Background: Sarcopenia is defined as the loss of muscle mass and strength. Despite the seriousness of this disease, a single diagnostic criterion has not yet been established. Few studies have reported the prevalence of sarcopenia globally, and there is a high level of heterogeneity between studies, stemmed from the diagnostic criteria of sarcopenia and the target population. The aims of this systematic review and meta‐analysis were (i) to identify and summarize the diagnostic criteria used to define sarcopenia and severe sarcopenia and (ii) to estimate the global and region‐specific prevalence of sarcopenia and severe sarcopenia by sociodemographic factors.Methods: Embase, MEDLINE, and Web of Science Core Collections were searched using relevant MeSH terms. The inclusion criteria were cross‐sectional or cohort studies in individuals aged ≥18 years, published in English, and with muscle mass measured using dual‐energy x‐ray absorptiometry, bioelectrical impedance, or computed tomography (CT) scan. For the meta‐analysis, studies were stratified by diagnostic criteria (classifications), cut‐off points, and instruments to assess muscle mass. If at least three studies reported the same classification, cut‐off points, and instrument to measure muscle mass, they were considered suitable for meta‐analysis. Following this approach, 6 classifications and 23 subgroups were created. Overall pooled estimates with inverse‐variance weights obtained from a random‐effects model were estimated using the metaprop command in Stata.Results: Out of 19 320 studies, 263 were eligible for the narrative synthesis and 151 for meta‐analysis (total n = 692 056, mean age: 68.5 years). Using different classifications and cut‐off points, the prevalence of sarcopenia varied between 10% and 27% in the studies included for meta‐analysis. The highest and lowest prevalence were observed in Oceania and Europe using the European Working Group on Sarcopenia in Older People (EWGSOP) and EWGSOP2, respectively. The prevalence ranged from 8% to 36% in individuals <60 years and from 10% to 27% in ≥60 years. Men had a higher prevalence of sarcopenia using the EWGSOP2 (11% vs. 2%) while it was higher in women using the International Working Group on Sarcopenia (17% vs. 12%). Finally, the prevalence of severe sarcopenia ranged from 2% to 9%.Conclusions: The prevalence of sarcopenia and severe sarcopenia varied considerably according to the classification and cut‐off point used. Considering the lack of a single diagnostic for sarcopenia, future studies should adhere to current guidelines, which would facilitate the comparison of results between studies and populations across the globe.

Physical activity is associated with lower cardiovascular and all-cause mortality. However, the effects of different exercise modalities on arterial stiffness are currently unclear. Our objectives were to investigate the effects of exercise modalities (aerobic, resistance or combined) on pulse wave velocity (PWV) and augmentation index (AIx), and to determine whether the effects on these indices differed according to the participants' or exercise characteristics. We searched the Medline, Embase and Cochrane Library databases from inception until April 2014 for randomized controlled trials lasting ≥4 weeks investigating the effects of exercise modalities on PWV and AIx in adults aged ≥18 years. Forty-two studies (1627 participants) were included in this analysis. Aerobic exercise improved both PWV (WMD: −0.63 m/s, 95% CI: −0.90, −0.35) and AIx (WMD:−2.63%, 95% CI: −5.25 to −0.02) significantly. Aerobic exercise training showed significantly greater reduction in brachial-ankle (WMD: −1.01 m/s, 95% CI: −1.57, −0.44) than in carotid-femoral (WMD: -0.39 m/s, 95% CI: −0.52, −0.27) PWV. Higher aerobic exercise intensity was associated with larger reductions in AIx (β: −1.55%, CI −3.09, 0.0001). In addition, aerobic exercise had a significantly larger effect in reducing PWV (WMD:−1.0 m/s, 95% CI: −1.43, −0.57) in participants with stiffer arteries (PWV ≥8 m/s). Resistance exercise had no effect on PWV and AIx. There was no significant effect of combined exercise on PWV and AIx. We conclude that aerobic exercise improved arterial stiffness significantly and that the effect was enhanced with higher aerobic exercise intensity and in participants with greater arterial stiffness at baseline. Database registration: CRD42014009744,.

Imprecise measurement of physical activity variables might attenuate estimates of the beneficial effects of activity on health-related outcomes. We aimed to compare the cardiometabolic risk factor dose-response relationships for physical activity and sedentary behaviour between accelerometer- and questionnaire-based activity measures. Physical activity and sedentary behaviour were assessed in 317 adults by 7-day accelerometry and International Physical Activity Questionnaire (IPAQ). Fasting blood was taken to determine insulin, glucose, triglyceride and total, LDL and HDL cholesterol concentrations and homeostasis model-estimated insulin resistance (HOMA_IR). Waist circumference, BMI, body fat percentage and blood pressure were also measured. For both accelerometer-derived sedentary time (50% lower for the IPAQ-reported compared to the accelerometer-derived measure (p<0.0001 for both interactions). The relationships for moderate-to-vigorous physical activity (MVPA) and risk factors were less strong than those observed for sedentary behaviours, but significant negative relationships were observed for both accelerometer and IPAQ MVPA measures with glucose, and insulin and HOMA_IR values (all p<0.05). For accelerometer-derived MVPA only, additional negative relationships were seen with triglyceride, total cholesterol and LDL cholesterol concentrations, BMI, waist circumference and percentage body fat, and a positive relationship was evident with HDL cholesterol (p = 0.0002). Regression coefficients for HOMA_IR, insulin and triglyceride were 43–50% lower for the IPAQ-reported compared to the accelerometer-derived MVPA measure (all p≤0.01). Using the IPAQ to determine sitting time and MVPA reveals some, but not all, relationships between these activity measures and metabolic and vascular disease risk factors. Using this self-report method to quantify activity can therefore underestimate the strength of some relationships with risk factors.

