Corrigendum

Introduction Fabry disease (FD) is an X-linked sphingolipidosis characterized by pathogenic variants in the GLA gene, which affect alpha-galactosidase A activity. Studies on body composition in FD patients have shown conflicting results. There is significant variability in weight and body mass index (BMI) among FD patients, likely due to chronic inflammatory status, gastrointestinal and renal disturbances, inactivity, exercise intolerance, and medications. However, there is no study that evaluate body composition using dual-energy X-ray absorptiometry (DXA) in FD patients compared to healthy controls. Objectives To assess body composition by DXA in Brazilian male FD patients and to compare the findings with those of healthy controls (HC). Additionally, to correlate the DXA measurements with Lyso-Gb3 concentrations, the main substrate accumulated in the disease. Method Fifteen genotype-confirmed classic male FD patients and 20 sex/age-matched HC had body composition evaluated by DXA. Lyso-Gb3 levels were obtained for FD patients. Results Mean age was 44.2 ± 12.3 years and 44.9 ± 11.8 years in FD patients and HC, respectively (p = 0.87). BMI in FD patients (22.9 ± 3.7 kg/m2) was not statistically different from HC (24.8 ± 2.4 kg/m2, p = 0.07). Appendicular lean mass was lower in FD patients (20,324 ± 2808 g) than HC (25529 ± 2535 g, p < 0.0001), as well as the appendicular lean mass index (7.24 ± 0.89 vs. 8.72 ± 0.80 kg/m2, p < 0.0001). There were no differences between patients and controls regarding fat mass or fat percentage. Lyso-Gb3 levels were inversely correlated with lean mass (r = - 0.63, p = 0.01), fat mass (r = - 0,68, p = 0.005) and fat percentage (r = - 0.64, p = 0.01). Conclusion Adult FD patients in this cohort had lower lean mass than controls. Lyso-Gb3 accumulation is associated with lower values of lean mass, fat mass and fat percentage in FD patients.

Sarcopenia is associated with poor health outcomes such as disability, institutionalization, and mortality. Efforts to manage sarcopenia clinically have been hindered by challenges in determining how to ascertain sarcopenia status correctly. The objective of this project was to assess the agreement between the different methods of ascertaining sarcopenia recommended by expert groups. Cross-sectional study of baseline data (2011-2015) from the Canadian Longitudinal Study on Aging. Population-based multicenter study of community-dwelling participants. Eligible participants (n = 12,646) aged 65 to 85 living within 25 to 50 km of 11 data collection sites in Canada. The analyses included 10,820 participants with the data required to diagnose sarcopenia. Sarcopenia was operationalized as appendicular lean mass (ALM), ALM and grip strength, ALM and gait speed, and grip strength and gait speed. Within each combination, ALM was adjusted for height squared, weight, body mass index, and the residual of regressing lean mass on height and fat mass. The lowest 20th sex-specific percentile values were used as the cutoffs for low ALM. Low grip strength cutoffs of 35.5 kg for men and 20 kg for women and a gait speed cutoff of .8 m/s were used. The mean age was 73.0 ± 5.6 years, and 51.9% of the sample was male. The agreement (Cohen's κ) between the different combinations of variables used to ascertain sarcopenia status was below .50. Agreement for the different lean mass adjustment techniques ranged from .04 to .76. The combination of variables used to ascertain sarcopenia and many of the ALM adjustment techniques have insufficient agreement to be considered equivalent. This has important clinical implications for the management of sarcopenia because treatments may differ based on how sarcopenia is identified. To improve the clinical utility of sarcopenia, a unified definition of sarcopenia is required.

This study sought to evaluate the associations between changes in glycemic status and changes in total body (TB), trunk, and appendicular fat (FM) and lean mass (LM) in men. A population-based study of men aged 20–66 years at baseline were included in cross-sectional (n = 430) and three-year longitudinal (n = 411) analyses. Prediabetes was defined as fasting glucose 100–125 mg/dL. Type 2 diabetes (T2D) was determined by: self-reported diabetes, current anti-diabetic drug use (insulin/oral hypoglycemic agents), fasting glucose (≥126 mg/dL), or non-fasting glucose (≥200 mg/dL). Body composition was evaluated by dual-energy X-ray absorptiometry. Longitudinal analyses showed that changes in TB FM and LM, and appendicular LM differed among glycemic groups. Normoglycemic men who converted to prediabetes lost more TB and appendicular LM than men who remained normoglycemic (all, p < 0.05). Normoglycemic or prediabetic men who developed T2D had a greater loss of TB and appendicular LM than men who remained normoglycemic (both, p < 0.05). T2D men had greater gains in TB FM and greater losses in TB and appendicular LM than men who remained normoglycemic (all, p < 0.05). Dysglycemia is associated with adverse changes in TB and appendicular LM.

