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Objectives Evidence on the association between frailty and quality of life (QoL) is mostly limited to cross-sectional studies. Thus, the temporal order and potential mechanisms of this association are largely unknown. Our study examines both the directionality of this association and the role of cognition in this association in longitudinal data. Methods Cross-lagged panel models were employed to examine the temporal relationship between frailty and QoL, as well as cognition's role among 19,649 older adults in Europe. Frailty, QoL, and cognition were assessed using the health deficit index, CASP-12, and 3 standard cognitive tests, respectively. Results We observed a bidirectional association between frailty and QoL and their dynamics. High initial levels of frailty predicted poorer QoL later and vice versa (β = −0.151 and −0.052, p <.001). The early change in frailty predicted the late change in QoL, and vice versa (β = −0.093 and −0.061, p <.001). Frailty or its early change drives this interrelationship. Cognition at Wave 5 partially mediated frailty's effect at Wave 4 on QoL at Wave 6 (indirect effect: β = −0.005, 95% confidence interval = −0.006, −0.004). Discussion Our findings supported that early prevention of frailty and its risk factors may have more influential protective effects on later physical and mental health, as well as the need for ongoing screening for mental health in aging population. Also, the maintenance of good cognitive performance may help interrupt this possible vicious cycle linking frailty and QoL decline. [ABSTRACT FROM AUTHOR]

Background This study aimed to investigate the associations between ultra-processed food (UPF) consumption and the risk of cardiovascular disease and all-cause mortality in the UK Biobank Cohort. Methods This observational prospective study evaluated 60 298 participants aged 40 years or older. We used the NOVA classification system to identify and categorize UPF. The associations among UPF consumption, cardiovascular disease (CVD) incidence and all-cause mortality were estimated using multivariable Cox proportional hazards models. Dose–response analysis of UPF consumption and CVD incidence and mortality was performed using a restricted cubic spline. Results After a median follow-up of 10.9 years, 6048 participants (10.0%) experienced CVD events, and 5327 (8.8%) and 1503 (2.5%) experienced coronary heart and cerebrovascular diseases, respectively. There were 2590 (4.3%) deaths, of which 384 (0.6%) deaths were caused by CVD. A higher intake of UPF was associated with a higher risk of CVD and all-cause mortality (all P  <   0.001). A higher intake of UPF was associated with a higher risk of CVD [hazard ratio (HR) = 1.17, 95% confidence interval (CI): 1.09–1.26], coronary heart disease (HR = 1.16, 95% CI: 1.07–1.25), cerebrovascular disease (HR = 1.30, 95% CI: 1.13–1.50) and all-cause mortality (HR = 1.22, 95% CI: 1.09–1.36). The association of UPF consumption with a range of CVD incidents and all-cause mortality was monotonic (all P for non-linearity > 0.30). Conclusions A higher proportion of UPF consumption was associated with CVD and all-cause mortality. Thus, actions to limit UPF consumption should be incorporated into the CVD and all-cause mortality prevention recommendations. [ABSTRACT FROM AUTHOR]