With considerable variation including potential sex-specific differential rate of skeletal muscle loss, identifying modifiable factors for sarcopenia will be pivotal to guide targeted interventions. This study seeks to identify clinical and biological correlates of sarcopenia in community-dwelling older adults, with emphasis on the role of anabolic and catabolic stimuli, and special reference to gender specificity. In this crosssectional study involving 200 community-dwelling and functionally independent older adults aged ≥50 years, sarcopenia was defined using the Asian Working Group for Sarcopenia criteria. Comorbidities, cognitive and functional performance, physical activity and nutritional status were routinely assessed. Biochemical parameters included haematological indices, lipid panel, vitamin D level, anabolic hormones [insulin-like growth factor-1 (IGF-1), free testosterone (males only)] and catabolic markers [inflammatory markers (interleukin-6, Creactive protein) and myostatin]. Multiple logistic regression was performed to identify independent predictors for sarcopenia. Age was associated with sarcopenia in both genders. Malnutrition conferred significantly higher odds for sarcopenia in women (OR=5.71, 95 % CI 1.13-28.84.44, p=0.035) while higher but acceptable range serum triglyceride was protective in men (OR=0.05, 95 % CI 0.00-0.52, p=0.012). Higher serum myostatin independently associated with higher odds for sarcopenia in men (OR=1.11, 95 % CI 1.00-1.24, p=0.041). Serum IGF-1 was significantly lower amongst female sarcopenic subjects, with demonstrable trend for protective effect against sarcopenia in multiple regression models, such that each 1 ng/ml increase in IGF-1 was associated with 1 % decline in odds of sarcopenia in women (p=0.095). Our findings support differential pathophysiological mechanisms for sarcopenia that, if corroborated, may have clinical utility in guiding sex-specific targeted interventions for community-dwelling older adults.

Notwithstanding the increasing body of evidence that links social determinants to health outcomes, social frailty is arguably the least explored among the various dimensions of frailty. Using available items from previous studies to derive a social frailty scale as guided by the Bunt social frailty theoretical framework, we aimed to examine the association of social frailty, independently of physical frailty, with salient outcomes of mood, nutrition, physical performance, physical activity, and life–space mobility. We studied 229 community-dwelling older adults (mean age 67.22 years; 72.6% females) who were non-frail (defined by the FRAIL criteria). Using exploratory factor analysis, the resultant 8-item Social Frailty Scale (SFS-8) yielded a three-factor structure comprising social resources, social activities and financial resource, and social need fulfilment (score range: 0–8 points). Social non-frailty (SNF), social pre-frailty (SPF), and social frailty (SF) were defined based on optimal cutoffs, with corresponding prevalence of 63.8%, 28.8%, and 7.4%, respectively. In logistic regression adjusted for significant covariates and physical frailty (Modified Fried criteria), there is an association of SPF with poor physical performance and low physical activity (odds ratio, OR range: 3.10 to 6.22), and SF with depressive symptoms, malnutrition risk, poor physical performance, and low physical activity (OR range: 3.58 to 13.97) compared to SNF. There was no significant association of SPF or SF with life–space mobility. In summary, through a theory-guided approach, our study demonstrates the independent association of social frailty with a comprehensive range of intermediary health outcomes in more robust older adults. A holistic preventative approach to frailty should include upstream interventions that target social frailty to address social gradient and inequalities.

No abstract

No abstract

Our proposed method based on machine learning produces accurate tissue quantification and showed an effective use of large information provided by the four contrast images from Dixon MRI.

No abstract

No abstract

ObjectiveSarcopenic obesity (SO) is associated with poorer physical outcomes and functional status in the older adult. A proinflammatory milieu associated with central obesity is postulated to enhance muscle catabolism. We set out to examine associations of the chemokine monocyte chemoattractant protein-1 (MCP-1) in groups of older adults, with sarcopenia, obesity, and the SO phenotypes.MethodsA total of 143 community dwelling, well, older adults were recruited. Cross-sectional clinical data, physical performance, and muscle mass measurements were collected. Obesity and sarcopenia were defined using revised National Cholesterol Education Program (NCEP) obesity guidelines and those of the Asian Working Group for Sarcopenia. Serum levels of MCP-1 were measured by enzyme-linked immunosorbent assay (ELISA).ResultsIn all, 25.2% of subjects were normal, 15.4% sarcopenic, 48.3% obese, and 11.2% were SO. The SO groups had the lowest appendicular lean mass, highest percentage body fat, and lowest performance scores on the Short Physical Performance Battery and grip strength. The MCP-1 levels were significantly different, with the highest levels found in SO participants (P<0.05).ConclusionSignificantly raised MCP-1 levels in obese and SO subjects support the theory of chronic inflammation due to excess adiposity. Longitudinal studies will reveal whether SO represents a continuum of obesity causing accelerated sarcopenia and cardiovascular events, or the coexistence of two separate conditions with synergistic effects affecting functional performance.