Psoriasis is a common inflammatory skin disease that has been reported to be associated with obesity. We aimed to investigate a possible causal relationship between body mass index (BMI) and psoriasis. Following a review of published epidemiological evidence of the association between obesity and psoriasis, mendelian randomization (MR) was used to test for a causal relationship with BMI. We used a genetic instrument comprising 97 single-nucleotide polymorphisms (SNPs) associated with BMI as a proxy for BMI (expected to be much less confounded than measured BMI). One-sample MR was conducted using individual-level data (396,495 individuals) from the UK Biobank and the Nord-Trøndelag Health Study (HUNT), Norway. Two-sample MR was performed with summary-level data (356,926 individuals) from published BMI and psoriasis genome-wide association studies (GWASs). The one-sample and two-sample MR estimates were meta-analysed using a fixed-effect model. To test for a potential reverse causal effect, MR analysis with genetic instruments comprising variants from recent genome-wide analyses for psoriasis were used to test whether genetic risk for this skin disease has a causal effect on BMI. Published observational data showed an association of higher BMI with psoriasis. A mean difference in BMI of 1.26 kg/m² (95% CI 1.02–1.51) between psoriasis cases and controls was observed in adults, while a 1.55 kg/m² mean difference (95% CI 1.13–1.98) was observed in children. The observational association was confirmed in UK Biobank and HUNT data sets. Overall, a 1 kg/m² increase in BMI was associated with 4% higher odds of psoriasis (meta-analysis odds ratio [OR] = 1.04; 95% CI 1.03–1.04; P = 1.73 × 10⁻⁶⁰). MR analyses provided evidence that higher BMI causally increases the odds of psoriasis (by 9% per 1 unit increase in BMI; OR = 1.09 (1.06–1.12) per 1 kg/m²; P = 4.67 × 10⁻⁹). In contrast, MR estimates gave little support to a possible causal effect of psoriasis genetic risk on BMI (0.004 kg/m² change in BMI per doubling odds of psoriasis (−0.003 to 0.011). Limitations of our study include possible misreporting of psoriasis by patients, as well as potential misdiagnosis by clinicians. In addition, there is also limited ethnic variation in the cohorts studied. Our study, using genetic variants as instrumental variables for BMI, provides evidence that higher BMI leads to a higher risk of psoriasis. This supports the prioritization of therapies and lifestyle interventions aimed at controlling weight for the prevention or treatment of this common skin disease. Mechanistic studies are required to improve understanding of this relationship.

Dementia is associated with a high burden of dependency and disability. Physical frailty (hereafter referred to as frailty) is a multisystem dysregulation that has been identified as a risk factor for dementia. The aim of this study was to examine the association of frailty and its individual components with all-cause dementia incidence in a cohort of UK adults. Participants in UK Biobank with data available for dementia incidence and without any form of dementia at baseline were included in this prospective study. Frailty was defined using a modified version of the frailty phenotype based on five individual components (weight loss, tiredness, physical activity, gait speed, and grip strength), with participants classified as pre-frail if they fulfilled one or two criteria or frail if they fulfilled three or more. Associations between frailty and dementia incidence were investigated using Cox proportional hazard models adjusted for sociodemographic factors, lifestyle factors, and morbidity count. The population attributable fraction was also estimated. Of 502 535 participants in UK Biobank, 143 215 met the inclusion criteria and were included in our analyses. 68 500 (47·8%) of the participants were pre-frail and 5565 (3·9%) were frail. During a median follow-up period of 5·4 years, 726 individuals developed dementia. Compared with non-frail individuals, the risk of dementia incidence was increased for individuals with pre-frailty (hazard ratio 1·21 [95% CI 1·04-1·42]) and frailty (1·98 [1·47-2·67]) in the fully adjusted model. Of the five components used to define frailty, weight loss (1·31 [1·09-1·58]), tiredness (1·48 [1·18-1·86]), low grip strength (1·38 [1·17-1·63]), and slow gait speed (1·55 [1·22-1·96]) were independently associated with incident dementia. Based on population attributable fraction analyses, in the study sample, pre-frailty and frailty accounted for 9·9% and 8·6% of dementia cases, respectively. Individuals with pre-frailty and frailty were at a higher risk of dementia incidence even after adjusting for a wide range of confounding factors. Early detection and interventions for frailty could translate into prevention or delayed onset of dementia. None.