BackgroundRecent genetic evidence supports a causal role for sarcopenia in osteoarthritis, which may be mediated by the occurrence of obesity or changes in circulating inflammatory protein levels. Here, we leveraged publicly available genome-wide association study data to investigate the intrinsic causal relationship between sarcopenia, obesity, circulating inflammatory protein levels, and osteoarthritis.MethodsIn this study, we used Mendelian randomization analyses to explore the causal relationship between sarcopenia phenotypes (Appendicular lean mass [ALM], Low hand-grip strength [LHG], and usual walking pace [UWP]) and osteoarthritis (Knee osteoarthritis [KOA], and Hip osteoarthritis [HOA]). Univariable Mendelian randomization (UVMR) analyses were performed using the inverse variance weighted (IVW) method, MR-Egger, weighted median method, simple mode, and weighted mode, with the IVW method being the primary analytical technique. Subsequently, the independent causal effects of sarcopenia phenotype on osteoarthritis were investigated using multivariate Mendelian randomization (MVMR) analysis. To further explore the mechanisms involved, obesity and circulating inflammatory proteins were introduced as the mediator variables, and a two-step Mendelian randomization analysis was used to explore the mediating effects of obesity and circulating inflammatory proteins between ALM and KOA as well as the mediating proportions.ResultsUVMR analysis showed a causal relationship between ALM, LHG, UWP and KOA [(OR = 1.151, 95% CI: 1.087–1.218, P = 1.19 × 10–6, PFDR = 7.14 × 10–6) (OR = 1.215, 95% CI: 1.004–1.470; P = 0.046, PFDR = 0.055) (OR = 0.503, 95% CI: 0.292–0.867; P = 0.013, PFDR = 0.027)], and a causal relationship between ALM, UWP and HOA [(OR = 1.181, 95% CI: 1.103–1.265, P = 2.05 × 10–6, PFDR = 6.15 × 10–6) (OR = 0.438, 95% CI: 0.226–0.849, P = 0.014, PFDR = 0.022)]. In the MVMR analyses adjusting for confounders (body mass index, insomnia, sedentary behavior, and bone density), causal relationships were observed between ALM, LHG, UWP and KOA [(ALM: OR = 1.323, 95%CI: 1.224- 1.431, P = 2.07 × 10–12), (LHG: OR = 1.161, 95%CI: 1.044- 1.292, P = 0.006), (UWP: OR = 0.511, 95%CI: 0.290- 0.899, P = 0.020)], and between ALM and HOA (ALM: OR = 1.245, 95%CI: 1.149- 1.348, P = 7.65 × 10–8). In a two-step MR analysis, obesity was identified to play a potential mediating role in ALM and KOA (proportion mediated: 5.9%).ConclusionsThe results of this study suggest that decreased appendicular lean mass, grip strength, and walking speed increase the risk of KOA and decreased appendicular lean mass increases the risk of HOA in patients with sarcopenia in a European population. Obesity plays a mediator role in the occurrence of KOA due to appendicular lean body mass reduction.

This study aimed to verify which of the different cutoff points of low muscle mass (LMM) based on appendicular lean mass (ALM) is associated with osteoporosis in postmenopausal women (PMW). Cross-sectional study. PMW (n = 355) were classified for the presence of osteoporosis (score <-2.5 standard deviations) at the femoral neck and lumbar spine and LMM (three cutoff points: ALM < 15 kg; ALM/height2 [ALM index] <5.67 kg/m2 and ratio between ALM and body mass index [ALMBMI] <0.512). After adjustments for confounding factors, binary logistic regression showed that ALM and ALM index were associated with osteoporosis at the lumbar spine (odds ratio [OR] = 5.3 [95% CI: 2.3-12.5] and OR = 2.5 [95% CI: 1.0-6.2], respectively) and only ALM was associated with osteoporosis at the femoral neck (OR = 16.1 [95% CI: 4.1-62.5]). When women were classified as having osteoporosis in at least one site, only ALM was associated with osteoporosis (OR = 7.7 [95% CI: 3.3-15.6]). There was no association between ALMBMI and osteoporosis. The predictive value of ALM for osteoporosis decreased after BMI or height were included as a covariate in the model. Absolute ALM (<15 kg) seems to be the most suitable for predicting osteoporosis based on LMM in PMW.

