selection needs to be standardized to better reflect the sarcopenia status comprehensively.…”