BackgroundEvidence indicates a negative link between glucosamine and age-related cognitive decline and sarcopenia. However, the causal relationship remains uncertain. This study aims to verify whether glucosamine is causally associated with cognitive function and sarcopenia.MethodForty-eight genetic variants linked to glucosamine use were extracted from the MRC-IEU consortium. Besides, we gathered cognition proxy indicators [cognitive performance and fluid intelligence score (FIS)], and sarcopenia-related indicators, namely, appendicular lean mass (ALM), whole body fat-free mass (WBFM), low hand grip strength, facial aging (FA), moderate to vigorous physical activity levels, usual walking pace and DNA methylation GrimAge acceleration from the large publicly available genome-wide association studies. Initially, Mendelian randomization (MR) analyses were conducted to ascertain the causal impact of glucosamine on cognition and sarcopenia-related traits. Subsequently, the two-step MR and multivariable MR (MVMR) were employed to examine whether any mediators causally mediated the observed associations.ResultMR analysis indicated that glucosamine was associated with increased cognitive performance (p = 8.46E-04), FIS (p = 7.50E-04), ALM (p = 6.45E-08), WBFM (p = 1.97E-03), usual walking pace (p = 2.55E-07), and moderate to vigorous physical activity levels (p = 3.29E-03), but associated with decreased FA risk (p = 3.77E-05) and DNA methylation GrimAge acceleration (p = 0.001). However, there were no significant causal associations between glucosamine and low hand grip strength. Multivariable MR showed that glucosamine continued to have a significant effect on cognitive performance, FIS, ALM, WBFM, usual walking pace, and moderate to vigorous physical activity levels after controlling for osteoarthritis (OA) and body mass index (BMI) (p &amp;lt; 0.05). We further found that C-reactive protein levels (CRP) may mediate the association of glucosamine and ALM, WBFM, usual walking pace, and physical activity (p &amp;lt; 0.05), and basal metabolic rate (BMR) may mediate the association of glucosamine and cognitive performance, FIS, ALM, WBFM, and usual walking pace (p &amp;lt; 0.05).ConclusionRegular glucosamine use enhances cognitive function and postpones sarcopenia for preserving the functional capacities necessary, and the impact of glucosamine on cognition and sarcopenia could be partially attributed to the mediation of BMR and CRP.

ObjectivesTo evaluate the prevalence of sarcopenia (SP) and associated factors in patients with rheumatoid arthritis (RA).Methods159 women (mean age 58.7±8.8) with confirmed RA according to ACR/EULAR criteria (2010) were enrolled....

It was recently hypothesized the existence of "cardiac-skeletal muscle axis." However, the relationship between skeletal muscle mass (SMM) and left ventricular mass (LVM) has never been investigated in the specific group of older individuals with low skeletal mass and physical performance. We tested this hypothesis in the SPRINT-T (Sarcopenia and Physical Frailty IN older people: multicomponenT Treatment strategies Trial) population using LVM as independent variable and SMM as dependent variable. SMM was assessed by dual-energy X-ray absorptiometry scan and expressed as appendicular lean mass (ALM), and LVM was estimated through echocardiography. Low ALM was defined according to Foundation for the National Institutes of Health Sarcopenia Project criteria, and Short Physical Performance Battery (SPPB) was used to assess physical performance. The population consisted of 100 persons (33 men and 67 women), aged 70 years or older (mean age = 79 ± 5 years) with low ALM and SPPB ranged between 3 and 9, suggestive of physical frailty. Charlson Comorbidity Index median score was 0. Mean value of LVM was 193 ± 67 g, indexed LVM/body surface area (LVM/BSA) was 112 ± 33 g/m2, and cardiac output (CO) was 65 ± 19 L/min. ALM was strongly and positively correlated with LVM (r = 0.54602; P < .0001), LVM/BSA (r = 0.30761; P < .002), CO (r = 0.49621; P < .0001), body mass index (BMI) (r = 0.52461; P < .0001), sex (r = 0.77; P < .001), fat mass (r = 0.38977; P < .0001), and hemoglobin (Hb) (r = 0.26001; P < .01). In the multivariate analysis, LVM (β = .019 ± .005; P < .0001), CO (β = .038 ± .016; P = .019), BMI (β = .286 ± .051; P < .0001), and Hb (β = .544 ± .175; P = .0025) remained associated to ALM. In a sample of older persons with low muscle mass and physical performance, LVM was positively and significantly correlated with ALM, independently from blood pressure, physical activity, and other potential confounders. Future studies are needed to address the effect of interventions targeting LVM and SMM.

Longitudinal changes in appendicular skeletal muscle mass among asthma and COPD subjects: The Rotterdam Study

Prognostic value of muscle mass assessed by DEXA in elderly hospitalized patients

Associations of accelerometer-determined physical activity and sedentary behavior with sarcopenia and incident falls over 12 months in community-dwelling Swedish older adults

As the human body ages, adverse body composition status such as sarcopenia and obesity become obvious phenotypes which can cause numerous health problems. We aimed to comprehensively investigate the association of sex hormones and body mass components in adult men of various age groups. We analysed national representative population data from the US National Health and Nutrition Examination Survey. Generalized linear model regression analyses were used to evaluate the association between sex hormones (total testosterone [TT], bio-available testosterone [BT], sex hormone-binding globulin [SHBG], estradiol [E2] and testosterone to estradiol ratio [T/E ratio]) and body mass components (weight, body mass index (BMI), total lean mass, appendicular lean mass, bone mineral content, total fat and trunk fat). The collection and testing time of blood samples were not fixed and there was no strict fasting, but in subsequent analysis we used statistical methods to minimize the impact of random testing. After screening for inclusion and exclusion, 3759 male participants aged 20-85 years old were included in this study. Higher levels of TT, SHBG, BT and T/E ratios were significantly associated with higher total lean mass, appendicular lean mass and bone mineral content, while lower weight, BMI, total fat and trunk fat. For E2 levels in men, we found an opposite trend, with higher E2 levels significantly associated with lower total lean mass and appendicular lean mass, and higher weight, BMI, total fat and trunk fat. Notably, in subgroup analysis, the results showed that there were significant interaction effects of age and smoking history in the association between sex hormones and body mass components. Higher TT levels, BT levels, SHBG levels and T/E ratios are associated with lower body weight and improved body composition in young adult men (characterized by higher lean body mass, higher bone density and lower fat mass). The relationship is especially pronounced among relatively young, nonsmoking men.

Weight change and risk of the foundation of National Institute of Health Sarcopenia-defined low lean mass: Data from the National Health and Nutrition examination surveys 1999-2004.

Appendicular lean mass (ALM) trajectory in males with Duchenne muscular dystrophy (DMD) has potential applicability for treatment and research and has not been characterized. This chart review included longitudinal data on 499 males with DMD receiving glucocorticoids and 693 controls, ages 5 to 22.9 y. ALM (kg) was measured by dual energy x-ray absorptiometry (DXA). Appendicular lean mass index (ALMI, kg/m2 ) was calculated for height adjustment. Reference centiles were generated using data from healthy controls, and ALM and ALMI Z-scores were calculated for patients with DMD. Generalized linear models were used to estimate median Z-scores by age and functional mobility status (FMS) score. ALM velocity by age was modeled using superimposition, translation and rotation (SITAR). Compared to controls, males with DMD had lower ALM from an early age. ALMI Z-scores dropped below 0 at age 8 y or FMS of 2, and below -2.0 at age 13 y or FMS of 3 (P < .05). Age at peak ALM velocity was similar in both groups, but the magnitude was higher in controls (3.5 vs. 0.7 kg/y, P < .0001). Patients with DMD had a transient loss of ALM around age 12 y, an increase at age 14 y, then a further decline at age 16 y, remaining low thereafter. Males with DMD have progressive decline in lean mass with age and worsening functional mobility. DXA measurement of ALM may be useful for monitoring lean mass status in patients with DMD, providing valuable information for individual treatment plans and research endeavors.

Low lean mass and cognitive impairment are both age-related diseases. In addition, these conditions share many risk factors. However, the association between them has been controversial in recent years. To investigate the association between low lean mass and cognitive performance in U.S. adults using NHANES data from 1999 to 2002. A total of 2550 participants were identified in the National Health and Nutrition Examination Survey Database (1999-2002). The independent variable was low lean mass, and the dependent variable was cognitive performance. Men and women were classified as having low lean mass if appendicular lean mass (ALM) adjusted for BMI (ALMBMI) was < 0.789 and < 0.512, respectively. Cognitive performance was assessed using the Digit Symbol Substitution Test (DSST). Higher scores on the DSST indicated better cognitive performance. The covariates included sex, age, race, poverty income ratio, comorbidity index, educational level, physical activity and smoking status. For the primary outcome, our multivariate linear regression analysis indicated that participants without low lean mass were associated with better cognitive performance (β = 1.50; 95% CI [0.12-2.89]). Subgroup analysis results indicated that the association was similar in sex, age, race, poverty income ratio, comorbidity index, educational level, physical activity and smoking status. Participants without low lean mass were associated with better cognitive performance. We might be able to improve cognitive performance by treating low lean mass, thus providing an opportunity for intervention at a younger age.